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10.3390/ijms18040693 http://scihub22266oqcxt.onion/10.3390/ijms18040693 C5412279!5412279 !28338624     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28338624 &cmd=llinks): Failed to open stream: HTTP request failed! 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Nerve Growth Factor Signaling from Membrane Microdomains to the Nucleus: Differential Regulation by Caveolins |pdf=|usr=}}{{28338624 }} gab.com Text Nerve Growth Factor Signaling from Membrane Microdomains to the Nucleus: Differential Regulation by Caveolins JO: Int J Mol Sci http://www.kidney.de/pget.php?&tw=1&pmid=28338624 #FOAvip Membrane microdomains or "lipid rafts" have emerged as essential functional modules of the cell, critical for the regulation of growth factor receptor-mediated responses. Herein we describe the dichotomy between caveolin-1 and caveolin-2, structural and regulatory components of microdomains, in modulating proliferation and differentiation. Caveolin-2 potentiates while caveolin-1 inhibits nerve growth factor (NGF) signaling and subsequent cell differentiation. Caveolin-2 does not appear to impair NGF receptor trafficking but elicits prolonged and stronger activation of MAPK (mitogen-activated protein kinase), Rsk2 (ribosomal protein S6 kinase 2), and CREB (cAMP response element binding protein). In contrast, caveolin-1 does not alter initiation of the NGF signaling pathway activation; rather, it acts, at least in part, by sequestering the cognate receptors, TrkA and p75(NTR), at the plasma membrane, together with the phosphorylated form of the downstream effector Rsk2, which ultimately prevents CREB phosphorylation. The non-phosphorylatable caveolin-1 serine 80 mutant (S80V), no longer inhibits TrkA trafficking or subsequent CREB phosphorylation. MC192, a monoclonal antibody towards p75(NTR) that does not block NGF binding, prevents exit of both NGF receptors (TrkA and p75(NTR)) from lipid rafts. The results presented herein underline the role of caveolin and receptor signaling complex interplay in the context of neuronal development and tumorigenesis. Twit Text FOAVip Nerve Growth Factor Signaling from Membrane Microdomains to the Nucleus: Differential Regulation by Caveolins ????Int J Mol Sci http://www.kidney.de/pget.php?&tw=1&pmid=28338624 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28338624 #FOAvip English Wikipedia <ref>{{Cite pmid|28338624 }}</ref> Nerve Growth Factor Signaling from Membrane Microdomains to the Nucleus: Differential Regulation by Caveolins #MMPMID28338624 Spencer A ; Yu L ; Guili V ; Reynaud F ; Ding Y ; Ma J ; Jullien J ; Koubi D ; Gauthier E ; Cluet D ; Falk J ; Castellani V ; Yuan C ; Rudkin BB Int J Mol Sci 2017[Mar]; 18 (4 ): ä PMID28338624 show ga Membrane microdomains or "lipid rafts" have emerged as essential functional modules of the cell, critical for the regulation of growth factor receptor-mediated responses. Herein we describe the dichotomy between caveolin-1 and caveolin-2, structural and regulatory components of microdomains, in modulating proliferation and differentiation. Caveolin-2 potentiates while caveolin-1 inhibits nerve growth factor (NGF) signaling and subsequent cell differentiation. Caveolin-2 does not appear to impair NGF receptor trafficking but elicits prolonged and stronger activation of MAPK (mitogen-activated protein kinase), Rsk2 (ribosomal protein S6 kinase 2), and CREB (cAMP response element binding protein). In contrast, caveolin-1 does not alter initiation of the NGF signaling pathway activation; rather, it acts, at least in part, by sequestering the cognate receptors, TrkA and p75(NTR), at the plasma membrane, together with the phosphorylated form of the downstream effector Rsk2, which ultimately prevents CREB phosphorylation. The non-phosphorylatable caveolin-1 serine 80 mutant (S80V), no longer inhibits TrkA trafficking or subsequent CREB phosphorylation. MC192, a monoclonal antibody towards p75(NTR) that does not block NGF binding, prevents exit of both NGF receptors (TrkA and p75(NTR)) from lipid rafts. The results presented herein underline the role of caveolin and receptor signaling complex interplay in the context of neuronal development and tumorigenesis. |Animals [MESH] |Antibodies, Monoclonal/immunology [MESH] |CREB-Binding Protein/metabolism [MESH] |Caveolin 1/antagonists & inhibitors/genetics/*metabolism [MESH] |Caveolin 2/antagonists & inhibitors/genetics/metabolism [MESH] |Cell Differentiation/drug effects [MESH] |Cell Nucleus/*metabolism [MESH] |Cells, Cultured [MESH] |Ganglia, Spinal/cytology/metabolism [MESH] |Membrane Microdomains/*metabolism [MESH] |Mice [MESH] |Nerve Growth Factor/*pharmacology [MESH] |Nerve Tissue Proteins [MESH] |PC12 Cells [MESH] |Phosphorylation/drug effects [MESH] |Protein Binding [MESH] |Protein Transport/drug effects [MESH] |RNA Interference [MESH] |RNA, Small Interfering/metabolism [MESH] |Rats [MESH] |Receptor, Nerve Growth Factor/metabolism [MESH] |Receptor, trkA/chemistry/immunology/metabolism [MESH] |Receptors, Growth Factor [MESH] |Receptors, Nerve Growth Factor/chemistry/immunology/metabolism [MESH] |Ribosomal Protein S6 Kinases, 90-kDa/metabolism [MESH]Nerve Growth Factor Signaling from Membrane Microdomains to the Nucleu(epmc).pdf DeepDyve Pubget Overpricing