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.

10.1016/j.canlet.2013.01.043 http://scihub22266oqcxt.onion/10.1016/j.canlet.2013.01.043 C3651913!3651913 !23376255     free     free     free Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\23376255 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Cancer+Lett 2013 ; 333 (2 ): 147-51 Nephropedia Template TP {{tp|p=23376255 |t=2013. Bit1 in anoikis resistance and tumor metastasis |pdf=|usr=}}{{23376255 }} gab.com Text Bit1 in anoikis resistance and tumor metastasis JO: Cancer Lett http://www.kidney.de/pget.php?&tw=1&pmid=23376255 #FOAvip Epithelial cells and most adherent normal cells rely on adhesion-dependent, integrin-mediated survival signals from the extracellular matrix (ECM) to survive. When these cells are deprived of adhesion to the ECM, they undergo a specific form of apoptosis termed "anoikis." In contrast, malignant cells have attained mechanisms to enable them to survive in the absence of adhesion and are considered anchorage-independent. This review will focus on the biological function of the Bcl2-inhibitor of transcription (Bit1) protein in the anoikis process, the underlying molecular mechanism of Bit1 apoptotic function, and its role in tumor metastasis. Twit Text FOAVip Bit1 in anoikis resistance and tumor metastasis ????Cancer Lett http://www.kidney.de/pget.php?&tw=1&pmid=23376255 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23376255 #FOAvip English Wikipedia <ref>{{Cite pmid|23376255 }}</ref> Bit1 in anoikis resistance and tumor metastasis #MMPMID23376255 Jenning S ; Pham T ; Ireland SK ; Ruoslahti E ; Biliran H Cancer Lett 2013[Jun]; 333 (2 ): 147-51 PMID23376255 show ga Epithelial cells and most adherent normal cells rely on adhesion-dependent, integrin-mediated survival signals from the extracellular matrix (ECM) to survive. When these cells are deprived of adhesion to the ECM, they undergo a specific form of apoptosis termed "anoikis." In contrast, malignant cells have attained mechanisms to enable them to survive in the absence of adhesion and are considered anchorage-independent. This review will focus on the biological function of the Bcl2-inhibitor of transcription (Bit1) protein in the anoikis process, the underlying molecular mechanism of Bit1 apoptotic function, and its role in tumor metastasis. |Animals [MESH] |Anoikis/*physiology [MESH] |Apoptosis/physiology [MESH] |Carboxylic Ester Hydrolases/genetics/*metabolism [MESH] |Epithelial Cells/metabolism/pathology [MESH] |Extracellular Matrix/metabolism/pathology [MESH] |Humans [MESH] |Mitochondrial Proteins/genetics/*metabolism [MESH]Bit1 in anoikis resistance and tumor metastasis (epmc).pdf DeepDyve Pubget Overpricing