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10.14348/molcells.2017.0225 http://scihub22266oqcxt.onion/10.14348/molcells.2017.0225 C5682248!5682248!29047262     free     free     free Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Mol+Cells 2017 ; 40 (10): 706-13 Nephropedia Template TP {{tp|p=29047262|t=2017. Current Understanding of RANK Signaling in Osteoclast Differentiation and Maturation |pdf=|usr=}}{{29047262}} gab.com Text Current Understanding of RANK Signaling in Osteoclast Differentiation and Maturation JO: Mol Cells http://www.kidney.de/pget.php?&tw=1&pmid=29047262 #FOAvip Osteoclasts are bone-resorbing cells that are derived from hematopoietic precursor cells and require macrophage-colony stimulating factor and receptor activator of nuclear factor-?B ligand (RANKL) for their survival, proliferation, differentiation, and activation. The binding of RANKL to its receptor RANK triggers osteoclast precursors to differentiate into osteoclasts. This process depends on RANKL-RANK signaling, which is temporally regulated by various adaptor proteins and kinases. Here we summarize the current understanding of the mechanisms that regulate RANK signaling during osteoclastogenesis. In the early stage, RANK signaling is mediated by recruiting adaptor molecules such as tumor necrosis factor receptor-associated factor 6 (TRAF6), which leads to the activation of mitogen-activated protein kinases (MAPKs), and the transcription factors nuclear factor-?B (NF-?B) and activator protein-1 (AP-1). Activated NF-?B induces the nuclear factor of activated T-cells cytoplasmic 1 (NFATc1), which is the key osteoclastogenesis regulator. In the intermediate stage of signaling, the co-stimulatory signal induces Ca2+ oscillation via activated phospholipase C?2 (PLC?2) together with c-Fos/AP-1, wherein Ca2+ signaling facilitates the robust production of NFATc1. In the late stage of osteoclastogenesis, NFATc1 translocates into the nucleus where it induces numerous osteoclast-specific target genes that are responsible for cell fusion and function. Twit Text FOAVip Current Understanding of RANK Signaling in Osteoclast Differentiation and Maturation ????Mol Cells http://www.kidney.de/pget.php?&tw=1&pmid=29047262 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29047262 #FOAvip English Wikipedia <ref>{{Cite pmid|29047262}}</ref> Current Understanding of RANK Signaling in Osteoclast Differentiation and Maturation #MMPMID29047262 Park JH; Lee NK; Lee SY Mol Cells 2017[Oct]; 40 (10): 706-13 PMID29047262show ga Osteoclasts are bone-resorbing cells that are derived from hematopoietic precursor cells and require macrophage-colony stimulating factor and receptor activator of nuclear factor-?B ligand (RANKL) for their survival, proliferation, differentiation, and activation. The binding of RANKL to its receptor RANK triggers osteoclast precursors to differentiate into osteoclasts. This process depends on RANKL-RANK signaling, which is temporally regulated by various adaptor proteins and kinases. Here we summarize the current understanding of the mechanisms that regulate RANK signaling during osteoclastogenesis. In the early stage, RANK signaling is mediated by recruiting adaptor molecules such as tumor necrosis factor receptor-associated factor 6 (TRAF6), which leads to the activation of mitogen-activated protein kinases (MAPKs), and the transcription factors nuclear factor-?B (NF-?B) and activator protein-1 (AP-1). Activated NF-?B induces the nuclear factor of activated T-cells cytoplasmic 1 (NFATc1), which is the key osteoclastogenesis regulator. In the intermediate stage of signaling, the co-stimulatory signal induces Ca2+ oscillation via activated phospholipase C?2 (PLC?2) together with c-Fos/AP-1, wherein Ca2+ signaling facilitates the robust production of NFATc1. In the late stage of osteoclastogenesis, NFATc1 translocates into the nucleus where it induces numerous osteoclast-specific target genes that are responsible for cell fusion and function. äCurrent Understanding of RANK Signaling in Osteoclast Differentiation (epmc).pdf DeepDyve Pubget Overpricing