| Application Area | Gene | KO Mice | cKO Mice | Description |
|---|---|---|---|---|
| Cardiovascular Disease(CVD) | Apoe（Atherosclerosis） | Apoe KO Mice | Apoe cKO Mice | Apolipoprotein E (APOE) is a plasma protein involved in cholesterol transportation. In humans, there are three major alleles (epsilon 2, epsilon 3, and epsilon 4) that related to Atherosclerosis and Alzheimer's disease (AD). Of these three types, epsilon 2 is the least common one. |
| Cardiovascular Disease(CVD) | Ldlr | Ldlr KO Mice | Ldlr cKO Mice | The plasma level of cholesterol increased 2-fold in LDLR deficient mice than the wild type, and low-density lipoprotein (LDL) receptor is more sensitive to high cholesterol. In addition, the LDLR gene in vivo overexpression in mice can inhibit high cholesterol caused by a high-fat diet. LDLR gene-deficient mouse model has significant clinical values in the research in diabetic nephropathy, atherosclerosis, hyperlipidemia, and hyperglycemia. |
| Cardiovascular Disease(CVD) | F9 | None | None | F9 deficiency can cause coagulation disorders in mice, and this model can be adopted in the research of coagulation disorders, F9 gene function, and gene therapy methods. |
| Cardiovascular Disease(CVD) | Apcs | Apcs KO Mice | Apcs cKO Mice | APCS is the coding gene of the serum amyloid P component (SAP), and SAP is the name of the amyloid P component (AP) in plasma. AP makes up 14% of the dry mass of amyloid deposits and is thought to be an important contributor to the pathogenesis of a related group of diseases called the Amyloidoses. APCS knockout mice can be used in the research of Atherosclerosis, Alzheimer's disease, and type II diabetes. |
| Cardiovascular Disease(CVD) | Mydgf | Mydgf KO Mice | Mydgf cKO Mice | Myeloid-derived growth factor (MYDGF, also known as C19orf10) is named based on its identification as a secreted monocyte/macrophage-derived mediator of cardiac repair following myocardial infarction in mice. |
| Cardiovascular Disease(CVD) | ApoB | ApoB KO Mice | ApoB cKO Mice | The gene polymorphism of Apolipoprotein (Apo) can influence the lipid metabolism, thus AOPB that closely related to the cardiovascular and cerebrovascular diseases is the coding gene of Apolipoprotein. Current research suggests that the change of blood lipids may be related to the absence or ectopicity of one or more of the genetic sites of Apob that leading to abnormal blood lipids. Relevant to lipid metabolism research and cardiovascular disease research. |
| Cardiovascular Disease(CVD) | Sirt7 | None | None | SIRT7 knockout mice undergo a reduction in mean and maximum life spans and tend to develop heart hypertrophy and inflammatory cardiomyopathy. |
| Cardiovascular Disease(CVD) | Sirt1 | None | None | Sirt1 plays a protective role in the pathological processes of atherosclerosis, myocardial ischemia, cardiac hypertrophy, diabetic cardiomyopathy, and other diseases. |
| Cardiovascular Disease(CVD) | Sirt2 | Sirt2 KO Mice | Sirt2 cKO Mice | During ischemia/reperfusion (I/R) injury, necrosis commonly occurs. RIP1 is deacetylated in a SIRT2-dependent fashion. Studies have found that Sirt2 deficient heart or heart that has been treated with a Sirt2 drug inhibitor will be basically protected from ischemic injury. Therefore, SIRT2 as an important regulator of programmed necrosis, is a promising target for drug action in preventing necrotic injury. |
| Cardiovascular Disease(CVD) | Ldlr | Ldlr KO Mice | Ldlr cKO Mice | The plasma level of cholesterol increased 2-fold in LDLR deficient mice than the wild type, and low-density lipoprotein (LDL) receptor is more sensitive to high cholesterol. In addition, the LDLR gene in vivo overexpression in mice can inhibit high cholesterol caused by a high-fat diet. LDLR gene-deficient mouse model has significant clinical values in the research in diabetic nephropathy, atherosclerosis, hyperlipidemia, and hyperglycemia. |
| Metabolic Disease | Pnliprp1 | Pnliprp1 KO Mice | Pnliprp1 cKO Mice | Fat metabolism, obesity, diabetes. Pnliprp1gene deficient mice will develop obesity after grown up and show some symptoms of early diabetes. Early glucose tolerance and insulin resistance phenomenon in obese and diabetic patients will be observed in adult mice. |
| Metabolic Disease | Ghsr | Ghsr KO Mice | Ghsr cKO Mice | The role of GHS-R(Growth Hormone Secretagogue Receptor) is thought to be in regulating energy homeostasis and body weight. Knockout of GHSR improves obesity and glucose metabolic disorders, suggesting a crucial role of ghrelin activity in insulin resistance. GHSR knockout may cause homeostatic control of energy imbalance, which can be used for related research on the digestive system, metabolism, diabetes and so on. |
| Metabolic Disease | Lepr（dbMice） | Lepr KO Mice | Lepr cKO Mice | Leptin receptor mutation mice are an important tool for research of diseases such as leptin resistance, insulin resistance, obesity, and type II diabetes. This mouse is also commonly called db mouse. |
| Metabolic Disease | Lep（ob/obMice） | Lep KO Mice | Lep cKO Mice | Mutation or deficient in leptin receptors can lead to severe obesity, hypogonadism caused by obesity, and closely related to the development of type II diabetes. Studies also found leptin receptors relevant to cardiovascular function as well. This mouse is also commonly called db mouse. |
| Metabolic Disease | Cpt1a | None | None | Cpt1a (Carnitine Palmitoyltransferase 1a) gene knockout heterozygous mice have certain changes in fasting plasma glucose (FPG) and serum-free fatty acid (FFA) concentrations. Circadian rhythm, fatty acid metabolism, CPT(Carnitine Palmitoyl Transferase) deficiency and so on. |
| Metabolic Disease | Sidt2 | Sidt2 KO Mice | Sidt2 cKO Mice | Plasma glucose, insulin secretion, diabetes and so on. Sidt2 is a lysosomal membrane protein that closely related to glucose metabolism. Studies have shown that Sidt2 deficiency can cause severe skeletal muscle disease. Sidt2 knockout mouse may influence the lung morphology, which can be presented as necrosis, capillary congestion, thickening of the basement membrane, and a massive amount of inflammatory infiltrate of cells and induce lung injury. Abnormal high expression in gastric oncology may participate in the occurrence and development of gastric oncology through influencing cell differentiation. |
| Metabolic Disease | Sirt5 | None | None | Sirt5 is used in the study of the influence of life span and sirtuin and food limitation on the ammonia degradation and CPS1 activation. Mice with deletion of SIRT5 show elevated ammonia levels after a prolonged fast, whereas, in contrast, mice overexpressing SIRT5 show increased CPS1 activity, suggesting one of the functions of SIRT5 may be to regulate the urea cycle. SIRT5 also interacts with and deacetylates cytochrome C. |
