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10.1093/jmcb/mjx006 http://scihub22266oqcxt.onion/10.1093/jmcb/mjx006 C5907827!5907827 !28096294     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28096294 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 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\28096294 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Mol+Cell+Biol 2017 ; 9 (1 ): 34-44 Nephropedia Template TP {{tp|p=28096294 |t=2017. Mouse modelling of the MDM2/MDMX-p53 signalling axis |pdf=|usr=}}{{28096294 }} gab.com Text Mouse modelling of the MDM2/MDMX-p53 signalling axis JO: J Mol Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=28096294 #FOAvip It is evident that p53 activity is critical for tumour prevention and stress response through its transcriptional activation of genes affecting cellular senescence, apoptosis, cellular metabolism, and DNA repair. The regulation of p53 is highly complex, and MDM2 and MDMX are thought to be critical for deciding the fate of p53, both through inhibitory binding and post-translational modification. Many mouse models have been generated to study the regulation of p53 in vivo, and they have altered our interpretations of how p53 is regulated by MDM2 and MDMX. Although MDM2 is absolutely required for p53 regulation, certain functions are dispensable under unstressed conditions, including the ability of MDM2 to degrade p53. MDMX, on the other hand, may only be required in select situations, like embryogenesis. These models have also clarified how cellular stress signals modify the p53-inhibiting activities of MDM2 and MDMX in vivo. It is clear that more work will need to be performed to further understand the contexts for each of these signals and the requirements of various MDM2 and MDMX functions. Here, we will discuss what we have learned from mouse modelling of MDM2 and MDMX and underscore the ways in which these models could inform future therapies. Twit Text FOAVip Mouse modelling of the MDM2/MDMX-p53 signalling axis ????J Mol Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=28096294 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28096294 #FOAvip English Wikipedia <ref>{{Cite pmid|28096294 }}</ref> Mouse modelling of the MDM2/MDMX-p53 signalling axis #MMPMID28096294 Tackmann NR ; Zhang Y J Mol Cell Biol 2017[Feb]; 9 (1 ): 34-44 PMID28096294 show ga It is evident that p53 activity is critical for tumour prevention and stress response through its transcriptional activation of genes affecting cellular senescence, apoptosis, cellular metabolism, and DNA repair. The regulation of p53 is highly complex, and MDM2 and MDMX are thought to be critical for deciding the fate of p53, both through inhibitory binding and post-translational modification. Many mouse models have been generated to study the regulation of p53 in vivo, and they have altered our interpretations of how p53 is regulated by MDM2 and MDMX. Although MDM2 is absolutely required for p53 regulation, certain functions are dispensable under unstressed conditions, including the ability of MDM2 to degrade p53. MDMX, on the other hand, may only be required in select situations, like embryogenesis. These models have also clarified how cellular stress signals modify the p53-inhibiting activities of MDM2 and MDMX in vivo. It is clear that more work will need to be performed to further understand the contexts for each of these signals and the requirements of various MDM2 and MDMX functions. Here, we will discuss what we have learned from mouse modelling of MDM2 and MDMX and underscore the ways in which these models could inform future therapies. |*Models, Biological [MESH] |*Signal Transduction [MESH] |Animals [MESH] |Mice [MESH] |Organ Specificity [MESH] |Protein Stability [MESH] |Proto-Oncogene Proteins c-mdm2/*metabolism [MESH]Mouse modelling of the MDM2/MDMX-p53 signalling axis (epmc).pdf DeepDyve Pubget Overpricing