Редактирование: STAT1 (раздел)

==Publications==

{{medline-entry
|title=Bioinformatic characterization of angiotensin-converting enzyme 2, the entry receptor for SARS-CoV-2.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33112891
|abstract=The World Health Organization declared the COVID-19 epidemic a public health emergency of international concern on March 11th, 2020, and the pandemic is rapidly spreading worldwide. COVID-19 is caused by a novel coronavirus SARS-CoV-2, which enters human target cells via angiotensin converting enzyme 2 ([[ACE2]]). We used a number of bioinformatics tools to computationally characterize [[ACE2]] by determining its cell-specific expression in trachea, lung, and small intestine, derive its putative functions, and predict transcriptional regulation. The small intestine expressed higher levels of [[ACE2]] mRNA than any other organ. By immunohistochemistry, duodenum, kidney and testis showed strong signals, whereas the signal was weak in the respiratory tract. Single cell RNA-Seq data from trachea indicated positive signals along the respiratory tract in key protective cell types including club, goblet, proliferating, and ciliary epithelial cells; while in lung the ratio of [[ACE2]]-expressing cells was low in all cell types (<2.6%), but was highest in vascular endothelial and goblet cells. Gene ontology analysis suggested that, besides its classical role in the renin-angiotensin system, [[ACE2]] may be functionally associated with angiogenesis/blood vessel morphogenesis. Using a novel tool for the prediction of transcription factor binding sites we identified several putative binding sites within two tissue-specific promoters of the [[ACE2]] gene as well as a new putative short form of [[ACE2]]. These include several interferon-stimulated response elements sites for [[STAT1]], [[IRF8]], and [[IRF9]]. Our results also confirmed that age and gender play no significant role in the regulation of [[ACE2]] mRNA expression in the lung.
|mesh-terms=* Aging
* Angiotensin-Converting Enzyme 2
* Betacoronavirus
* Binding Sites
* COVID-19
* Carrier Proteins
* Computational Biology
* Coronavirus Infections
* Female
* Gene Expression Regulation, Enzymologic
* Gene Ontology
* Humans
* Interferons
* Lung
* Male
* Metalloproteases
* Neovascularization, Physiologic
* Organ Specificity
* Pandemics
* Peptidyl-Dipeptidase A
* Pneumonia, Viral
* Promoter Regions, Genetic
* RNA, Messenger
* Receptors, Virus
* Renin-Angiotensin System
* SARS-CoV-2
* Sex Characteristics
* Single-Cell Analysis
* Transcription Factors
* Transcription Initiation Site
* Virus Attachment

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7592753
}}
{{medline-entry
|title=[[STAT1]]-p53-p21axis-dependent stress-induced progression of chronic nephrosis in adriamycin-induced mouse model.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32953802
|abstract=Chronic nephrosis (CN) is an aging-related disease with high mortality. Signal transduction and transcriptional activator 1 ([[STAT1]]) protein promotes senescence in human glomerular mesangial cells (HMCs), but whether it affects the progression of adriamycin (ADR)-induced CN [i]in vivo[/i] remains unclear. We established an ADR-induced CN mouse model that was completed in wild-type (wt) mice by a single intravenous injection of 10 mg/kg ADR for 2 or 4 weeks. Clinical indexes in each group were determined. Hematoxylin and eosin staining (H