Though the current situation regarding COVID-19 is still severe, since July, many successes have been achieved on SARS-CoV-2 neutralizing antibody and Phase II clinical trials of SARS-CoV-2 vaccines. With the effort of scientists worldwide, results indicate that research will continue to make progress in the fight against COVID-19.
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The heterogenous nuclear ribonucleoprotein (hnRNP) family are multifunctional complexes of RNA and protein present in the cell nucleus that serve critical roles in gene regulation. Multiple lines of evidence have linked hnRNP abnormalities as key pathobiological drivers of cancer and neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).
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Humanized mice can be developed through a variety of genetic modification techniques, wherein human genes may directly replace endogenous mouse genes or be inserted into a safe locus, such as Rosa26.
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The predominant animal models currently used in the research of Alzheimer's disease (AD) are genetically modified mice. Although promising results have been achieved in this field, almost all corresponding clinical trials have failed, especially with regards to drug development centered on the amyloid hypothesis.
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The human S100A9 gene encodes the S100 calcium-binding protein A9 (S100A9). In mammals, S100A8 and S100A9 proteins form a heterodimer known as calprotectin. Calprotectin is involved in the inflammatory process - it is known to be present as a soluble protein in the cytosol of neutrophil granulocytes, and is found in lower concentrations among in monocytes, macrophages, and squamous epithelial cells.
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Recent news continues to show that the COVID-19 pandemic situation globally is far from being over. Across the entire world, the pneumonia-like COVID-19 caused by the novel coronavirus (SARS-CoV-2) remains a huge medical challenge. To provide a wholistic guide for developing clinical treatments, vaccines, and antiviral drugs, it is of great significance to study the interaction mechanisms between severe acute respiratory syndrome (SARS) coronaviruses and host molecules, while also exploring the pathogenic process of coronaviruses. Accurate animal models are necessary for verifying the pathogenesis and immune mechanisms of the illness to accelerate research across vaccine development, new drug development, gene therapy, and more.
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Although the origin of the new coronavirus remains inconclusive, according to the analysis of existing genomic data, the scientific community has drawn preliminary conclusions that bats may be the reservoir species for the novel coronavirus (SARS-CoV-2). If this view is proved to be credible, how does the virus jump from a bat to a human? With the development of the pandemic, the novel coronavirus (SARS-CoV-2) has demonstrated its power to infect human beings with continuous improvement. Herein, we discuss how the coronavirus has been transferred from bats to humans, why SARS-CoV-2 is so deadly, and explore whether it may disappear someday.
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The MYD88 gene encodes a cytosolic adapter protein, MyD88, which is involved in signaling for both the innate and adaptive immune response. The MyD88 adapter protein is essential for transducing signals in the interleukin-1 (IL-1) and toll-like receptor (TLR) pathways, which regulate activation of proinflammatory genes, and stimulating signaling molecules that activate interacting proteins called nuclear factor-kappa-B (NF-κB).
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The World Health Organization (WHO) announced the reclassification of the COVID-19 outbreak as a global pandemic on March 11, 2020. With the rapid spread of the disease across the globe, countries worldwide have joined the war against the SARS-CoV-2 virus. It is of great significance to study the interaction mechanisms between human coronaviruses (hCoVs) and host molecules, and also explore the pathogenic process of viruses to provide a wholistic guide for developing clinical treatments, vaccines, and antiviral drugs.
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Although most cases of Parkinson’s Disease (PD) are idiopathic, there is a small fraction of cases that have known genetic factors – presented in diagnoses of familial PD. Roughly 5% -15% of PD cases are due to a mutation occurring in one of several specific genes, commonly designated as PARK genes (due to their association with PD). The genetic mutations that lead to PD can be transmitted in either an autosomal-recessive or autosomal-dominant pattern, and can contribute to the pathogenesis of either familial or sporadic PD depending on the specific gene mutated.
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