| Metabolic Disease | Sirt3 | None | None | SIRT3 protein expression is significantly lower in tumor samples from women with breast oncology compared to normal breast tissue. Therefore, the SIRT3 knockout model can be used in the research of ER/PR-positive mammary tumors development. Besides, this mouse model can also be used for studying the function of fatty acid oxidation in diabetes, cardiovascular disease, steatosis, fasting, cold exposure, and longevity. |
| Metabolic Disease | Fgf21 | Fgf21 KO Mice | Fgf21 cKO Mice | To study the function of fibroblast growth factor 21 (Fgf21) in the pathogenesis of metabolic diseases such as non-alcoholic fatty liver disease (NAFLD), obesity and diabetes. The functions of Fgf21 are mainly manifested in glucose metabolism, lipid metabolism, and insulin resistance. Fgf21 liver-specific knockout mice occur symptoms like fatty liver and hyperlipidemia, along with decreased serum ketones concentrations. |
| Metabolic Disease | Fto | Fto KO Mice | Fto cKO Mice | FTO gene is an obesity-associated protein, also known as obese gene. Obesity gives rise to the occurrence of type II diabetes, heart diseases, oncology, and other diseases. The m6A methylation modification is mediated by a multi-protein complex. The components of this complex are currently known to include METTL3, METTL14, and WTAP, while the responsibility of demethylase FTO and ALKBH5 is erasing the methylation modification group. |
| Metabolic Disease | Adora1 | Adora1 KO Mice | Adora1 cKO Mice | The adenosine Adora 1 receptor is one member of the adenosine receptor group of GPCRs (G Protein-Coupled Receptors) with adenosine as endogenous ligand. Adora 1 is the key gene in regulating lipid deposition. |
| Metabolic Disease | Nr1h4 | Nr1h4 KO Mice | Nr1h4 cKO Mice | FXR(farnesoid X receptor)/Nr1h4 is a ligand-activated transcription factor that exists in various different tissues, which belongs to the metabolic nuclear receptor. And this factor plays an important role in bile acid metabolism, lipid metabolism, glucose metabolism, liver protection, growth of intestinal bacteria and the occurrence and development of atherosclerosis. |
| Metabolic Disease | Cth | Cth KO Mice | Cth cKO Mice | This model is used in the research of metabolism, liver function, kidney function and other diseases. |
| Metabolic Disease | Mfn2 | None | None | Mfn2 knockout can promote the occurrence of inflammation in the mice model, the increased triglyceride accumulation, and can contribute to the occurrence of hepatic fibrosis and liver oncology. While after increasing the Mfn2 expression in the liver through the adoption of the AAV virus receptor, symptoms of Nonalcoholic fatty liver disease (NAFLD) were alleviated. |
| Neurological Disease | Mecp2 | None | None | Rett syndrome, autism. |
| Neurological Disease | Pink1 | Pink1 KO Mice | Pink1 cKO Mice | Pink 1 gene is the Park6 gene, which is the first and the only protein of various PD-related genes that linking the mitochondrial dysfunction to the pathogenesis of PD. |
| Neurological Disease | Park2（Parkinson） | Park2 KO Mice | Park2 cKO Mice | Park2 gene, also named as Parkin gene (PRKN), is expressed as Parkin protein. In 1998, Kitada et al found that the mutation of this gene could lead to autosomal recessive juvenile Parkinson’s disease. It has been reported in the literature that the expression of Park2 plays an important role in maintaining the nervous system function. Parkin enhances cell survival by suppressing both mitochondria-dependent and -independent apoptosis. Thus, Parkin was defined as the tumor suppressor with antiglycolytic and antioxidant abilities. The mutation is associated with mitochondrial dysfunction, which contributes to the neuronal cell death and aberrant metabolism in tumorigenesis. |
| Neurological Disease | Park7 | Park3 KO Mice | Park3 cKO Mice | Parkinson, DJ-1 gene is the Park7 gene, and its pathogenic mechanism may be the DJ-1 protein level reduction after mutation, which weakens the body's scavenging oxygen free radicals abilities, and eventually causes the damage of oxidative substances to neuronal cells increased. |
| Neurological Disease | Park 8 | None | None | Lrrk2 gene is also known as the Park8 gene, more than 100 kinds of Lrrk2 mutations were found in PD patients. It has been confirmed that around 20 mutation sites are associated with PD, and different mutation sites located in different domains with the apparent region and ethnic difference. Lrrk2 mutation can cause increased protein kinase activity and apoptosis, thereby exerting toxic effects leading to the occurrence of PD. |
| Neurological Disease | Park9 | None | None | Atp13a2 is also known as the Park9 gene. The mutation of this gene has diversity, which affects the transmembrane domain directly or indirectly, leads to the degradation of lysosomes and the formation of toxic aggregates, and induces the degeneration of substantia nigra and the occurrence of PD. |
| Neurological Disease | Park14 | None | None | Pla2g6 gene is also known as the Park14 gene. The mutation of this gene can cause weakened or completely lost of its mitochondrial protective function, therefore lost the oxidative stress damage repairment ability, and leads to axonal degeneration, finally cause PD. |
| Neurological Disease | Park15 | None | None | Fbxo7 gene is also known as the Park15 gene. The mutation of this gene can cause function disorder in its encoded protein Fbxo7, and studies have also reported that PD-related brain imaging examination suggests a large number of substantia nigra (SN) dopamine neurons are lost in the nigrostriatal region. |
| Neurological Disease | Nfe2l2 | Nfe2l2 KO Mice | Nfe2l2 cKO Mice | Nrf2 can regulate the expression of peroxiredoxins, and prevent oxidative damage caused by injury and inflammation. The genetic activation of Nrf2 may promote the development of neoplastic neoplasms and atherosclerosis through increasing the plasma cholesterol levels and cholesterol levels in the liver. This mouse model can be used in various research: age-related macular degeneration, diabetes, Parkinson's disease and oxidative stress in the pathogenesis of other inflammatory degenerative diseases, as well as oncology, multiple sclerosis, liver cirrhosis, atherosclerosis, injury and wound healing research. |
| Neurological Disease | Trem2 | Trem2 KO Mice | Trem2 cKO Mice | TREM2(myeloid cells 2) mutation has increased the risk of neurodegenerative diseases, such as Alzheimer's disease, amyotrophic lateral sclerosis, and Parkinson's disease. The interaction of REM2 with DAP12 (DNAX-activating protein of 12 kDa) in microglia can trigger the phagocytosis of the amyloidogenic Aβ (amyloid-β) and apoptotic neurons of non-inflammation. Mutation in TREM2 impairs the normal proteolytic maturation of proteins, which in turn interferes with phagocytosis, thus lead to the pathogenesis of Alzheimer's disease. |
