https://transhumanist.ru/index.php?action=history&feed=atom&title=EPHA3 2026-06-09T05:06:07Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=EPHA3&diff=6483&oldid=prev 2021-05-12T15:33:01Z

<p>Новая страница: «Ephrin type-A receptor 3 precursor (EC 2.7.10.1) (EPH-like kinase 4) (EK4) (hEK4) (HEK) (Human embryo kinase) (Tyrosine-protein kinase TYRO4) (Tyrosine-protein ki...»</p> <p><b>Новая страница</b></p><div>Ephrin type-A receptor 3 precursor (EC 2.7.10.1) (EPH-like kinase 4) (EK4) (hEK4) (HEK) (Human embryo kinase) (Tyrosine-protein kinase TYRO4) (Tyrosine-protein kinase receptor ETK1) (Eph-like tyrosine kinase 1) [ETK] [ETK1] [HEK] [TYRO4]<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=A high-content cellular senescence screen identifies candidate tumor suppressors, including [[EPHA3]].<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/23324396<br /> |abstract=Activation of a cellular senescence program is a common response to prolonged oncogene activation or tumor suppressor loss, providing a physiological mechanism for tumor suppression in premalignant cells. The link between senescence and tumor suppression supports the hypothesis that a loss-of-function screen measuring bona fide senescence marker activation should identify candidate tumor suppressors. Using a high-content siRNA screening assay for cell morphology and proliferation measures, we identify 12 senescence-regulating kinases and determine their senescence marker signatures, including elevation of senescence-associated β-galactosidase, DNA damage and p53 or p16 (INK4a) expression. Consistent with our hypothesis, SNP array CGH data supports loss of gene copy number of five senescence-suppressing genes across multiple tumor samples. One such candidate is the [[EPHA3]] receptor tyrosine kinase, a gene commonly mutated in human cancer. We demonstrate that selected intracellular [[EPHA3]] tumor-associated point mutations decrease receptor expression level and/or receptor tyrosine kinase (RTK) activity. Our study therefore describes a new strategy to mine for novel candidate tumor suppressors and provides compelling evidence that [[EPHA3]] mutations may promote tumorigenesis only when key senescence-inducing pathways have been inactivated.<br /> |mesh-terms=* Cell Line, Tumor<br /> * Cell Transformation, Neoplastic<br /> * Cellular Senescence<br /> * Cyclin-Dependent Kinase Inhibitor p16<br /> * Gene Expression Profiling<br /> * Gene Expression Regulation, Neoplastic<br /> * High-Throughput Screening Assays<br /> * Humans<br /> * Models, Molecular<br /> * Mutation<br /> * Oligonucleotide Array Sequence Analysis<br /> * Polymorphism, Single Nucleotide<br /> * RNA, Small Interfering<br /> * Receptor Protein-Tyrosine Kinases<br /> * Receptor, EphA3<br /> * Signal Transduction<br /> * Tumor Suppressor Protein p53<br /> * beta-Galactosidase<br /> |keywords=* DDR<br /> * EPHA3/RTK<br /> * p16INK4a<br /> * p53<br /> * senescence<br /> * tumor suppressor<br /> |full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3594263<br /> }}</div>

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