Livin: On a Prayer

Livin is a member of the inhibitor of apoptosis proteins (IAP) family that regulates programmed cell death. The Livin protein contains a single baculovirus IAP repeat (BIR) essential for function, along with a COOH-terminal RING-type zinc finger domain. In general, IAP proteins block apoptosis by binding and inhibiting caspases through this BIR domain. Two Livin splicing variants, alpha and beta, have been identified, and each has different anti-apoptotic properties. With Livin expression low in adult tissues, it is somewhat higher in developmental tissues. Many RING finger-containing IAPs possess E3 ubiquitin ligase activity, with Livin utilizing a Smac/DIABLO-mediated pathway. There is a large body of literature that establishes Livin as a player in a wide spectrum of tumor types, thus it holds significant potential as a both a diagnostic and prognostic tumor marker. IAP overexpression and the resulting apoptotic resistance that occurs play a key role in cancer progression.

Western Blot: Livin Antibody

A Norwegian group performed Livin antibody immunoblotting to generate their comparative expression profiles of X-linked IAP (XIAP), survivin, and livin in malignant mesotheliomas¹. A multivariate analysis included the Livin antibody and explored the effects of ectopic Livin expression in bladder cancer cells, and found that Livin clearly stimulated proliferation and blocked chemically-induced apoptosis². Slagsvold et al used Livin antibody in colon cancer cells to evaluate how docosahexaenoic acid (DHA) affects cell cycle checkpoint proteins and IAP signaling³. They were able to show that DHA favorably causes both G1 and G2 cell cycle arrest and could be used as a chemotherapy and radiotherapy adjuvant. Some studies out of an Israel lab used the Livin antibody to determine that in melanoma cells, several caspases cleave Livin into a novel truncated form with complex and paradoxical functions⁴. Liu’s group examined the role of Livin in clinical sensitivity of epitheloid ovarian cancer⁵. By using the Livin antibody, they were able to show that specific livin silencing was enough to promote apoptosis and enhance chemotherapy sensitivity.