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10.1681/ASN.2008030312 http://scihub22266oqcxt.onion/10.1681/ASN.2008030312 18776119!2573016!18776119     free     free     free Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Am+Soc+Nephrol 2008 ; 19 (11): 2159-69 Nephropedia Template TP {{tp|p=18776119|t=2008. Podocyte-selective deletion of dicer induces proteinuria and glomerulosclerosis |pdf=|usr=}}{{18776119}} gab.com Text Podocyte-selective deletion of dicer induces proteinuria and glomerulosclerosis JO: J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=18776119 #FOAvip Dicer is an enzyme that generates microRNA (miRNA), which are small, noncoding RNA that function as important regulators of gene and protein expression. For exploration of the functional roles of miRNA in glomerular biology, Dicer was inactivated selectively in mouse podocytes. Mutant mice developed proteinuria 4 to 5 weeks after birth and died several weeks later, presumably from kidney failure. Multiple abnormalities were observed in glomeruli of mutant mice, including foot process effacement, irregular and split areas of the glomerular basement membrane, podocyte apoptosis and depletion, mesangial expansion, capillary dilation, and glomerulosclerosis. Gene profiling revealed upregulation of 190 genes in glomeruli isolated from mutant mice at the onset of proteinuria compared with control littermates. Target sequences for 16 miRNA were significantly enriched in the 3'-untranslated regions of the 190 upregulated genes. Further suggesting validity of the in silico analysis, six of the eight top-candidate miRNA were identified in miRNA libraries generated from podocyte cultures; these included four members of the mir-30 miRNA family, which are known to degrade target transcripts directly. Among 15 upregulated target genes of the mir-30 miRNA, four genes known to be expressed and/or functional in podocytes were identified, including receptor for advanced glycation end product, vimentin, heat-shock protein 20, and immediate early response 3. Receptor for advanced glycation end product and immediate early response 3 are known to mediate podocyte apoptosis, whereas vimentin and heat-shock protein-20 are involved in cytoskeletal structure. Taken together, these results provide a knowledge base for ongoing investigations to validate functional roles for the mir-30 miRNA family in podocyte homeostasis and podocytopathies. Twit Text FOAVip Podocyte-selective deletion of dicer induces proteinuria and glomerulosclerosis ????J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=18776119 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=18776119 #FOAvip English Wikipedia <ref>{{Cite pmid|18776119}}</ref> Podocyte-selective deletion of dicer induces proteinuria and glomerulosclerosis #MMPMID18776119 Shi S; Yu L; Chiu C; Sun Y; Chen J; Khitrov G; Merkenschlager M; Holzman LB; Zhang W; Mundel P; Bottinger EP J Am Soc Nephrol 2008[Nov]; 19 (11): 2159-69 PMID18776119show ga Dicer is an enzyme that generates microRNA (miRNA), which are small, noncoding RNA that function as important regulators of gene and protein expression. For exploration of the functional roles of miRNA in glomerular biology, Dicer was inactivated selectively in mouse podocytes. Mutant mice developed proteinuria 4 to 5 weeks after birth and died several weeks later, presumably from kidney failure. Multiple abnormalities were observed in glomeruli of mutant mice, including foot process effacement, irregular and split areas of the glomerular basement membrane, podocyte apoptosis and depletion, mesangial expansion, capillary dilation, and glomerulosclerosis. Gene profiling revealed upregulation of 190 genes in glomeruli isolated from mutant mice at the onset of proteinuria compared with control littermates. Target sequences for 16 miRNA were significantly enriched in the 3'-untranslated regions of the 190 upregulated genes. Further suggesting validity of the in silico analysis, six of the eight top-candidate miRNA were identified in miRNA libraries generated from podocyte cultures; these included four members of the mir-30 miRNA family, which are known to degrade target transcripts directly. Among 15 upregulated target genes of the mir-30 miRNA, four genes known to be expressed and/or functional in podocytes were identified, including receptor for advanced glycation end product, vimentin, heat-shock protein 20, and immediate early response 3. Receptor for advanced glycation end product and immediate early response 3 are known to mediate podocyte apoptosis, whereas vimentin and heat-shock protein-20 are involved in cytoskeletal structure. Taken together, these results provide a knowledge base for ongoing investigations to validate functional roles for the mir-30 miRNA family in podocyte homeostasis and podocytopathies. |3' Untranslated Regions[MESH] |Animals[MESH] |Apoptosis[MESH] |Base Sequence[MESH] |DEAD-box RNA Helicases/*deficiency/genetics/metabolism[MESH] |DNA Primers/genetics[MESH] |Endoribonucleases/*deficiency/genetics/metabolism[MESH] |Gene Expression Profiling[MESH] |Glomerulosclerosis, Focal Segmental/enzymology/*etiology/genetics/pathology[MESH] |Mice[MESH] |Mice, Knockout[MESH] |MicroRNAs/genetics/metabolism[MESH] |Podocytes/*enzymology/pathology[MESH] |Proteinuria/enzymology/*etiology/genetics[MESH]Podocyte-selective deletion of dicer induces proteinuria and glomerulo(epmc).pdf DeepDyve Pubget Overpricing