https://transhumanist.ru/index.php?action=history&feed=atom&title=ERBB4 2026-04-12T04:44:46Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=ERBB4&diff=4447&oldid=prev 2021-04-29T19:18:36Z

<p>Новая страница: «Receptor tyrosine-protein kinase erbB-4 precursor (EC 2.7.10.1) (Proto-oncogene-like protein c-ErbB-4) (Tyrosine kinase-type cell surface receptor HER4) (p180erbB...»</p> <p><b>Новая страница</b></p><div>Receptor tyrosine-protein kinase erbB-4 precursor (EC 2.7.10.1) (Proto-oncogene-like protein c-ErbB-4) (Tyrosine kinase-type cell surface receptor HER4) (p180erbB4) [Contains: ERBB4 intracellular domain (4ICD) (E4ICD) (s80HER4)] [HER4]<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=Overexpression of [[ERBB4]] rejuvenates aged mesenchymal stem cells and enhances angiogenesis via PI3K/AKT and MAPK/ERK pathways.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30566395<br /> |abstract=The age-related functional exhaustion limits potential efficacy of mesenchymal stem cells ([[MSC]]) in treating cardiovascular disease. Therefore, rejuvenation of aged [[MSC]] in the elderly population is of great interest. We have previously reported that Erb-B2 receptor tyrosine kinase 4 ( [[ERBB4]]) plays a critical role in regulating [[MSC]] survival under hypoxia. The aim of this study was to investigate whether [[ERBB4]] rejuvenates aged [[MSC]] and how [[ERBB4]] enhances therapeutic efficacy of aged [[MSC]] in treating myocardial infarction (MI). Compared with vector aged [[MSC]] (aged-[[MSC]]), [[ERBB4]]-engineered aged [[MSC]] (ER4-aged-[[MSC]]) conferred resistance to oxidative stress-induced cell death and ameliorated the senescent phenotype in vitro. Four weeks after MI, the ER4-aged-[[MSC]] group exhibited enhanced blood vessel density, reduced cardiac remodeling and apoptosis with improved heart function compared with the aged-[[MSC]] group. Overexpression of [[ERBB4]] caused an increase in phosphorylated v-akt murine thymoma viral oncogene homolog 1 (AKT), and phosphorylated ERK expression under hypoxia. ER4-aged-[[MSC]] secreted higher levels of angiopoietin, epithelial neutrophil activating peptide 78, VEGF, and fibroblast growth factor 2, and enhanced tube formation in HUVEC. The impact of [[ERBB4]] on protein expression, proangiogenesis, cell behavior, and cytokine secretion was abolished by inhibiting PI3K/AKT and MAPK/ERK signaling pathway.-Liang, X., Ding, Y., Lin, F., Zhang, Y., Zhou, X., Meng, Q., Lu, X., Jiang, G., Zhu, H., Chen, Y., Lian, Q., Fan, H., Liu, Z. Overexpression of [[ERBB4]] rejuvenates aged mesenchymal stem cells and enhances angiogenesis via PI3K/AKT and MAPK/ERK pathways.<br /> |mesh-terms=* Adult<br /> * Aged<br /> * Aged, 80 and over<br /> * Aging<br /> * Animals<br /> * Apoptosis<br /> * Cells, Cultured<br /> * Cellular Senescence<br /> * Female<br /> * Human Umbilical Vein Endothelial Cells<br /> * Humans<br /> * MAP Kinase Signaling System<br /> * Male<br /> * Mesenchymal Stem Cell Transplantation<br /> * Mesenchymal Stem Cells<br /> * Mice<br /> * Mice, Inbred C57BL<br /> * Mice, Inbred NOD<br /> * Mice, SCID<br /> * Myocardial Infarction<br /> * Neovascularization, Physiologic<br /> * Oxidative Stress<br /> * Phosphatidylinositol 3-Kinases<br /> * Proto-Oncogene Proteins c-akt<br /> * Random Allocation<br /> * Receptor, ErbB-4<br /> * Recombinant Proteins<br /> * Telomere Homeostasis<br /> * Ventricular Remodeling<br /> * Young Adult<br /> |keywords=* MSC<br /> * aging<br /> * myocardial infarction<br /> |full-text-url=https://sci-hub.do/10.1096/fj.201801690R<br /> }}</div>

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