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10.1007/978-94-017-9211-0_2 http://scihub22266oqcxt.onion/10.1007/978-94-017-9211-0_2 C5356026!5356026!25201187     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25201187&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 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\25201187.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Subcell+Biochem 2014 ; 85 (ä): 17-40 Nephropedia Template TP {{tp|p=25201187|t=2014. Chapter: Alterations of p63 and p73 in human cancers |pdf=|usr=}}{{25201187}} gab.com Text Chapter: Alterations of p63 and p73 in human cancers JO: Subcell Biochem http://www.kidney.de/pget.php?&tw=1&pmid=25201187 #FOAvip p53 and its related genes, p63 and p73 constitute the p53 gene family. While p53 is the most frequently mutated gene in human tumors, p63 and p73 are rarely mutated or deleted in cancers. Many studies have reported p63/p73 overexpression in human cancers while others showed that a loss of p63/p73 is associated with tumor progression and metastasis. Thus, whether p63 or p73 is a tumor suppressor gene or an oncogene has been a matter of debate. This controversy has been attributed to the existence of multiple splicing isoforms with distinct functions; the full-length TA isoform of p63 has structural and functional similarity to wild-type p53, whereas the ?Np63 acts primarily in dominant-negative fashion against all family members of p53. Differential activities of TA and ?N isoforms have been shown in vivo by creating isoform-specific gene knockout mice. All p53, p63, p73 proteins bind to and activate target genes with p53-response elements; p63 also binds to distinct p63-response elements and regulate expression of specific target genes involved in skin, limb, and craniofacial development. Interestingly, several studies have shown that both p63 and p73 are involved in cellular response to cancer therapy and others have indicated that both of these molecules are required for p53-induced apoptosis, suggesting functional interplay among p53 family proteins. Consistent with these findings, aberrant splicing that result in ?Np63 or ?Np73 overexpression are frequently found in human cancers, and is associated with poor clinical outcomes of patients in the latter. Thus immunohistochemical staining of tumor specimen with ?Np73-specific antibody might have diagnostic values in cancer clinics. Twit Text FOAVip Chapter: Alterations of p63 and p73 in human cancers ????Subcell Biochem http://www.kidney.de/pget.php?&tw=1&pmid=25201187 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25201187 #FOAvip English Wikipedia <ref>{{Cite pmid|25201187}}</ref> Chapter: Alterations of p63 and p73 in human cancers #MMPMID25201187 Inoue K; Fry EA Subcell Biochem 2014[]; 85 (ä): 17-40 PMID25201187show ga p53 and its related genes, p63 and p73 constitute the p53 gene family. While p53 is the most frequently mutated gene in human tumors, p63 and p73 are rarely mutated or deleted in cancers. Many studies have reported p63/p73 overexpression in human cancers while others showed that a loss of p63/p73 is associated with tumor progression and metastasis. Thus, whether p63 or p73 is a tumor suppressor gene or an oncogene has been a matter of debate. This controversy has been attributed to the existence of multiple splicing isoforms with distinct functions; the full-length TA isoform of p63 has structural and functional similarity to wild-type p53, whereas the ?Np63 acts primarily in dominant-negative fashion against all family members of p53. Differential activities of TA and ?N isoforms have been shown in vivo by creating isoform-specific gene knockout mice. All p53, p63, p73 proteins bind to and activate target genes with p53-response elements; p63 also binds to distinct p63-response elements and regulate expression of specific target genes involved in skin, limb, and craniofacial development. Interestingly, several studies have shown that both p63 and p73 are involved in cellular response to cancer therapy and others have indicated that both of these molecules are required for p53-induced apoptosis, suggesting functional interplay among p53 family proteins. Consistent with these findings, aberrant splicing that result in ?Np63 or ?Np73 overexpression are frequently found in human cancers, and is associated with poor clinical outcomes of patients in the latter. Thus immunohistochemical staining of tumor specimen with ?Np73-specific antibody might have diagnostic values in cancer clinics. äChapter: Alterations of p63 and p73 in human cancers (epmc).pdf DeepDyve Pubget Overpricing