Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1038/srep18395 http://scihub22266oqcxt.onion/10.1038/srep18395 C4680877!4680877!26671672     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Sci+Rep 2015 ; 5 (ä): ä Nephropedia Template TP {{tp|p=26671672|t=2015. Hepatocystin is Essential for TRPM7 Function During Early Embryogenesis |pdf=|usr=}}{{26671672}} gab.com Text Hepatocystin is Essential for TRPM7 Function During Early Embryogenesis JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=26671672 #FOAvip Mutations in protein kinase C substrate 80K-H (PRKCSH), which encodes for an 80?KDa protein named hepatocystin (80K-H, PRKCSH), gives rise to polycystic liver disease (PCLD). Hepatocystin functions as the noncatalytic beta subunit of Glucosidase II, an endoplasmic reticulum (ER)-resident enzyme involved in processing and quality control of newly synthesized glycoproteins. Patients harboring heterozygous germline mutations in PRKCSH are thought to develop renal cysts as a result of somatic loss of the second allele, which subsequently interferes with expression of the TRP channel polycystin-2 (PKD2). Deletion of both alleles of PRKCSH in mice results in embryonic lethality before embryonic day E11.5. Here, we investigated the function of hepatocystin during Xenopus laevis embryogenesis and identified hepatocystin as a binding partner of the TRPM7 ion channel, whose function is required for vertebrate gastrulation. We find that TRPM7 functions synergistically with hepatocystin. Although other N-glycosylated proteins are critical to early development, overexpression of TRPM7 in Xenopus laevis embryos was sufficient to fully rescue the gastrulation defect caused by loss of hepatocystin. We observed that depletion of hepatocystin in Xenopus laevis embryos decreased TRPM7 expression, indicating that the early embryonic lethality caused by loss of hepatocystin is mainly due to impairment of TRPM7 protein expression. Twit Text FOAVip Hepatocystin is Essential for TRPM7 Function During Early Embryogenesis ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=26671672 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26671672 #FOAvip English Wikipedia <ref>{{Cite pmid|26671672}}</ref> Hepatocystin is Essential for TRPM7 Function During Early Embryogenesis #MMPMID26671672 Overton JD; Komiya Y; Mezzacappa C; Nama K; Cai N; Lou L; Fedeles SV; Habas R; Runnels LW Sci Rep 2015[]; 5 (ä): ä PMID26671672show ga Mutations in protein kinase C substrate 80K-H (PRKCSH), which encodes for an 80?KDa protein named hepatocystin (80K-H, PRKCSH), gives rise to polycystic liver disease (PCLD). Hepatocystin functions as the noncatalytic beta subunit of Glucosidase II, an endoplasmic reticulum (ER)-resident enzyme involved in processing and quality control of newly synthesized glycoproteins. Patients harboring heterozygous germline mutations in PRKCSH are thought to develop renal cysts as a result of somatic loss of the second allele, which subsequently interferes with expression of the TRP channel polycystin-2 (PKD2). Deletion of both alleles of PRKCSH in mice results in embryonic lethality before embryonic day E11.5. Here, we investigated the function of hepatocystin during Xenopus laevis embryogenesis and identified hepatocystin as a binding partner of the TRPM7 ion channel, whose function is required for vertebrate gastrulation. We find that TRPM7 functions synergistically with hepatocystin. Although other N-glycosylated proteins are critical to early development, overexpression of TRPM7 in Xenopus laevis embryos was sufficient to fully rescue the gastrulation defect caused by loss of hepatocystin. We observed that depletion of hepatocystin in Xenopus laevis embryos decreased TRPM7 expression, indicating that the early embryonic lethality caused by loss of hepatocystin is mainly due to impairment of TRPM7 protein expression. äHepatocystin is Essential for TRPM7 Function During Early Embryogenesi(epmc).pdf DeepDyve Pubget Overpricing