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10.1002/hep.27987 http://scihub22266oqcxt.onion/10.1002/hep.27987 C4618247!4618247!26174965     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 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 Deprecated: Implicit conversion from float 253.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Hepatology 2015 ; 62 (5): 1466-79 Nephropedia Template TP {{tp|p=26174965|t=2015. NUMB Phosphorylation Destabilizes p53 and Promotes Self-renewal of Tumor-Initiating Cells by NANOG-dependent Mechanism in Liver Cancer |pdf=|usr=}}{{26174965}} gab.com Text NUMB Phosphorylation Destabilizes p53 and Promotes Self-renewal of Tumor-Initiating Cells by NANOG-dependent Mechanism in Liver Cancer JO: Hepatology http://www.kidney.de/pget.php?&tw=1&pmid=26174965 #FOAvip Stem cell populations are maintained through self-renewing divisions in which one daughter cell commits to a particular fate while the other retains the multipotent characteristics of its parent. The NUMB, a tumor suppressor, in conjunctions with another tumor suppressor protein p53, preserves this property and acts as a barrier against deregulated expansion of Tumor-associated stem cells. In this context, NUMB-p53 interaction plays a crucial role to maintain the proper homeostasis of both stem cells, as well as differentiated cells. As the molecular mechanism governing the assembly and stability of the NUMB-p53 interaction/complex are poorly understood, we tried to identify the molecule/s govern this process. Using cancer cell lines, tumor-initiating cells (TICs) of liver, the mouse model and clinical samples, we identified that phosphorylations of NUMB destabilize p53 and promotes self-renewal of TICs by pluripotency-associated transcription factor NANOG dependent manner. NANOG phosphorylates NUMB via aPKC?, through the direct induction of Aurora A kinase (AURKA) and the repression of an aPKC? inhibitor, LGL-2. By radioactivity based kinase activity assays, we showed that NANOG enhances kinase activities of both AURKA and aPKC?, an important upstream process for NUMB phosphorylation. Phosphorylation of NUMB by aPKC? destabilizes the NUMB-p53 interaction, p53 proteolysis and to deregulate self-renewal in TICs.Conclusion: Posttranslational modification of NUMB by NANOG-AURKA-aPKC? pathway is an important event in TICs self-renewal and tumorigenesis. Hence, our work identifies the NANOG-NUMB-p53 signaling axis is an important regulatory pathway for TICS event in TICs self-renewal and liver tumorigenesis and suggest a therapeutic strategy by targeting NUMB-phosphorylation. However, further in depth in vivo and clinical studies are warranted to verify this suggestion. Twit Text FOAVip NUMB Phosphorylation Destabilizes p53 and Promotes Self-renewal of Tumor-Initiating Cells by NANOG-dependent Mechanism in Liver Cancer ????Hepatology http://www.kidney.de/pget.php?&tw=1&pmid=26174965 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26174965 #FOAvip English Wikipedia <ref>{{Cite pmid|26174965}}</ref> NUMB Phosphorylation Destabilizes p53 and Promotes Self-renewal of Tumor-Initiating Cells by NANOG-dependent Mechanism in Liver Cancer #MMPMID26174965 Siddique HR; Feldman DE; Chen CL; Punj V; Tokumitsu H; Machida K Hepatology 2015[Nov]; 62 (5): 1466-79 PMID26174965show ga Stem cell populations are maintained through self-renewing divisions in which one daughter cell commits to a particular fate while the other retains the multipotent characteristics of its parent. The NUMB, a tumor suppressor, in conjunctions with another tumor suppressor protein p53, preserves this property and acts as a barrier against deregulated expansion of Tumor-associated stem cells. In this context, NUMB-p53 interaction plays a crucial role to maintain the proper homeostasis of both stem cells, as well as differentiated cells. As the molecular mechanism governing the assembly and stability of the NUMB-p53 interaction/complex are poorly understood, we tried to identify the molecule/s govern this process. Using cancer cell lines, tumor-initiating cells (TICs) of liver, the mouse model and clinical samples, we identified that phosphorylations of NUMB destabilize p53 and promotes self-renewal of TICs by pluripotency-associated transcription factor NANOG dependent manner. NANOG phosphorylates NUMB via aPKC?, through the direct induction of Aurora A kinase (AURKA) and the repression of an aPKC? inhibitor, LGL-2. By radioactivity based kinase activity assays, we showed that NANOG enhances kinase activities of both AURKA and aPKC?, an important upstream process for NUMB phosphorylation. Phosphorylation of NUMB by aPKC? destabilizes the NUMB-p53 interaction, p53 proteolysis and to deregulate self-renewal in TICs.Conclusion: Posttranslational modification of NUMB by NANOG-AURKA-aPKC? pathway is an important event in TICs self-renewal and tumorigenesis. Hence, our work identifies the NANOG-NUMB-p53 signaling axis is an important regulatory pathway for TICS event in TICs self-renewal and liver tumorigenesis and suggest a therapeutic strategy by targeting NUMB-phosphorylation. However, further in depth in vivo and clinical studies are warranted to verify this suggestion. äNUMB Phosphorylation Destabilizes p53 and Promotes Self-renewal of Tum(epmc).pdf DeepDyve Pubget Overpricing