| Neurological Disease | Adora1 | Adora1 KO Mice | Adora1 cKO Mice | Adoral 1 gene is related to the pathogenesis of schizophrenia. The adenosine A1 receptor is one member of the adenosine receptor group of G protein-coupled receptors with adenosine as endogenous ligand. As a key gene that regulates fat deposition, Adora1 is widely distributed in the central nervous system of the brain, and has a high-density distribution in the cerebral cortex, hippocampus, cerebellum, thalamus, brain stem and bone marrow, is a neurotransmitter of the nervous system. |
| Neurological Disease | Mapt | Mapt KO Mice | Mapt cKO Mice | This model is used for the research of Alzheimer's disease, Pick's disease, and neurofibrillary tangles (NFT) related to other neurological syndromes. |
| Neurological Disease | Apoe（Alzheimer's disease） | Apoe KO Mice | Apoe cKO Mice | Apolipoprotein E (APOE) is a plasma protein involved in cholesterol transportation. In humans, there are three major alleles (epsilon 2, epsilon 3, and epsilon 4) that related to Atherosclerosis and Alzheimer's disease (AD). Of these three types, epsilon 2 is the least common one. |
| Neurological Disease | APP | APP KO Mice | APP cKO Mice | Mutations in the amyloid protein precursor (APP), presenilin-1 (PSEN1), and presenilin-2 (PSEN2) genes are a known cause of familia Alzheimer disease(fAD). |
| Neurological Disease | PSEN1 | / | ||
| Neurological Disease | PSEN2 | PSEN2 KO Mice | ||
| Neurological Disease | GCH1 | None | GCH1 cKO Mice | Guanosine triphosphate cyclohydrolase I (GCH1) mutations are associated with a variety of neuronal disease including dopa-responsive dystonia (DRD), neuropathic pain and Parkinson's disease (PD). GCH1 may play a role in the immune system or amyloid-β–associated metabolic pathway. |
| Neurological Disease | 5-HTT | 5-HTT KO Mice | 5-HTT cKO Mice | Depression phenotype in 5-HTT knockout mouse is related to genetic background, and C57BL/6J mouse corresponds to the non-depressive phenotype unless a repeat stress induction protocol was applied. CD1 mouse is more likely to exhibit behavioral despair and lack of pleasure. The depression phenotype of 129S6 mice is somewhere in between. |
| Neurological Disease | 5-HT4R | None | None | 5-Hydroxytryptamine receptor 4(5-HT4R) is a G protein-coupled receptor, which can regulate gastrointestinal function, eating behavior, learning and memory functions, and widely used in research. More and more studies adopted 5-HT4R as a potential antidepressant target for the excitement of this receptor can produce rapid antidepressant effects. |
| Neurological Disease | MAGE-D1 | MAGE-D1 KO Mice | MAGE-D1 cKO Mice | MAGE-D1 deficient mice exhibit various symptoms in familiar and unfamiliar environments, such as reduced activity, decreased social activity, prolonged FST immobility time, decreased sucrose consumption rate in the sucrose preference experiment, which correspondingly represents depression fatigue, decreased interest, behavioral despair, and lack of pleasure. All these symptoms can be fully or partially reversed by acute and chronic antidepressants. In other behavioral experiments like Elevated Plus Maze, Novel Object Recognition (NOR), hint and related fear conditioning, and Rotor-Rod, no anxiety, recognition disorder and dyskinesia found in MAGE-D1 knockout mice. Besides, the knockdown of MAGE-DI in the prefrontal cortex of adult mice can also exhibit the depressive behavior in MAGE-D1 knockout mice. |
| Neurological Disease | P11 | P11 KO Mice | P11 cKO Mice | P11 has played an important role in various depression pathological and physical related brain regions. P11 knockout mice exhibit depression phenotype and decreased response to antidepressant treatment. |
| Neurological Disease | Akt2 | Akt2 KO Mice | Akt2 cKO Mice | Akt2 deficient mice exhibit decreased activity, increased anxiety, increased depressive behavior, and less exploratory behavior. Akt2 exerts some antidepressant effects and that reduced stimulation of Akt2 may lead to depressive disorders. Research results suggest an involvement of Akt2 in anxiety and depressive behavior in mice and identify Akt2 as a potential therapeutic target for the treatment and prevention of anxiety disorders and depression. |
| Neurological Disease | Trek-1 | Trek-1 KO Mice | Trek-1 cKO Mice | The physiological functions of Trek-1 potassium channels include the regulation of menstrual flow, response to certain physical and chemical stimuli, and the participation in neuroprotection and pain perception activities. Trek-1 deficient mice exhibit antidepressant behavior, while similar antidepressant behavior was observed in wild type mice through the systematic treatment by Trek-1 potassium channels inhibitor. |
| Immunity and imflammation | Fcgr2b | None | None | As a low-affinity immunoglobulin G receptor, FcgRIIß protein inhibits the activation of different effector functions such as phagocytosis, antibody-dependent cytotoxicity, and release of inflammatory mediators. In addition, it is known that this protein takes effect on B cells and mast cells as an inhibitory receptor. This protein is used in the research of feedback inhibition pathways that regulate antibody production, and also for allergic and autoimmune disorders studies. |
| Immunity and imflammation | Fcer1g | Fcer1g KO Mice | Fcer1g cKO Mice | Deficiency in these Fc receptors has brought the functional impairment of macrophages, neutrophils, mast cells, basophils, and NK cells. T cell thymic and peripheral T cell development is normal in mice, which can be adopted for determining the function of Fc receptors that have a similar structure in effector immune response mediation, and the pleiotropic role of the γ chain subunit. The display of different immunodeficiency types makes it suitable for the research in distinguishing the role Fc receptors played in antibody-mediated effector responses, and to evaluate the contribution of effector pathways triggered by IgG and IgE. |
| Immunity and imflammation | CX3CL1 | CX3CL1 KO Mice | CX3CL1 cKO Mice | As the receptor of chemokine Fractalkine (CX3CL1), CX3CR1 was found in monocytes, T cells, NK cells, and neurons, microglia cells, and astrocytes. According to the initial analysis, Cx3cr1 knockout mice on an atherogenic Apoe knockout background exhibit lower susceptibility towards atherosclerosis. The interaction between CX3CL1 and its receptor has played an important role in a series of inflammatory, infection, neurology and neoplastic disease, which is believed to be the new target of disease treatment for humans. |
| Immunity and imflammation | IL-4Ra | IL-4Ra KO Mice | IL-4Ra cKO Mice | The alpha chain of the interleukin 4 receptor (IL-4Ra) is a subunit shared by the IL-4 and IL-13 receptors, which explains their overlapping biological functions. Therefore, in contrast to IL-4 knockout mice, IL-4Ra knockout has inhibited the function of these two cytokines. The parallel study that comparing the immunoreaction of BALB / c IL-4 and IL-4Ra mice has revealed the unique function of IL-13 in an allergic reaction, and the susceptibility towards infections come from Nippostrongylus Brasiliensis, Schistosoma Mansoni, and some strains of Leishmania major parasites. |
