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10.1042/CS20171525

http://scihub22266oqcxt.onion/10.1042/CS20171525
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29352074!5817097!29352074
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suck abstract from ncbi

pmid29352074      Clin+Sci+(Lond) 2018 ; 132 (2): 173-183
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  • Aldosterone, SGK1, and ion channels in the kidney #MMPMID29352074
  • Valinsky WC; Touyz RM; Shrier A
  • Clin Sci (Lond) 2018[Jan]; 132 (2): 173-183 PMID29352074show ga
  • Hyperaldosteronism, a common cause of hypertension, is strongly connected to Na(+), K(+), and Mg(2+) dysregulation. Owing to its steroidal structure, aldosterone is an active transcriptional modifier when bound to the mineralocorticoid receptor (MR) in cells expressing the enzyme 11beta-hydroxysteroid dehydrogenase 2, such as those comprising the aldosterone-sensitive distal nephron (ASDN). One such up-regulated protein, the ubiquitous serum and glucocorticoid regulated kinase 1 (SGK1), has the capacity to modulate the surface expression and function of many classes of renal ion channels, including those that transport Na(+) (ENaC), K(+) (ROMK/BK), Ca(2+) (TRPV4/5/6), Mg(2+) (TRPM7/6), and Cl(-) (ClC-K, CFTR). Here, we discuss the mechanisms by which ASDN expressed channels are up-regulated by SGK1, while highlighting newly discovered pathways connecting aldosterone to nonselective cation channels that are permeable to Mg(2+) (TRPM7) or Ca(2+) (TRPV4).
  • |Aldosterone/*metabolism[MESH]
  • |Animals[MESH]
  • |Humans[MESH]
  • |Immediate-Early Proteins/*metabolism[MESH]
  • |Ion Channels/*metabolism[MESH]
  • |Kidney/*metabolism[MESH]
  • |Nephrons/metabolism[MESH]
  • |Protein Serine-Threonine Kinases/*metabolism[MESH]
  • |Signal Transduction[MESH]


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