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10.1681/ASN.2014070639 http://scihub22266oqcxt.onion/10.1681/ASN.2014070639 C4552111!4552111 !25556166     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25556166 &cmd=llinks): Failed to open stream: HTTP request failed! 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Kelch-Like Protein 2 Mediates Angiotensin II-With No Lysine 3 Signaling in the Regulation of Vascular Tonus |pdf=|usr=}}{{25556166 }} gab.com Text Kelch-Like Protein 2 Mediates Angiotensin II-With No Lysine 3 Signaling in the Regulation of Vascular Tonus JO: J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=25556166 #FOAvip Recently, the kelch-like protein 3 (KLHL3)-Cullin3 complex was identified as an E3 ubiquitin ligase for with no lysine (WNK) kinases, and the impaired ubiquitination of WNK4 causes pseudohypoaldosteronism type II (PHAII), a hereditary hypertensive disease. However, the involvement of WNK kinase regulation by ubiquitination in situations other than PHAII has not been identified. Previously, we identified the WNK3-STE20/SPS1-related proline/alanine-rich kinase-Na/K/Cl cotransporter isoform 1 phosphorylation cascade in vascular smooth muscle cells and found that it constitutes an important mechanism of vascular constriction by angiotensin II (AngII). In this study, we investigated the involvement of KLHL proteins in AngII-induced WNK3 activation of vascular smooth muscle cells. In the mouse aorta and mouse vascular smooth muscle (MOVAS) cells, KLHL3 was not expressed, but KLHL2, the closest homolog of KLHL3, was expressed. Salt depletion and acute infusion of AngII decreased KLHL2 and increased WNK3 levels in the mouse aorta. Notably, the AngII-induced changes in KLHL2 and WNK3 expression occurred within minutes in MOVAS cells. Results of KLHL2 overexpression and knockdown experiments in MOVAS cells confirmed that KLHL2 is the major regulator of WNK3 protein abundance. The AngII-induced decrease in KLHL2 was not caused by decreased transcription but increased autophagy-mediated degradation. Furthermore, knockdown of sequestosome 1/p62 prevented the decrease in KLHL2, suggesting that the mechanism of KLHL2 autophagy could be selective autophagy mediated by sequestosome 1/p62. Thus, we identified a novel component of signal transduction in AngII-induced vascular contraction that could be a promising drug target. Twit Text FOAVip Kelch-Like Protein 2 Mediates Angiotensin II-With No Lysine 3 Signaling in the Regulation of Vascular Tonus ????J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=25556166 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25556166 #FOAvip English Wikipedia <ref>{{Cite pmid|25556166 }}</ref> Kelch-Like Protein 2 Mediates Angiotensin II-With No Lysine 3 Signaling in the Regulation of Vascular Tonus #MMPMID25556166 Zeniya M ; Morimoto N ; Takahashi D ; Mori Y ; Mori T ; Ando F ; Araki Y ; Yoshizaki Y ; Inoue Y ; Isobe K ; Nomura N ; Oi K ; Nishida H ; Sasaki S ; Sohara E ; Rai T ; Uchida S J Am Soc Nephrol 2015[Sep]; 26 (9 ): 2129-38 PMID25556166 show ga Recently, the kelch-like protein 3 (KLHL3)-Cullin3 complex was identified as an E3 ubiquitin ligase for with no lysine (WNK) kinases, and the impaired ubiquitination of WNK4 causes pseudohypoaldosteronism type II (PHAII), a hereditary hypertensive disease. However, the involvement of WNK kinase regulation by ubiquitination in situations other than PHAII has not been identified. Previously, we identified the WNK3-STE20/SPS1-related proline/alanine-rich kinase-Na/K/Cl cotransporter isoform 1 phosphorylation cascade in vascular smooth muscle cells and found that it constitutes an important mechanism of vascular constriction by angiotensin II (AngII). In this study, we investigated the involvement of KLHL proteins in AngII-induced WNK3 activation of vascular smooth muscle cells. In the mouse aorta and mouse vascular smooth muscle (MOVAS) cells, KLHL3 was not expressed, but KLHL2, the closest homolog of KLHL3, was expressed. Salt depletion and acute infusion of AngII decreased KLHL2 and increased WNK3 levels in the mouse aorta. Notably, the AngII-induced changes in KLHL2 and WNK3 expression occurred within minutes in MOVAS cells. Results of KLHL2 overexpression and knockdown experiments in MOVAS cells confirmed that KLHL2 is the major regulator of WNK3 protein abundance. The AngII-induced decrease in KLHL2 was not caused by decreased transcription but increased autophagy-mediated degradation. Furthermore, knockdown of sequestosome 1/p62 prevented the decrease in KLHL2, suggesting that the mechanism of KLHL2 autophagy could be selective autophagy mediated by sequestosome 1/p62. Thus, we identified a novel component of signal transduction in AngII-induced vascular contraction that could be a promising drug target. |Adaptor Proteins, Signal Transducing/genetics [MESH] |Angiotensin II/*pharmacokinetics/pharmacology [MESH] |Animals [MESH] |Aorta [MESH] |Autophagy/drug effects [MESH] |Cells, Cultured [MESH] |Gene Knockdown Techniques [MESH] |Heat-Shock Proteins/genetics [MESH] |Mice [MESH] |Microfilament Proteins/drug effects/genetics/*metabolism [MESH] |Muscle Tonus/*physiology [MESH] |Muscle, Smooth, Vascular/metabolism [MESH] |Myocytes, Smooth Muscle/metabolism [MESH] |Nerve Tissue Proteins/drug effects/genetics/*metabolism [MESH] |Protein Serine-Threonine Kinases/drug effects/*metabolism [MESH] |Sequestosome-1 Protein [MESH] |Signal Transduction/*drug effects [MESH] |Sodium, Dietary/pharmacology [MESH] |Solute Carrier Family 12, Member 2/metabolism [MESH]Kelch-Like Protein 2 Mediates Angiotensin II-With No Lysine 3 Signalin(epmc).pdf DeepDyve Pubget Overpricing