| Immunity and imflammation | Flt3l | None | None | FMS-like tyrosine kinase 3 (flt3) ligand (flt3l) is the growth factor of hemopoietic progenitors, which induces the mobilization of hemopoietic progenitors and stem cell in vivo. With promising potential in antineoplastic, flt3l has bright application prospects in anti-infection, radiation protection, allergic diseases treatment, and other aspects. |
| Immunity and imflammation | Ifnar1 | Ifnar1 KO Mice | Ifnar1 cKO Mice | The function of IFNAR mainly depends on its activation of specific signal transduction pathways after binding to interferon, thereby exerting functions like antiviral, immune regulation and antitumor in multiple systems. Recently, research on IFNAR mainly focused on its antiviral effect. Ifnar1 knockout mice lack the function of type I interferon receptor, which results in decreased immunoreaction and increased susceptibility to viral infection. This model can be used for studying the antiviral immune response, interferon stimulation and JAK-STAT signaling. |
| Immunity and imflammation | Nos2 | Nos2 KO Mice | Nos2 cKO Mice | Nitric oxide synthase (iNOS or Nos2) plays a critical role in the host defense of mammals towards infectious agents and tumors. Nos2 knockout mice are suitable for inflammatory disease research, which includes rheumatoid arthritis, inflammatory bowel disease, cardiac allograft rejection, liver toxicity, myocardial ischemia-reperfusion, and septic shock. |
| Immunity and imflammation | Gpr183 | Gpr183 KO Mice | Gpr183 cKO Mice | Gpr183 is also known as EBI2, belongs to the Class A rhodopsin family of G protein-coupled receptors (GPCRs), which can inhibit the Notch1 signaling in the development of normal hematopoietic cells and to promote the endothelial-to-hematopoietic transition. Gpr183 is highly expressed in the chronic lymphoblastic leukemia(CLL), which drives the migration of B cells to the outer follicular region, reduces the germinal center-dependent immune response, lower its secreted levels of IgM and IgG, up-regulates c-MYC oncogene expression, and promotes cell proliferation. Studies have shown that Gpr183 promotes the infiltration of inflammatory cells in colitis, and pr183 gene-deficient mice have reduced susceptibility to colitis. |
| Immunity and imflammation | Tlr2 | Tlr2 KO Mice | Tlr2 cKO Mice | Toll-like receptors (TLRs) family is the major pattern recognition receptors in the innate immune system, most of the identThere are currently 10 members, of which Tlr2 is responsible for the peptidoglycan of the gram-positive bacterium and the membrane lipoprotein infection of treponema pallidum. A variety of studies shown that TLRs activate the pro-inflammatory factors and antimicrobial peptides of the innate immune system through identifying the PAMP of different pathogens, and against the invasion of pathogenic microorganisms, meanwhile, send alert to antigen-presenting cell(APC)， and release inflammatory cytokines and co-stimulator, eventually initiate cellular and humoral adaptive immunity. |
| Immunity and imflammation | Myd88 | Myd88 KO Mice | Myd88 cKO Mice | This model can be used in the research of innate and adaptive immune response，because Myd88 is part of Interleukin-1 receptor (IL-1R), Interleukin-18 receptor (IL-18R) and the majority of TLR signaling pathways that regulate pro-inflammatory reaction. |
| Immunity and imflammation | Rag1（ Immunodeficient Mouse） | Rag1 KO Mice | Rag1 cKO Mice | Immunodeficient mouse, NOD. Deficient in the Rag1 gene (also recombinase reactivating gene 1) and therefore does not develop endogenous mature T or B cells. Subcutaneous inoculation of liver cancer tissue mass and tumor cells to form and grow tumors. |
| Immunity and imflammation | Ripk3 | Ripk3 KO Mice | Ripk3 cKO Mice | The product of this gene is a member of the receptor-interacting protein (RIP) family of serine/threonine protein kinases and contains a C-terminal domain unique from other RIP family members. As a component of the tumor necrosis factor (TNF) receptor-I signaling complex, Ripk3 can induce apoptosis and weakly activates NF-kappaB transcription factor through activating the tumor necrosis factor-α-RIPK1 signaling pathway and its downstream pathways under the influence of stimulus factors such as inflammation, injury, and infection in vivo and in vitro. |
| Immunity and imflammation | Tmem173 | Tmem173 KO Mice | Tmem173 cKO Mice | Stimulator Of Interferon Genes (STING), is also known as Transmembrane Protein 173 (TMEM173). STING has played an important role in the innate immune system. When cell infects intracellular pathogens, STING induces the occurrence of type I interferons such as viruses, mycobacteria, and intracellular parasites. STING-mediated type I interferons prevent infected cells and neighboring cells from partial infection through integrating with cells that secrete it (autocrine signaling) and neighboring cells (paracrine signaling). |
| Immunity and imflammation | Il17a | Il17a KO Mice | Il17a cKO Mice | High-level Il17a cytokines are associated with severe kinds of chronic inflammatory disease, which include rheumatoid arthritis, psoriasis, and multiple sclerosis. Application: autoimmune disease(AD), lung disease, host defense, oncology research, and drug targets. |
| Immunity and imflammation | NLRP1 | None | None | The inflammasome of the NOD-like receptor family pyrin domain containing 1 (NLRP1) is the protein complex integration of NLRP1 after recognizing intracellular pathogen-associated molecular patterns (PAMP) and apoptosis-related speckle-like protein (ASC) and caspases like caspase-1 and Caspase-5. After activation, it promotes the maturation and release of inflammatory factors such as IL-1β, IL-18, and IL-33, and plays an important role in innate immunity. |
| Immunity and imflammation | NLRP3 | None | None | As a significant component of innate immunity, NLRP3 inflammasome plays important role in organic immune response and disease development, its over-activation can cause several major human diseases such as Alzheimer's disease(AD), inflammatory bowel disease(IBD), diabetes and malignant tumors. |
| Immunity and imflammation | NLRP6 | NLRP6 KO Mice | NLRP6 cKO Mice | NLRP6, short for the NOD-like receptor family pyrin domain containing 6, is a protein with a unique function in the NLRs family. NLRP6 is highly expressed in intestine, which can inhibit inflammation and repair damaged intestine. According to research, its deficient expression with inflamed colon and colorectal oncology indicates that NLPR6 could be the potential new targeting treatment of oncology for its function in promoting apoptosis and preventing tumor development. |
| Immunity and imflammation | NLRP10 | NLRP10 KO Mice | NLRP10 cKO Mice | NLRP10 can promotes the NOD1 mediated immune reponse as well as inhibit the activation of NLRP3 inflammasome. |
