Masao Saitoh

TL;DR: Evidence that Trx is a negative regulator of ASK1 suggests possible mechanisms for redox regulation of the apoptosis signal transduction pathway as well as the effects of antioxidants against cytokine‐ and stress‐induced apoptosis.

TL;DR: Overexpression of ASK1 induced apoptotic cell death, andASK1 was activated in cells treated with tumor necrosis factor-α, and TNF-α-induced apoptosis was inhibited by a catalytically inactive form of AsK1.

TL;DR: It is shown that ASK1 interacts with members of the TRAF family and is activated by TRAF2, TRAF5, and TRAF6 overexpression and is a mediator of TRAf2-induced JNK activation.

TL;DR: It is shown that phosphorylation of Thr845 at the activation loop is essential for ASK1 to be activated by H2O2, and it is proposed that this potential Thr8 45 kinase may be an ignition kinase that triggers Thr 845 phosphorylated in oligomerized and activation‐competent forms of AsK1.

TL;DR: A small molecule inhibitor, A‐83‐01, is synthesized and characterized, which is structurally similar to previously reported ALK‐5 inhibitors and blocks signaling of type I serine/threonine kinase receptors for cytokines of the TGF‐β superfamily (known as activin receptor‐like kinases; ALKs), suggesting that A‐ 83–01 and related molecules may be useful for preventing the progression of advanced cancers.