protein

Livin/BIRC7 Protein, Human (His)

HY-P77065

5 μg;10 μg;50 μg

40;70;185 USD

Livin/BIRC7 Protein, Human (His)

proteins

E. coli

5 μg;10 μg;50 μg

40;70;185 USD

Livin/BIRC7 is an apoptosis regulator that coordinates pro- and anti-apoptotic activities and is critical for apoptosis, cell proliferation, and cell cycle control. Its anti-apoptotic functions include inhibition of CASP3, CASP7 and CASP9, as well as E3 ubiquitin protein ligase activity. Livin/BIRC7 Protein, Human (His) is the recombinant human-derived Livin/BIRC7 protein, expressed by E. coli , with C-His labeled tag.

Human

Livin/BIRC7, an apoptotic regulator, intricately modulates both proapoptotic and anti-apoptotic activities, holding pivotal roles in apoptosis, cell proliferation, and cell cycle control. Its anti-apoptotic prowess stems from the inhibition of CASP3, CASP7, and CASP9, coupled with its E3 ubiquitin-protein ligase activity. Despite its classification as a weak caspase inhibitor, Livin's anti-apoptotic function is attributed to its capability to ubiquitinate DIABLO/SMAC, directing it for degradation and thereby fostering cell survival. Furthermore, Livin may hinder DIABLO/SMAC from disrupting XIAP/BIRC4-caspase interactions, potentially contributing to caspase inhibition. Notably, Livin safeguards against apoptosis induced by TNF or chemical agents like adriamycin, etoposide, or staurosporine. This protective effect is facilitated through the activation of MAPK8/JNK1 and possibly MAPK9/JNK2, contingent upon TAB1 and MAP3K7/TAK1. Livin's multifaceted functions also extend to inhibiting CASP3 and impeding the proteolytic activation of pro-CASP9 in vitro, as well as blocking staurosporine-induced apoptosis. Moreover, Livin promotes natural killer (NK) cell-mediated killing, underscoring its diverse regulatory roles in cellular processes.

Baculoviral IAP repeat-containing protein 7; KIAP; MLIAP; RNF50

Greater than 95% as determined by reducing SDS-PAGE

Supplied as a 0.2 μm filtered solution of 50 mM Tris, 200 mM NaCl, pH 8.0.

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