| Immunity and imflammation | NLRP12 | NLRP12 KO Mice | NLRP12 cKO Mice | Some research showed that NLPR12 is closely associated with inflammatory bowel disease (IBD), and it may play a dual function in the development of enteritis. Increased colonic inflammation and antimicrobial peptide production in Nlrp12-/- mice may promote dysbacteriosis. After high-fat feeding, Nlrp12 mice display dysbiosis marked by increased obesity-associated Erysipelotrichaceae but reduced Lachnospiraceae and clostridium required for short-chain fatty acid (SCFA) synthesis. |
| Immunity and imflammation | TLRs Family | TLR1-9；TLR11-13 KO Mice | TLR1-9；TLR11-13 cKO Mice | TLRs are currently known to be involved in the pathogenesis of autoimmune, chronic inflammation and infectious diseases. |
| Immunity and imflammation | IL-10 | IL-10 KO Mice | IL-10 cKO Mice | Immunosuppression, anti-inflammatory |
| Immunity and imflammation | IL-19 | IL-19 KO Mice | IL-19 cKO Mice | Skin development and immune regulation |
| Immunity and imflammation | IL-20 | IL-20 KO Mice | IL-20 cKO Mice | Skin development, inflammation, hematopoiesis |
| Immunity and imflammation | IL-22 | None | None | Acute phase response, innate immunity |
| Immunity and imflammation | IL-24 | IL-24 KO Mice | IL-24 cKO Mice | Cell apoptosis, skin function, inflammatory cascade |
| Immunity and imflammation | IL-26 | None | None | Mucous membrane and skin immunity |
| Immunity and imflammation | IL-28、IL-29 | None | None | Antiviral immunity |
| Tumor (oncology） | Apc | Apcs KO Mice | Apcs cKO Mice | APC(adenomatosis polyposis coli) gene-encoded protein is a tumor suppressor protein, functions as an antagonist of the Wnt signaling pathway. Apc-β-catenin-TCF mediated Wnt pathway disorder is the main cause of familial adenomatous polyposis coli (FAP). |
| Tumor (oncology） | Smad4 | None | None | Smad4 can be used to study cell proliferation and tumor suppression. For example, pancreas specific-knockout can be used in the research of anomalies of pancreatic ducts and pancreatic cancer. |
| Tumor (oncology） | Brca1 | None | None | Breast cancr, cancer research |
| Tumor (oncology） | P53 | P53 KO Mice | P53 cKO Mice | As a star tumor-suppressive gene, p53 regulates the cell cycle and prevents cell canceration, which is known as "guardian of the genome", and also one of the tumor-suppressive genes that with the most frequent mutation. P53 mutation was observed in 50% of oncology types, and the remaining types are frequently finding other ways to inactivate P53. |
| Tumor (oncology） | Nfe2l2 | Nfe2l2 KO Mice | Nfe2l2 cKO Mice | Nrf2 regulates the expression of antioxidant proteins and prevents oxidative damage caused by injury and inflammation. The genetic activation of Nrf2 can be achieved through increasing plasma cholesterol levels and cholesterol concentration in the liver, to promote the development of neoplastic neoplasm and atherosclerosis. This mouse model can be used to study oxidative stress in the pathogenesis of age-related macular degeneration, diabetes, Parkinson's disease(PD), and other inflammatory degenerative diseases as well as studies of cancer, multiple sclerosis, liver cirrhosis, atherosclerosis, injury and wound healing. |
| Tumor (oncology） | Sirt3 | Sirt3 KO Mice | Sirt3 cKO Mice | Endogenous SIRT3 is a soluble protein located in the mitochondrial matrix, and a large amount of published literature indicates that there is a strong mechanism link between mitochondrial function, aging, and carcinogenesis. Compared with normal breast tissue, Sirt3 expression is lower in tumor samples from women with breast cancer. Therefore, the Sirt3 knockout model can be used to study the development of ER / PR-positive breast tumors. In addition, this model can also be used to study the role of fatty acid oxidation in diabetes, cardiovascular disease, steatosis, fasting, cold exposure, and longevity. |
| Tumor (oncology） | Ifnar1 | Ifnar1 KO Mice | Ifnar1 cKO Mice | The function of IFNAR mainly depends on its activation of specific signal transduction pathways after binding to interferon, thereby exerting antiviral, immune regulation and antitumor functions in multiple systems. Recent research on this gene mainly focused on antiviral efficacy. Ifnar1 knockout mice lack the role of type I interferon(IFN) receptor, which causes a decrease in immune response and an increase in susceptibility to viral infections. This model can be used to study antiviral immune response, interferon stimulation and JAK-STAT signaling. |
| Tumor (oncology） | Ythdf3 | Ythdf3 KO Mice | Ythdf3 cKO Mice | This model is used to study m6A and its corresponding functions, such as stem cell differentiation, piRNA, lncRNA, susceptible gene, circRNA, tumor, miRNA methylation, exosome miRNA and so on. |
| Tumor (oncology） | Ythdf1 | Ythdf1 KO Mice | Ythdf1 cKO Mice | Due to the versatility of m6A in various physiological processes, it has relations with a large number of human diseases. This model can be used to study m6A and its corresponding functions, such as stem cell differentiation, piRNA, lncRNA, susceptible gene, circRNA, tumor, miRNA methylation, exosome miRNA and so on. |
| Tumor (oncology） | Prkn(帕金森） | Prkn KO Mice | Prkn cKO Mice | This model can be used to simulate the most common exon3 deficiency mutation among patients with autosomal recessive juvenile Parkinson's disease, and to study Parkinson's disease, dopamine regulation, substantia nigra striatum function, mitochondrial function, tumor, and other neurobiological topics. |
| Tumor (oncology） | Il17a | Il17a KO Mice | Il17a cKO Mice | High-level Il17a cytokines are associated with severe kinds of chronic inflammatory disease, which include rheumatoid arthritis, psoriasis, and multiple sclerosis. Application: autoimmune disease(AD), lung disease, host defense, oncology research, and drug targets. |
| Tumor (oncology） | Per2 | Per2 KO Mice | Per2 cKO Mice | Human PER2 is involved in the sleep disorder and oncology formation of humans. Decreased PER2 expression is observed in many tumor cells in vivo, which indicates that the necessity of PER2 in normal activities, while the lower levels of this gene can promote the development of the tumor. |
| Tumor (oncology） | Pten | None | None | PTEN protein can inhibit the occurrence and development of tumors through antagonizing the activity of tyrosine kinase and other phosphorylases. It is the first tumor suppressor gene with the activity of alkaline phosphatase, and it's closely related to tumorigenesis as a tumor suppressor gene after P53 and Rb gene, the main mechanism of PTEN is the main negative regulator factor of PI3K/Akt pathway. In addition, PTEN protein can indirectly inhibit the activity of insulin-mediated phosphoinositol -3 kinase by dephosphorylating the third phosphoric acid of IP3 specifically, while IP3 is the second important messanger in the insulin-regulated cell growth signaling pathway, which shows that PTEN protein plays an important role in this pathway. |
