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10.1083/jcb.201511055 http://scihub22266oqcxt.onion/10.1083/jcb.201511055 C5223597!5223597 !27998989     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27998989 &cmd=llinks): Failed to open stream: HTTP request failed! 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INPP5E regulates phosphoinositide-dependent cilia transition zone function |pdf=|usr=}}{{27998989 }} gab.com Text INPP5E regulates phosphoinositide-dependent cilia transition zone function JO: J Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=27998989 #FOAvip Human ciliopathies, including Joubert syndrome (JBTS), arise from cilia dysfunction. The inositol polyphosphate 5-phosphatase INPP5E localizes to cilia and is mutated in JBTS. Murine Inpp5e ablation is embryonically lethal and recapitulates JBTS, including neural tube defects and polydactyly; however, the underlying defects in cilia signaling and the function of INPP5E at cilia are still emerging. We report Inpp5e(-/-) embryos exhibit aberrant Hedgehog-dependent patterning with reduced Hedgehog signaling. Using mouse genetics, we show increasing Hedgehog signaling via Smoothened M2 expression rescues some Inpp5e(-/-) ciliopathy phenotypes and "normalizes" Hedgehog signaling. INPP5E's phosphoinositide substrates PI(4,5)P(2) and PI(3,4,5)P(3) accumulated at the transition zone (TZ) in Hedgehog-stimulated Inpp5e(-/-) cells, which was associated with reduced recruitment of TZ scaffolding proteins and reduced Smoothened levels at cilia. Expression of wild-type, but not 5-phosphatase-dead, INPP5E restored TZ molecular organization and Smoothened accumulation at cilia. Therefore, we identify INPP5E as an essential point of convergence between Hedgehog and phosphoinositide signaling at cilia that maintains TZ function and Hedgehog-dependent embryonic development. Twit Text FOAVip INPP5E regulates phosphoinositide-dependent cilia transition zone function ????J Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=27998989 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27998989 #FOAvip English Wikipedia <ref>{{Cite pmid|27998989 }}</ref> INPP5E regulates phosphoinositide-dependent cilia transition zone function #MMPMID27998989 Dyson JM ; Conduit SE ; Feeney SJ ; Hakim S ; DiTommaso T ; Fulcher AJ ; Sriratana A ; Ramm G ; Horan KA ; Gurung R ; Wicking C ; Smyth I ; Mitchell CA J Cell Biol 2017[Jan]; 216 (1 ): 247-263 PMID27998989 show ga Human ciliopathies, including Joubert syndrome (JBTS), arise from cilia dysfunction. The inositol polyphosphate 5-phosphatase INPP5E localizes to cilia and is mutated in JBTS. Murine Inpp5e ablation is embryonically lethal and recapitulates JBTS, including neural tube defects and polydactyly; however, the underlying defects in cilia signaling and the function of INPP5E at cilia are still emerging. We report Inpp5e(-/-) embryos exhibit aberrant Hedgehog-dependent patterning with reduced Hedgehog signaling. Using mouse genetics, we show increasing Hedgehog signaling via Smoothened M2 expression rescues some Inpp5e(-/-) ciliopathy phenotypes and "normalizes" Hedgehog signaling. INPP5E's phosphoinositide substrates PI(4,5)P(2) and PI(3,4,5)P(3) accumulated at the transition zone (TZ) in Hedgehog-stimulated Inpp5e(-/-) cells, which was associated with reduced recruitment of TZ scaffolding proteins and reduced Smoothened levels at cilia. Expression of wild-type, but not 5-phosphatase-dead, INPP5E restored TZ molecular organization and Smoothened accumulation at cilia. Therefore, we identify INPP5E as an essential point of convergence between Hedgehog and phosphoinositide signaling at cilia that maintains TZ function and Hedgehog-dependent embryonic development. |*Second Messenger Systems [MESH] |Abnormalities, Multiple/*enzymology/genetics [MESH] |Animals [MESH] |Cell Line [MESH] |Cerebellum/*abnormalities/enzymology [MESH] |Cilia/*enzymology [MESH] |Disease Models, Animal [MESH] |Embryo, Mammalian/*enzymology [MESH] |Eye Abnormalities/*enzymology/genetics [MESH] |Gene Expression Regulation, Developmental [MESH] |Genetic Predisposition to Disease [MESH] |Hedgehog Proteins/genetics/metabolism [MESH] |Humans [MESH] |Kidney Diseases, Cystic/*enzymology/genetics [MESH] |Kruppel-Like Transcription Factors/genetics/metabolism [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Phenotype [MESH] |Phosphatidylinositol 4,5-Diphosphate/*metabolism [MESH] |Phosphatidylinositol Phosphates/*metabolism [MESH] |Phosphoric Monoester Hydrolases/deficiency/genetics/*metabolism [MESH] |Retina/*abnormalities/enzymology [MESH] |Retinal Pigment Epithelium/*enzymology [MESH] |Smoothened Receptor/genetics/metabolism [MESH] |Time Factors [MESH] |Transfection [MESH]INPP5E regulates phosphoinositide-dependent cilia transition zone func(epmc).pdf DeepDyve Pubget Overpricing