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10.1172/JCI92893 http://scihub22266oqcxt.onion/10.1172/JCI92893 C5663351!5663351!28945203     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Clin+Invest ä ; 127 (11): 4001-17 Nephropedia Template TP {{tp|p=28945203|t=ä. mTORC1 loss impairs epidermal adhesion via TGF-?/Rho kinase activation |pdf=|usr=}}{{28945203}} gab.com Text mTORC1 loss impairs epidermal adhesion via TGF- /Rho kinase activation JO: J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=28945203 #FOAvip Despite its central position in oncogenic intracellular signaling networks, the role of mTORC1 in epithelial development has not been studied extensively in vivo. Here, we have used the epidermis as a model system to elucidate the cellular effects and signaling feedback sequelae of mTORC1 loss of function in epithelial tissue. In mice with conditional epidermal loss of the mTORC1 components Rheb or Rptor, mTORC1 loss of function unexpectedly resulted in a profound skin barrier defect with epidermal abrasions, blistering, and early postnatal lethality, due to a thinned epidermis with decreased desmosomal protein expression and incomplete biochemical differentiation. In mice with mTORC1 loss of function, we found that Rho kinase (ROCK) signaling was constitutively activated, resulting in increased cytoskeletal tension and impaired cell-cell adhesion. Inhibition or silencing of ROCK1 was sufficient to rescue keratinocyte adhesion and biochemical differentiation in these mice. mTORC1 loss of function also resulted in marked feedback upregulation of upstream TGF-? signaling, triggering ROCK activity and its downstream effects on desmosomal gene expression. These findings elucidate a role for mTORC1 in the regulation of epithelial barrier formation, cytoskeletal tension, and cell adhesion, underscoring the complexity of signaling feedback following mTORC1 inhibition. Twit Text FOAVip mTORC1 loss impairs epidermal adhesion via TGF- /Rho kinase activation ????J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=28945203 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28945203 #FOAvip English Wikipedia <ref>{{Cite pmid|28945203}}</ref> mTORC1 loss impairs epidermal adhesion via TGF-?/Rho kinase activation #MMPMID28945203 Asrani K; Sood A; Torres A; Georgess D; Phatak P; Kaur H; Dubin A; Talbot CC; Elhelu L; Ewald AJ; Xiao B; Worley P; Lotan TL J Clin Invest ä[]; 127 (11): 4001-17 PMID28945203show ga Despite its central position in oncogenic intracellular signaling networks, the role of mTORC1 in epithelial development has not been studied extensively in vivo. Here, we have used the epidermis as a model system to elucidate the cellular effects and signaling feedback sequelae of mTORC1 loss of function in epithelial tissue. In mice with conditional epidermal loss of the mTORC1 components Rheb or Rptor, mTORC1 loss of function unexpectedly resulted in a profound skin barrier defect with epidermal abrasions, blistering, and early postnatal lethality, due to a thinned epidermis with decreased desmosomal protein expression and incomplete biochemical differentiation. In mice with mTORC1 loss of function, we found that Rho kinase (ROCK) signaling was constitutively activated, resulting in increased cytoskeletal tension and impaired cell-cell adhesion. Inhibition or silencing of ROCK1 was sufficient to rescue keratinocyte adhesion and biochemical differentiation in these mice. mTORC1 loss of function also resulted in marked feedback upregulation of upstream TGF-? signaling, triggering ROCK activity and its downstream effects on desmosomal gene expression. These findings elucidate a role for mTORC1 in the regulation of epithelial barrier formation, cytoskeletal tension, and cell adhesion, underscoring the complexity of signaling feedback following mTORC1 inhibition. ämTORC1 loss impairs epidermal adhesion via TGF-?/Rho kinase activation(epmc).pdf DeepDyve Pubget Overpricing