https://transhumanist.ru/index.php?action=history&feed=atom&title=EML6 2026-08-21T06:21:21Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=EML6&diff=6474&oldid=prev 2021-05-12T15:32:29Z

<p>Новая страница: «microtubule-associated protein-like 6 (EMAP-6) (Echinoderm microtubule-associated protein-like 5-like) [EML5L] ==Publications== {{medline-entry |title=Cell fate...»</p> <p><b>Новая страница</b></p><div>microtubule-associated protein-like 6 (EMAP-6) (Echinoderm microtubule-associated protein-like 5-like) [EML5L]<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=Cell fate regulation by reticulon-4 in human prostate cancers.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30480803<br /> |abstract=Reticulon-4 ([[RTN4]]), a reticulon family protein localized in the endoplasmic reticulum, is reported to be involved in multiple physiological processes like neuroendocrine secretion and membrane trafficking in neuroendocrine cells. Previous studies have presented a great potential of [[RTN4]] for the treatment of autoimmune-mediated demyelinating diseases and spinal cord injury regeneration. While interaction with Bcl-2 and Bcl-2-like family in apoptosis modulation implicated its possible role in various human cancers. However, the investigation of this gene in prostate cancer is mainly ignored. Here in our current study, we focused on its role in prostate cancer and found that [[RTN4]] DNA copy numbers were higher in prostate cancer than normal prostate gland while its RNA and protein expressions were relatively lower. Chromosomal neighbor gene [[EML6]] had similar expression patterns with [[RTN4]] in prostate cancer tissues and cell lines, and further research found that they could be both targeted by miR-148a-3p. Lentivirus-mediated [[RTN4]] overexpression potently inhibited DU145 and LNCaP cells proliferation. Cell cycle was blocked in G2/M phase and significant cell senescence was observed in [[RTN4]] overexpressed prostate cancer cells. Finally, interaction networks in the normal prostate gland and cancer tissues further revealed that [[RTN4]] maybe phosphorylated by [[MAPKAPK2]] and [[FYN]] at tyrosine 591 and serine 107, respectively. All these results implied that [[RTN4]] might somehow participate in prostate tumor progression, and this elicits possibility to develop or identify selective agents targeting [[RTN4]] for prostate cancer therapy.<br /> |mesh-terms=* Apoptosis<br /> * Cell Cycle<br /> * Cell Line<br /> * Cell Line, Tumor<br /> * Cell Proliferation<br /> * Endoplasmic Reticulum<br /> * Gene Expression Regulation, Neoplastic<br /> * HEK293 Cells<br /> * Humans<br /> * Intracellular Signaling Peptides and Proteins<br /> * Male<br /> * MicroRNAs<br /> * Nogo Proteins<br /> * PC-3 Cells<br /> * Phosphorylation<br /> * Prostatic Neoplasms<br /> * Protein-Serine-Threonine Kinases<br /> * Proteomics<br /> * Proto-Oncogene Proteins c-bcl-2<br /> |keywords=* cell proliferation<br /> * cell senescence<br /> * miR-148a-3p<br /> * prostate cancer<br /> * reticulon-4<br /> |full-text-url=https://sci-hub.do/10.1002/jcp.27704<br /> }}</div>

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