| Tumor (oncology） | kars | None | None | As the main sub-type in the RAS gene family, KRAS triggers various fatal tumors in humans, such as lung, colon and pancreatic cancer. However, for the complexity of KARS signaling pathway regulation and resistance of its mutant tumor to clinical drugs, therefore, there are no effective drugs of methods in treating KRAS mutant tumors clinically. |
| Tumor (oncology） | Rb | Rb KO Mice | Rb cKO Mice | tumor suppressor gene (PTEN) |
| Tumor (oncology） | p16 | p16 KO Mice | p16 cKO Mice | tumor suppressor gene (PTEN) |
| Tumor (oncology） | nm23 | / | / | tumor suppressor gene (PTEN) |
| Tumor (oncology） | TP53 （P53） |
P53 KO Mice | P53 cKO Mice | P53 is a gate-kepper that prevent normal cells turn into oncocytes. |
| Tumor (oncology） | EGFR （ErbB1） |
EGFR KO Mice | EGFR cKO Mice | EGFR is the most important target of tumor-targeted therapy, and its mutation can largely influence the effectiveness of multiple targeted therapies. |
| Tumor (oncology） | HER2（ErbB2） | / | / | HER2 gene is a significant biomarker in breast and gastric oncology-targeted therapy. |
| Tumor (oncology） | ALK | ALK KO Mice | ALK cKO Mice | For the ALK gene, the generation of fusion gene mutation is an important form of oncogene mutation. The mutated ALK protein is widely involved in activated downstream signaling pathways. These signaling pathways are directing cell proliferation, apoptosis resistance, promotion of angiogenesis, and induce cancer eventually. |
| Tumor (oncology） | BRAF | None | None | BRAF is a targeted gene that related to melanoma. |
| Genitourinary system | kif18A | None | None | Kif18A knockout homozygous male mice exhibits infertility, testicular atrophy and sperm loss. |
| Genitourinary system | Mettl3 | Mettl3 KO Mice | Mettl3 cKO Mice | The m6A modification mediated by METTL3 plays a significant role in biorhythm, DNA damage response (DDR），regulation of stem cell self-renewal and pluripotency, parent-zygote transformation, neuro-regulation and sex determination in drosophila, various biological processes and ontogenesis development of eukaryotes such as early embryonic development of mice. The knockout of Mettl3 can cause the death of mice embryo. |
| Genitourinary system | Mettl14 | Mettl14 KO Mice | Mettl14 cKO Mice | Germ cell-specific Mettl3 or Mettl14 knockout with Vasa-Cre in mice can bring the loss of m6A, then cause proliferation of spermatogonial stem cells (SSCs) and translation dysfunction of differentiation-associated gene transcript, eventually result in the depletion of spermatogonial stem cells (SSCs). |
| Genitourinary system | Alkbh5 | None | Alkbh5 cKO Mice | Alkbh5-deficient m6A demethylase male mice exhibit phenotypes like testicle decrescent, spermatogenesis abnormality, sperm motility abnormality, while obviously increase of primary and secondary spermatocytes, significantly decrease of the number of pachytene spermatocytes and mature sperm are detected in the seminiferous tubule developing to Ⅶ period, along with cell apoptosis. |
| Genitourinary system | NLRP2 | NLRP2 KO Mice | NLRP2 cKO Mice | Nlrp2 gene was needed in the development of an early embryo in mice. |
| Genitourinary system | NLRP4 | NLRP4a、NLRP4f、NLRP4b KO Mice | NLRP4a、NLRP4b、NLRP4e、NLRP4f cKO Mice | NLRP4 in mice has been duplicated during gene evolution, a total of 7 genes from Nlrp4a to Nlrp4g were identified so far. Studies have shown that these 7 Nlrp4 genes have similar expression profiles, which are expressed in oocytes and early embryos in the mouse, while NLRP4 protein does not affect the process of oocyte maturation, but mainly plays a role in early embryonic development. |
| Genitourinary system | NLRP5 | None | None | NLPR5 plays a vital role in the early embryonic development of mice. |
| Genitourinary system | NLRP7 | None | None | The human NLRP7 gene is expressed in oocytes and early embryos. Gene mutation cause changes in the encoded protein, and furtherly leading to abnormal development in the earlier human embryonic period. |
| Genitourinary system | NLRP8 | None | None | / |
| Genitourinary system | NLRP9 | NLRP9 KO Mice | NLRP9 cKO Mice | NLRP9b model available |
| Genitourinary system | NLRP11 | None | None | / |
| Genitourinary system | NLRP13 | None | None | / |
| Genitourinary system | NLRP14 | NLRP14 KO Mice | NLRP14 cKO Mice | The silencing of the NLRP14 gene from zygotes is known to generate various degrees of developmental arrest during early embryogenesis and cause developmental failure. Besides, the NLRP14 gene also expresses in the sperms of humans and mouse, the mutation of this gene in the human will cause spermatogenic failure. If NLRP14 mutation happens on humans, it will lead to Infertility. |
| Bone Diseases | Tnfrsf11b | Tnfrsf11b KO Mice | Tnfrsf11b cKO Mice | Encoded by Tnfrsf11b gene, Osteoprotegerin(Opg) knockout mouse model (short in "osteoporosis mouse") exhibits definite osteoporosis symptoms. |
| Bone Diseases | BMP-2 （BMP-2A) |
None | None | 1)Regulates bone and cartilage formation during embryonic development. 2)Regulates bone morphogenesis. 3)Induces mesenchymal precursor cells to differentiate into osteoblasts. 4)Regulates the apoptosis cell signal. 5)Expressed in lung, spleen, and colon. |
| Bone Diseases | BMP-3 （BMP-3A) |
BMP-3 KO Mice | BMP-3 cKO Mice | 1)Regulates bone and cartilage formation. 2)Functioned as chemical attractions. 3)Induces the synthesis and secretion of TGF-β1 by monocytes. 4)Expressed in lungs, ovaries and small intestine. |
| Bone Diseases | BMP-3B (GDF-10) |
BMP-3B KO Mice | BMP-3B cKO Mice | 1)Induces cartilage osteogenesis. 2)Expressed in cerebellum, lungs, pancreas, testicles and femur. |
| Bone Diseases | BMP-4 （BMP2B） |
None | None | 1)Function as the developmental regulator. 2)Mesoderm formation during mediation, bone induction, lower limb development, bone fracture repair, tooth development and so on. 3)Regulates the formation of myelin sheaths. 4)Induces the formation of embryonic hematopoietic tissue. 5)Expressed in lungs and kidneys. |
| Bone Diseases | BMP-5 | None | None | 1)Regulates the bone formation during embryonic development. 2)Expressed in lungs and liver. |
| Bone Diseases | BMP-6 （VGR） |
BMP-6 KO Mice | BMP-6 cKO Mice | 1)Regulates bone and cartilage formation. 2)Induces mesenchymal precursor cells to differentiate into osteoblasts. 3)Higher concentration in fetal cartilage. |
| Bone Diseases | BMP-7 （OP-1 ） |
None | None | 1)Induces cartilage and bone formation. 2)Induces the lens and glomerulus formation. 3)Osteoinductive factor (OIF) of epithelial osteogenesis. 4)Regulates the steady-state internal bone environment and calcium concentration. 5)Expressed in brains, kidneys, and bladder. |
| Bone Diseases | BMP-12 （GDF-7, CDMP-3） |
None | None | 1)Induces cartilage formation. 2)Promotes the formation of tendon and ligament, and repair after injury. |
| Bone Diseases | BMP-13 （ GDF-6, CDMP-2） |
