From January through June of 2020, Cyagen received over 70 citations for our animal models, contributing to many advances across research fields. We have put together the below list of articles from high impact factor (IF) journals to provide insights into a variety of mouse model types, gene targets, research applications, and some of the most recent developments shown in scientific literature.
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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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The TurboKnockout® gene targeting service by Cyagen is based on traditional embryonic stem cell (ESC)-mediated targeting techniques, which can be used for complex gene knockout projects to provide C57BL/6 or (new) BALB/c mouse models with accurate genetic modification and no off-target effects.
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The COVID-19 epidemic is now a huge challenge for the entire world. Since the epidemic in most of the countries is controlled, colleges, universities and institutes worldwide, gradually returned to school or lab and started their scientific research work. However, the recent local restrictions and measures against COVID-19 and the unclear prospect of the epidemic have made many scientific researchers anxious.
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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 following publications demonstrate the use of custom genetically modified mouse and rat models across a broad range of human disease studies, including immunological disorders, inflammatory disorders, cardiovascular disease, oncology, immunology, and liver disease.
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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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