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10.1002/stem.1963 http://scihub22266oqcxt.onion/10.1002/stem.1963 25639853!ä!25639853 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Stem+Cells 2015 ; 33 (5): 1447-55 Nephropedia Template TP {{tp|p=25639853|t=2015. Enhanced SMAD1 Signaling Contributes to Impairments of Early Development in CFC-iPSCs |pdf=|usr=}}{{25639853}} gab.com Text Enhanced SMAD1 Signaling Contributes to Impairments of Early Development in CFC-iPSCs JO: Stem Cells http://www.kidney.de/pget.php?&tw=1&pmid=25639853 #FOAvip Cardio-facio-cutaneous (CFC) syndrome is a developmental disorder caused by constitutively active ERK signaling manifesting mainly from BRAF mutations. Little is known about the role of elevated ERK signaling in CFC syndrome during early development. Here, we show that both SMAD1 and ERK signaling pathways may contribute to the developmental defects in CFC syndrome. Induced pluripotent stem cells (iPSCs) derived from dermal fibroblasts of a CFC syndrome patient (CFC-iPSCs) revealed early developmental defects in embryoid body (EB) development, beta-catenin localization, and neuronal differentiation. Both SMAD1 and ERK signalings were significantly activated in CFC-iPSCs during EB formation. Most of the beta-catenin was dissociated from the membrane and preferentially localized into the nucleus in CFC-EBs. Furthermore, activation of SMAD1 signaling recapitulated early developmental defects in wild-type iPSCs. Intriguingly, inhibition of SMAD1 signaling in CFC-iPSCs rescued aberrant EB morphology, impaired neuronal differentiation, and altered beta-catenin localization. These results suggest that SMAD1 signaling may be a key pathway contributing the pathogenesis of CFC syndrome during early development. Twit Text FOAVip Enhanced SMAD1 Signaling Contributes to Impairments of Early Development in CFC-iPSCs ????Stem Cells http://www.kidney.de/pget.php?&tw=1&pmid=25639853 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25639853 #FOAvip English Wikipedia <ref>{{Cite pmid|25639853}}</ref> Enhanced SMAD1 Signaling Contributes to Impairments of Early Development in CFC-iPSCs #MMPMID25639853 Han KM; Kim SK; Kim D; Choi JY; Im I; Hwang KS; Kim CH; Lee BH; Yoo HW; Han YM Stem Cells 2015[May]; 33 (5): 1447-55 PMID25639853show ga Cardio-facio-cutaneous (CFC) syndrome is a developmental disorder caused by constitutively active ERK signaling manifesting mainly from BRAF mutations. Little is known about the role of elevated ERK signaling in CFC syndrome during early development. Here, we show that both SMAD1 and ERK signaling pathways may contribute to the developmental defects in CFC syndrome. Induced pluripotent stem cells (iPSCs) derived from dermal fibroblasts of a CFC syndrome patient (CFC-iPSCs) revealed early developmental defects in embryoid body (EB) development, beta-catenin localization, and neuronal differentiation. Both SMAD1 and ERK signalings were significantly activated in CFC-iPSCs during EB formation. Most of the beta-catenin was dissociated from the membrane and preferentially localized into the nucleus in CFC-EBs. Furthermore, activation of SMAD1 signaling recapitulated early developmental defects in wild-type iPSCs. Intriguingly, inhibition of SMAD1 signaling in CFC-iPSCs rescued aberrant EB morphology, impaired neuronal differentiation, and altered beta-catenin localization. These results suggest that SMAD1 signaling may be a key pathway contributing the pathogenesis of CFC syndrome during early development. |*Signal Transduction[MESH] |Cell Differentiation[MESH] |Cell Nucleus/metabolism[MESH] |Ectodermal Dysplasia/*metabolism/*pathology[MESH] |Embryoid Bodies/metabolism[MESH] |Facies[MESH] |Failure to Thrive/*metabolism/*pathology[MESH] |Heart Defects, Congenital/*metabolism/*pathology[MESH] |Humans[MESH] |Induced Pluripotent Stem Cells/*metabolism[MESH] |Male[MESH] |Neurons/pathology[MESH] |Protein Transport[MESH] |Smad Proteins/*metabolism[MESH]Enhanced SMAD1 Signaling Contributes to Impairments of Early Developme(epmc).pdf DeepDyve Pubget Overpricing