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10.1073/pnas.1714313114 http://scihub22266oqcxt.onion/10.1073/pnas.1714313114 C5776978!5776978 !29158412     free     free     free Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 253.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 253.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 253.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 253.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\29158412 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Proc+Natl+Acad+Sci+U+S+A 2018 ; 115 (3 ): E418-E427 Nephropedia Template TP {{tp|p=29158412 |t=2018. Induced Gnas(R201H) expression from the endogenous Gnas locus causes fibrous dysplasia by up-regulating Wnt/?-catenin signaling |pdf=|usr=}}{{29158412 }} gab.com Text Induced Gnas(R201H) expression from the endogenous Gnas locus causes fibrous dysplasia by up-regulating Wnt/ -catenin signaling JO: Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=29158412 #FOAvip Fibrous dysplasia (FD; Online Mendelian Inheritance in Man no. 174800) is a crippling skeletal disease caused by activating mutations of the GNAS gene, which encodes the stimulatory G protein G?(s) FD can lead to severe adverse conditions such as bone deformity, fracture, and severe pain, leading to functional impairment and wheelchair confinement. So far there is no cure, as the underlying molecular and cellular mechanisms remain largely unknown and the lack of appropriate animal models has severely hampered FD research. Here we have investigated the cellular and molecular mechanisms underlying FD and tested its potential treatment by establishing a mouse model in which the human FD mutation (R201H) has been conditionally knocked into the corresponding mouse Gnas locus. We found that the germ-line FD mutant was embryonic lethal, and Cre-induced Gnas FD mutant expression in early osteochondral progenitors, osteoblast cells, or bone marrow stromal cells (BMSCs) recapitulated FD features. In addition, mosaic expression of FD mutant G?(s) in BMSCs induced bone marrow fibrosis both cell autonomously and non-cell autonomously. Furthermore, Wnt/?-catenin signaling was up-regulated in FD mutant mouse bone and BMSCs undergoing osteogenic differentiation, as we have found in FD human tissue previously. Reduction of Wnt/?-catenin signaling by removing one Lrp6 copy in an FD mutant line significantly rescued the phenotypes. We demonstrate that induced expression of the FD G?(s) mutant from the mouse endogenous Gnas locus exhibits human FD phenotypes in vivo, and that inhibitors of Wnt/?-catenin signaling may be repurposed for treating FD and other bone diseases caused by G?(s) activation. Twit Text FOAVip Induced Gnas(R201H) expression from the endogenous Gnas locus causes fibrous dysplasia by up-regulating Wnt/ -catenin signaling ????Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=29158412 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29158412 #FOAvip English Wikipedia <ref>{{Cite pmid|29158412 }}</ref> Induced Gnas(R201H) expression from the endogenous Gnas locus causes fibrous dysplasia by up-regulating Wnt/?-catenin signaling #MMPMID29158412 Khan SK ; Yadav PS ; Elliott G ; Hu DZ ; Xu R ; Yang Y Proc Natl Acad Sci U S A 2018[Jan]; 115 (3 ): E418-E427 PMID29158412 show ga Fibrous dysplasia (FD; Online Mendelian Inheritance in Man no. 174800) is a crippling skeletal disease caused by activating mutations of the GNAS gene, which encodes the stimulatory G protein G?(s) FD can lead to severe adverse conditions such as bone deformity, fracture, and severe pain, leading to functional impairment and wheelchair confinement. So far there is no cure, as the underlying molecular and cellular mechanisms remain largely unknown and the lack of appropriate animal models has severely hampered FD research. Here we have investigated the cellular and molecular mechanisms underlying FD and tested its potential treatment by establishing a mouse model in which the human FD mutation (R201H) has been conditionally knocked into the corresponding mouse Gnas locus. We found that the germ-line FD mutant was embryonic lethal, and Cre-induced Gnas FD mutant expression in early osteochondral progenitors, osteoblast cells, or bone marrow stromal cells (BMSCs) recapitulated FD features. In addition, mosaic expression of FD mutant G?(s) in BMSCs induced bone marrow fibrosis both cell autonomously and non-cell autonomously. Furthermore, Wnt/?-catenin signaling was up-regulated in FD mutant mouse bone and BMSCs undergoing osteogenic differentiation, as we have found in FD human tissue previously. Reduction of Wnt/?-catenin signaling by removing one Lrp6 copy in an FD mutant line significantly rescued the phenotypes. We demonstrate that induced expression of the FD G?(s) mutant from the mouse endogenous Gnas locus exhibits human FD phenotypes in vivo, and that inhibitors of Wnt/?-catenin signaling may be repurposed for treating FD and other bone diseases caused by G?(s) activation. |Cell Differentiation [MESH] |Chromogranins/genetics/*metabolism [MESH] |Fibrous Dysplasia of Bone/*genetics [MESH] |GTP-Binding Protein alpha Subunits, Gs/genetics/*metabolism [MESH] |Gene Expression Regulation [MESH] |Humans [MESH] |Mesenchymal Stem Cells/physiology [MESH] |Mutation [MESH] |Osteoblasts/physiology [MESH] |Signal Transduction [MESH] |Up-Regulation [MESH] |Wnt Proteins/genetics/*metabolism [MESH]Induced Gnas(R201H) expression from the endogenous Gnas locus causes f(epmc).pdf DeepDyve Pubget Overpricing