Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1111/j.1582-4934.2007.00030.x http://scihub22266oqcxt.onion/10.1111/j.1582-4934.2007.00030.x C3822825!3822825!17488475     free     free     free       J+Cell+Mol+Med 2007 ; 11 (2): 239-51 Nephropedia Template TP {{tp|p=17488475|t=2007. E2F1 death pathways as targets for cancer therapy |pdf=|usr=}}{{17488475}} gab.com Text E2F1 death pathways as targets for cancer therapy JO: J Cell Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=17488475 #FOAvip Defects in apoptotic programs contribute to a number of human diseases, ranging from neurodegenerative disorders to malignancy, and treatment failure. The genetic basis for apoptosis implies that cell death can be disrupted by mutations, raising the intriguing possibility that cell numbers can be regulated by factors that influence cell survival. It is well documented that the E2F1 transcription factor is a key regulator of apoptotic programs. E2F1-induced cell death occurs via multiple pathways, some of which involve the tumour suppressor p53, and autonomous of p53. This has led to the opinion that E2F1 functions as a tumour surveillance factor, detecting aberrant proliferation and engaging apoptotic pathways to protect the organism from developing tumours. Frequently, novel players are discovered that expand the interpretation of apoptosis control by E2F1. This information will help to produce new strategies to exploit E2F1-induced apoptosis for therapeutic benefit. Twit Text FOAVip E2F1 death pathways as targets for cancer therapy ????J Cell Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=17488475 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=17488475 #FOAvip English Wikipedia <ref>{{Cite pmid|17488475}}</ref> E2F1 death pathways as targets for cancer therapy #MMPMID17488475 Pützer BM J Cell Mol Med 2007[Mar]; 11 (2): 239-51 PMID17488475show ga Defects in apoptotic programs contribute to a number of human diseases, ranging from neurodegenerative disorders to malignancy, and treatment failure. The genetic basis for apoptosis implies that cell death can be disrupted by mutations, raising the intriguing possibility that cell numbers can be regulated by factors that influence cell survival. It is well documented that the E2F1 transcription factor is a key regulator of apoptotic programs. E2F1-induced cell death occurs via multiple pathways, some of which involve the tumour suppressor p53, and autonomous of p53. This has led to the opinion that E2F1 functions as a tumour surveillance factor, detecting aberrant proliferation and engaging apoptotic pathways to protect the organism from developing tumours. Frequently, novel players are discovered that expand the interpretation of apoptosis control by E2F1. This information will help to produce new strategies to exploit E2F1-induced apoptosis for therapeutic benefit. äE2F1 death pathways as targets for cancer therapy (epmc).pdf DeepDyve Pubget Overpricing