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Kwon, Hyug Moo
Immunometabolism and Cancer Lab
Research Interests
  • TonEBP, Obesity, Cancer, Chronic inflammatory diseases, Brain disorder, Kidney disorder, Genomic instability


Involvement of multiple kinase pathways in stimulation of gene transcription by hypertonicity

DC Field Value Language Nahm, O ko Woo, SK ko Handler, JS ko Kwon, H. Moo ko 2014-06-03T00:54:39Z - 2014-06-02 ko 2002-01 ko
dc.identifier.citation AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, v.282, no.1, pp.C49 - C58 ko
dc.identifier.issn 0363-6143 ko
dc.identifier.uri -
dc.description.abstract Osmolality of the mammalian renal medulla is high because of the operation of the urinary concentrating mechanism. To understand molecular events during the early phase of cellular adaptation to hypertonicity, we performed comprehensive searches for genes induced in response to hypertonicity using a cell line (mIMCD3) derived from the inner medullary collecting duct of mouse kidney. PCR-based subtractive hybridization of cDNA pools and cDNA microarray analysis were used. We report 12 genes whose mRNA expression is significantly increased within 4 h after exposure to hypertonicity. The increase in mRNA expression was the result of increased transcription. Many are either stress response genes or growth regulatory genes, supporting the notion that hypertonicity evokes the stress response and growth regulation in cells. Experiments using inhibitors revealed that mitogen-activated protein kinases were commonly involved in signaling for the induction of genes by hypertonicity. Tyrosine kinases and phosphatidylinositol 3-kinase also play a significant role. Signaling pathways for stimulation of transcription appeared quite diverse in that each gene was sensitive to different combinations of inhibitors. ko
dc.description.statementofresponsibility close -
dc.language 영어 ko
dc.title Involvement of multiple kinase pathways in stimulation of gene transcription by hypertonicity ko
dc.type ARTICLE ko
dc.identifier.scopusid 2-s2.0-0036079677 ko
dc.identifier.wosid 000172721700004 ko
dc.type.rims ART ko
dc.description.wostc 44 *
dc.description.scopustc 43 * 2015-05-06 * 2014-06-02 *
dc.identifier.url ko
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