BMP-13 KO Mice | BMP-13 cKO Mice | 1)Induces cartilage formation. 2)Promotes the formation of tendon and ligament, and repair after injury. 3)Expressed in long bones. |
| Bone Diseases | BMP-14 （ GDF-6, CDMP-2） |
None | None | 1)Induces cartilage formation. 2)Improves the healing of tendon and bone formation. 3)The neurotrophic factor (BDNF) of dopaminergic neurons. 4)Expressed in long bones. |
| Bone Diseases | FGF3 (Int2) |
FGF3 KO Mice | FGF3 cKO Mice | Bone development |
| m6A DNA methylation | Mettl3 | Mettl3 KO Mice | Mettl3 cKO Mice | METTL3 and METTL14 in the METTL family are studied more than others. The m6A modification mediated by METTL3 plays a significant role in biorhythm, DNA damage response (DDR），regulation of stem cell self-renewal and pluripotency, parent-zygote transformation, neuro-regulation and sex determination in drosophila, various biological processes and ontogenesis development of eukaryotes such as early embryonic development of mice. The knockout of Mettl3 can cause the death of mice embryo, and the in vivo biology function of Mettl3-mediated m6A RNA modification in tissue development is largely unknown in mammals. For germ cell-specific( (Vasa-Cre) Mettl3 knockout mice (Mettl3 cKO) model, the ablation of Mettl3 in germ cells severely inhibited spermatogonial differentiation and blocked the initiation of meiosis in mice, resulting in male infertility. Specific inactivation of Mettl3 in the central nervous system (CNS) can cause severe dyskinesia or even death in mice during lactation. |
| m6A DNA methylation | Mettl14 | Mettl14 KO Mice | Mettl14 cKO Mice | Germ cell-specific Mettl3 or Mettl14 knockout with Vasa-Cre in mice can bring the loss of m6A, then cause proliferation of spermatogonial stem cells (SSCs) and translation dysfunction of differentiation-associated gene transcript, eventually result in the depletion of spermatogonial stem cells (SSCs). Combined deletion of Mettl3 and Mettl14 will impair the translation of haploid-specific genes for spermiogenesis, and finally result in spermatogenesis arrest. Specificl inactivation of Mettl14 in central nervous system (CNS)in mice can cause severe impact on its cerebral cortical development. |
| m6A DNA methylation | Ythdf1 | Ythdf1 KO Mice | Ythdf1 cKO Mice | YTHDF Family is the most popular research object in "reader" for it participates in the translation and degradation of protein extranuclear. YTHDF1 protein, mainly binding to the m6A site of mRNA, it plays an essential role in brain development, dopamine secretion, synaptogenesis, and other processes. |
| m6A DNA methylation | Ythdf2 | / | Ythdf2 cKO Mice | YTHDF2 is the first protein being identified as the reader of m6A. YTHDF2-mediated degradation of m6A-containing mRNA is also the first aspect that known by humankind in the influence of m6A on the fate of mRNA. |
| m6A DNA methylation | Ythdf3 | Ythdf3 KO Mice | Ythdf3 cKO Mice | Together with YTHDF1 and YTHDF2, YTDHF3 plays a critic role in speeding up the metabolism of m6A-mediated mRNA in the cytoplasm. All these 3 YTHDF proteins can influence the m6A RNA DNA methylation related basic biology process through integration and collaboration. |
| m6A DNA methylation | FTO | FTO KO Mice | FTO cKO Mice | FTO disorder is relevant to obesity, brain malformations and growth retardation, while m6A plays an important role in these diseases as a regulator. |
| ADMET （Pharmacokinetics） |
Slco1a/1b Family | Slco1a1、Slco1a4、Slco1a5、Slco1a6、Slco1b2、Slco1c1 KO Mice |
Slco1a1、Slco1a4、Slco1a5、Slco1a6、Slco1b2、Slco1c1 cKO Mice | Slco1a/1b family used to call as OATPSlco1a/1b family. OATP promotes the sodium independent intake transport of multiple organic endogenous and exogenous compounds, such as, bile acid, steroid, thyroid hormone(TH）and its conjugate, and many drugs and toxins, which is helpful in studying the contribution of Slco1a / 1b family in these processes. |
| ADMET （Pharmacokinetics） |
Abcb1a | Abcb1a KO Mice | Abcb1a cKO Mice | Encoded p-glycoprotein 3 is a multidrug resistance gene. P-glycoprotein 3 actively squeezes out multiple drugs from cells and attaches multiple drug resistance to tumor cells. Without the protection function of p-glycoprotein 3, this model exhibits functional defects in the blood-brain barrier. Abcb1a and Abcb1b dual KO Mice are suitable for central nervous system research, including neurotoxicology, drug transport, oral bioavailability, and multidrug resistance research. |
| ADMET （Pharmacokinetics） |
Abcb1b | Abcb1b KO Mice | Abcb1b cKO Mice | Encoded p-glycoprotein 1 is a multidrug resistance gene. Abcb1a and Abcb1b dual KO Mice are suitable for central nervous system research, including neurotoxicology, drug transport, oral bioavailability, and multidrug resistance research. |
| ADMET （Pharmacokinetics） |
Abcc1 | Abcc1 KO Mice | Abcc1 cKO Mice | ATP-binding cassette protein transport-related protein 1(MRP1, ABCCl) is a multidrug resistance protein, which can identify, transport and discharge substrate(drugs) that incorporated with glutathione conjugates. This model can be used to study the function of ATP-dependent transport protein in mediating inflammatory response and testing drug disposition. |
| ADMET （Pharmacokinetics） |
Abcg2 | Abcg2 KO Mice | Abcg2 cKO Mice | Bcrp actively transports various anticancer drugs when expressing in cancer cells, which can cause multi-drug resistance (MDR), and this model can be used to study the in vivo drug disposition and immunity of ATP-dependent transporter. |
| ADMET （Pharmacokinetics） |
Cyp2c | Cyp2c29、Cyp2c66、Cyp2c70、Cyp2c44、Cyp2c50、Cyp2c65、Cyp2c54、Cyp2c55 KO Mice | Cyp2c29、Cyp2c66、Cyp2c70、Cyp2c44、Cyp2c50、Cyp2c65、Cyp2c54、Cyp2c55 cKO Mice | In humans, CYP2C metabolic enzymes up to 30% in the marketed drugs, which is helpful in analyzing the contribution of the Cyp2c family in total bioavailability of drugs. |
| ADMET （Pharmacokinetics） |
Cyp3a | Cyp3a11、Cyp3a13、Cyp3a57 KO Mice | Cyp3a11、Cyp3a13、Cyp3a57 cKO Mice | In humans, CYP3A metabolic enzymes exist in most drugs, which is helpful in analyzing the contribution of the Cyp3a family in total bioavailability of drugs. |
| ADMET （Pharmacokinetics） |
Cyp2d | Cyp2d10、Cyp2d22、Cyp2d26、Cyp2d34 KO Mice | Cyp2d10、Cyp2d22、Cyp2d26、Cyp2d34 cKO Mice | In humans, CYP2D6 metabolic enzymes account for 25% of the marketed drugs, which is helpful in analyzing the contribution of the Cyp2d family in total bioavailability of drugs. |
| ADMET （Pharmacokinetics） |
Cyp1a1 | Cyp1a1 KO Mice | Cyp1a1 cKO Mice | Cytochrome P450 monooxygenases are the major enzyme system for drug metabolism in humans, among which CYP1A1 in charge of estrogen and multiple exogenous as an important metabolic enzyme. As an extrahepatic enzyme, CYP1A1 is widely distributed in extrahepatic tissues such as the lung, kidney, and gastrointestinal tract. It is involved in the metabolism of hydrocarbon carcinogens. As the important constructional material of environmental chemical carcinogens, PAHs(polycyclic aromatic hydrocarbons) cause cancer after metabolized by CYP1A1 into active intermediates, and the main carcinogenic target organs are lung and skin. This model can be used to study the relevance between CYP1A1 genetic polymorphisms and tumor susceptibility. |
