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10.3389/fcell.2021.662915 http://scihub22266oqcxt.onion/10.3389/fcell.2021.662915 33898465!8063699!33898465     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=33898465&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Front+Cell+Dev+Biol 2021 ; 9 (?): 662915 Nephropedia Template TP {{tp|p=33898465|t=2021. Calcium State-Dependent Regulation of Epithelial Cell Quiescence by Stanniocalcin 1a |pdf=|usr=}}{{33898465}} gab.com Text Calcium State-Dependent Regulation of Epithelial Cell Quiescence by Stanniocalcin 1a JO: Front Cell Dev Biol http://www.kidney.de/pget.php?&tw=1&pmid=33898465 #FOAvip The molecular mechanisms regulating cell quiescence-proliferation balance are not well defined. Using a zebrafish model, we report that Stc1a, a secreted glycoprotein, plays a key role in regulating the quiescence-proliferation balance of Ca(2+) transporting epithelial cells (ionocytes). Zebrafish stc1a, but not the other stc genes, is expressed in a Ca(2+) state-dependent manner. Genetic deletion of stc1a, but not stc2b, increased ionocyte proliferation, leading to elevated body Ca(2+) levels, cardiac edema, body swelling, and premature death. The increased ionocyte proliferation was accompanied by an increase in the IGF1 receptor-mediated PI3 kinase-Akt-Tor signaling activity in ionocytes. Inhibition of the IGF1 receptor, PI3 kinase, Akt, and Tor signaling reduced ionocyte proliferation and rescued the edema and premature death in stc1a(-/-) fish, suggesting that Stc1a promotes ionocyte quiescence by suppressing local IGF signaling activity. Mechanistically, Stc1 acts by inhibiting Papp-aa, a zinc metalloproteinase degrading Igfbp5a. Inhibition of Papp-aa proteinase activity restored ionocyte quiescence-proliferation balance. Genetic deletion of papp-aa or its substrate igfbp5a in the stc1a(-/-) background reduced ionocyte proliferation and rescued the edema and premature death. These findings uncover a novel and Ca(2+) state-dependent pathway regulating cell quiescence. Our findings also provide new insights into the importance of ionocyte quiescent-proliferation balance in organismal Ca(2+) homeostasis and survival. Twit Text FOAVip Calcium State-Dependent Regulation of Epithelial Cell Quiescence by Stanniocalcin 1a ????Front Cell Dev Biol http://www.kidney.de/pget.php?&tw=1&pmid=33898465 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33898465 #FOAvip English Wikipedia <ref>{{Cite pmid|33898465}}</ref> Calcium State-Dependent Regulation of Epithelial Cell Quiescence by Stanniocalcin 1a #MMPMID33898465 Li S; Liu C; Goldstein A; Xin Y; Ke C; Duan C Front Cell Dev Biol 2021[]; 9 (?): 662915 PMID33898465show ga The molecular mechanisms regulating cell quiescence-proliferation balance are not well defined. Using a zebrafish model, we report that Stc1a, a secreted glycoprotein, plays a key role in regulating the quiescence-proliferation balance of Ca(2+) transporting epithelial cells (ionocytes). Zebrafish stc1a, but not the other stc genes, is expressed in a Ca(2+) state-dependent manner. Genetic deletion of stc1a, but not stc2b, increased ionocyte proliferation, leading to elevated body Ca(2+) levels, cardiac edema, body swelling, and premature death. The increased ionocyte proliferation was accompanied by an increase in the IGF1 receptor-mediated PI3 kinase-Akt-Tor signaling activity in ionocytes. Inhibition of the IGF1 receptor, PI3 kinase, Akt, and Tor signaling reduced ionocyte proliferation and rescued the edema and premature death in stc1a(-/-) fish, suggesting that Stc1a promotes ionocyte quiescence by suppressing local IGF signaling activity. Mechanistically, Stc1 acts by inhibiting Papp-aa, a zinc metalloproteinase degrading Igfbp5a. Inhibition of Papp-aa proteinase activity restored ionocyte quiescence-proliferation balance. Genetic deletion of papp-aa or its substrate igfbp5a in the stc1a(-/-) background reduced ionocyte proliferation and rescued the edema and premature death. These findings uncover a novel and Ca(2+) state-dependent pathway regulating cell quiescence. Our findings also provide new insights into the importance of ionocyte quiescent-proliferation balance in organismal Ca(2+) homeostasis and survival. ?Calcium State-Dependent Regulation of Epithelial Cell Quiescence by St(epmc).pdf DeepDyve Pubget Overpricing