By Jane K. Setlow

This quantity provides cutting-edge discussions in Genetics and Genetic engineering through concentrating on plant technology and know-how, shipping protein biochemistry, phone biology and gene remedy learn.

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Given these structural features, it has been shown that the anti-apoptotic effects of FLIPs arise in part from their recruitment to the receptor-associated DISC via DED-DED interactions with pro-caspase-8 and/or FADD (116, 117, 123, 124). This interaction apparently hinders further recruitment of pro-caspase-8 and its proteolytic processing, thus preventing the activation of downstream effector caspases. The precise role of FLIPs in apoptosis under physiological conditions is unclear as most data obtained to date were derived from protein overexpression, and in some cases a pro-apoptotic function for c-FLIP has been suggested (118-120, 122).

As is the case with other signaling pathways, much of our understanding of the diverse functions of Jak and STAT proteins in vivo has been revealed through the generation of knock-out mice (16). As anticipated, STAT1-deficient mice display dramatically increased sensitivity towards viral and microbial pathogens, presumably due to their inability to respond to interferons (17, 18). Disruption of the STAT3 gene results in early embryonic lethality, and only the use of conditional gene targeting revealed an essential role for STAT3 in T cell and macrophage function (19, 20).

123, 121-134. , Stears, R. and Gullans, S. R. (1998) Contrib. Nephrol. 123, 110-120. , Martin, P. , Favre, H. and Feraille, E. (1999) J. Biol. Chem. 274, 34103-34110. , Michel, L. and Dubertret, L. (1995) J. Leukoc. Biol. 57, 851-855. MECHANISMS OF APOPTOSIS REPRESSION 33 165 Hughes, F. , Bortner, C. , Purdy, G. D. and Cidlowski, J. A. (1997) J. Biol. Chem. 272, 30567-30576. 166 Yu, S. , Yeh, C. , Sensi, S. , Gwag, B. , Canzoniero, L. , Farhangrazi, Z. , Ying, H. , Dugan, L. L. and Choi, D. W. (1997) Science 278, 114117.

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