| ADMET （Pharmacokinetics） |
Cyp1a2 | Cyp1a2 KO Mice | Cyp1a2 cKO Mice | As an important cytochrome P450 enzyme, CYP1A2 plays critical role in drug metabolism, and the process of activation of pretoxicants and precarcinogens. |
| ADMET （Pharmacokinetics） |
Nr1i2 | Nr1i2 KO Mice | Nr1i2 cKO Mice | Encoded nuclear receptor PXR(pregnane X receptor), can be used to define the influence of PXR towards CYP induction, therefore give definition to pharmacokinetics, drug toxicity and efficacy, used to study xenobiotics metabolism, cholestasis and hepatotoxicity. Related gene: Car, Ahr |
| ADMET （Pharmacokinetics） |
Nr1i3 | Nr1i3 KO Mice | Nr1i3 cKO Mice | Encoded nuclear receptor CAR(constitutive androstane receptor), can be used to define the influence of CAR towards CYP induction, therefore give definition to pharmacokinetics, drug toxicity and efficacy. Related gene: Car, Ahr |
| ADMET （Pharmacokinetics） |
Ahr | None | Ahr cKO Mice | Mice AHR(aryl hydrocarbon receptor) gene, can be used to define the influence of AHR towards CYP induction, therefore give definition to pharmacokinetics, drug toxicity and efficacy. Related gene: Car, Pxr |
| Others | Ahi1 | None | None | Study the retinopathy, nephronophthisis (NPH) and Joubert syndrome. |
| Others | Ar | Ar KO Mice | Ar cKO Mice | Androgen insensitivity syndrome (AIS), obesity, diabetes, prostatic cancer and so on. |
| Others | Ern1 | Ern1 KO Mice | Ern1 cKO Mice | AD (Alzheimer's Disease), NAFLD (non-alcoholic fatty liver disease) |
| Others | Nipbl | None | None | Cornelia de Lange syndrome (CdLS) |
| Others | Wls | None | None | Keratinocyte cKO mouse exhibits psoriasis-like dermatitis phenotype，and this model can be used to study the Wnt signaling pathway. |
| Others | Tgfb1 | Tgfb1 KO Mice | Tgfb1 cKO Mice | TGF-β is an important subtype of cell factors, which can influence cell proliferation and differentiation, cell apoptosis and regulate cell stability. TGF-β1 plays a crucial role in immune system regulation and can show different activation at different developmental stages in different cells. The majority of immune cells(or white blood cells, WBCs) can release TGF-β1. This strain of mouse is important to the research in the function of TGF-β1 signaling in tumor, wound healing, tissue fibrosis, and muscle, neuro, eyes, cardiovascular and immunity dysfunction, as well as other diseases such as Marfan syndrome, and progressive diaphyseal dysplasia(PDD). |
| Others | Mlkl | Mlkl KO Mice | Mlkl cKO Mice | Mlkl gene belongs to the protein kinase superfamily. This protein plays a crucial role in tumor necrosis factor(TNF)-induced necroptosis through interacting with RIP3(Receptor-interacting protein 3), this process is a programmed cell death, in which RIP3 is functioned as the key signaling molecule in necroptosis pathway. This model is used to study inhibitor and the inhibition of Mlkl knockdown on TNF-induced necrosis. A high level of Mlkl protein and RIP3 are associated with inflammatory bowel disease(IBD) in children. |
| Others | Arntl | Arntl KO Mice | Arntl cKO Mice | ARNTL Protein 1 is a protein in humans that encoded by the ARNTL(Aryl Hydrocarbon Receptor Nuclear Translocator Like) gene, also known as BMAL1, MOP3 and so on. BMAL1 protein plays a critical role in auto-regulatory Transcriptional-Translational Negative Feedback Loop (TTFL) in mammals as the active components, and TTFL charges the production of molecular circadian rhythms. BMAL1 has also been defined as the candidate gene for susceptibility towards hypertension, diabetes, and obesity, and its mutation is associated with infertility, problems with gluconeogenesis and lipogenesis, and altered sleep patterns. Arnt1 is the positive element of the regulation network of the mammalian circadian clock. Arnt1 is a sensitive point of this network because it is the only gene in the mouse model where single knockout exhibits arrhythmias at the molecular and behavioral levels. Besides, these Arntl knockout mice also had reproductive problems, short stature, age quickly, and suffered from progressive joint disease. |
| Others | Nr4a1 | Nr4a1 KO Mice | Nr4a1 cKO Mice | Nuclear receptor NR4A1 is one of the members of nuclear receptor NR4A family, it can participate in cell proliferation and apoptosis regulation, and plays an important role in various life activities such as oncogenesis, vascular remodeling, and steroidogenesis, as well as immune response and energetic metabolism, additionally, its function was regulated by phosphorylation, protein interaction, and other multiple methods. |
| Others | Selo | Selo KO Mice | Selo cKO Mice | The number of the report on the function of selenoprotein O (Selo) is few and not been fully confirmed yet. Until now, it is generally believed that selenoprotein with oxidoreductase activity is the main performer of various biological functions of trace element selenium. Through their own enzymatic activity, they play an important role in enhancing immunity, anti-aging, preventing cardiovascular disease and cancer, and maintaining male reproductive function. |
| Others | Kdm5a | Kdm5a KO Mice | Kdm5a cKO Mice | As a kind of Histone Lysine Demethylase, KDM5A (Lysine Demethylase 5A) can specifically demethylate H3K4me2/3, thereby playing a role in gene inhibition. KDM5A is a macromolecular protein with multiple functional domains, can regulate several biological processes, such as cell proliferation and differentiation, and cell aging, and related to embryonic differentiation, morphogenesis, tumorigenesis, and prognosis. Homozygous mice cause death. |
| Others | Jmy | Jmy KO Mice | Jmy cKO Mice | JMY is a junction-mediating and regulatory protein, which interacts with p300, and has the function of regulating p53 activation. JMY is the member of WASp(Wiskott–Aldrich syndrome protein) actin nucleation factor family, which expressed in normal and tumor tissue, has the function of inhibiting tumor and promoting tumor metastasis. WAVE2 and JMY participate in the embryonic development of mice, and it is important to the early pig embryonic development. JMY polymorphism is associated with the severity of Ankylosing Spondylitis(AS) in Han Chinese. JMC is the negative regulator of neurogenesis. |
| Others | Trpv4 | Trpv4 KO Mice | Trpv4 cKO Mice | Trpv4 is the member of the family of transient receptor potential(TRP) channel and the nonselective calcium ion channel. The function of Trpv4 is regulating the systemic osmotic pressure induced by the brain, vascular function, function of liver, intestinal, renal and bladder, as well as skin barrier function and response to UV-B radiation, growth and structural integrity of the skeleton, joint function, airway and lung function, retinal and inner ear function, and pain. |
