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10.1681/ASN.2014030281 http://scihub22266oqcxt.onion/10.1681/ASN.2014030281 C4413762!4413762!25168025     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Am+Soc+Nephrol 2015 ; 26 (5): 1081-91 Nephropedia Template TP {{tp|p=25168025|t=2015. Nonmuscle Myosin II Regulates the Morphogenesis of Metanephric Mesenchyme?Derived Immature Nephrons |pdf=|usr=}}{{25168025}} gab.com Text Nonmuscle Myosin II Regulates the Morphogenesis of Metanephric Mesenchyme Derived Immature Nephrons JO: J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=25168025 #FOAvip The kidney develops from reciprocal interactions between the metanephric mesenchyme and ureteric bud. The mesenchyme transforms into epithelia and forms complicated nephron structures, whereas the ureteric bud extends its pre-existing epithelial ducts. Although the roles are well established for extracellular stimuli, such as Wnt and Notch, it is unclear how the intracellular cytoskeleton regulates these morphogenetic processes. Myh9 and Myh10 encode nonmuscle myosin II heavy chains, and Myh9 mutations in humans are implicated in congenital kidney diseases and focal segmental glomerulosclerosis in adults. Here, we analyzed the roles of Myh9 and Myh10 in the developing kidney. Ureteric bud-specific depletion of Myh9 resulted in no apparent phenotypes, whereas mesenchyme-specific Myh9 deletion caused proximal tubule dilations and renal failure. Mesenchyme-specific Myh9/Myh10 mutant mice died shortly after birth and showed a severe defect in nephron formation. The nascent mutant nephrons failed to form a continuous lumen, which likely resulted from impaired apical constriction of the elongating tubules. In addition, nephron progenitors lacking Myh9/Myh10 or the possible interactor Kif26b were less condensed at midgestation and reduced at birth. Taken together, nonmuscle myosin II regulates the morphogenesis of immature nephrons derived from the metanephric mesenchyme and the maintenance of nephron progenitors. Our data also suggest that Myh9 deletion in mice results in failure to maintain renal tubules but not in glomerulosclerosis. Twit Text FOAVip Nonmuscle Myosin II Regulates the Morphogenesis of Metanephric Mesenchyme Derived Immature Nephrons ????J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=25168025 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25168025 #FOAvip English Wikipedia <ref>{{Cite pmid|25168025}}</ref> Nonmuscle Myosin II Regulates the Morphogenesis of Metanephric Mesenchyme?Derived Immature Nephrons #MMPMID25168025 Recuenco MC; Ohmori T; Tanigawa S; Taguchi A; Fujimura S; Conti MA; Wei Q; Kiyonari H; Abe T; Adelstein RS; Nishinakamura R J Am Soc Nephrol 2015[May]; 26 (5): 1081-91 PMID25168025show ga The kidney develops from reciprocal interactions between the metanephric mesenchyme and ureteric bud. The mesenchyme transforms into epithelia and forms complicated nephron structures, whereas the ureteric bud extends its pre-existing epithelial ducts. Although the roles are well established for extracellular stimuli, such as Wnt and Notch, it is unclear how the intracellular cytoskeleton regulates these morphogenetic processes. Myh9 and Myh10 encode nonmuscle myosin II heavy chains, and Myh9 mutations in humans are implicated in congenital kidney diseases and focal segmental glomerulosclerosis in adults. Here, we analyzed the roles of Myh9 and Myh10 in the developing kidney. Ureteric bud-specific depletion of Myh9 resulted in no apparent phenotypes, whereas mesenchyme-specific Myh9 deletion caused proximal tubule dilations and renal failure. Mesenchyme-specific Myh9/Myh10 mutant mice died shortly after birth and showed a severe defect in nephron formation. The nascent mutant nephrons failed to form a continuous lumen, which likely resulted from impaired apical constriction of the elongating tubules. In addition, nephron progenitors lacking Myh9/Myh10 or the possible interactor Kif26b were less condensed at midgestation and reduced at birth. Taken together, nonmuscle myosin II regulates the morphogenesis of immature nephrons derived from the metanephric mesenchyme and the maintenance of nephron progenitors. Our data also suggest that Myh9 deletion in mice results in failure to maintain renal tubules but not in glomerulosclerosis. äNonmuscle Myosin II Regulates the Morphogenesis of Metanephric Mesench(epmc).pdf DeepDyve Pubget Overpricing