Miao-Der (Sophie) Chen
Our laboratory has previously shown that heat shock-induced apoptosis does not require any of the known initiator caspase-activating complexes. We have recently observed that heat shock induces endo-lysosomal membrane permealization (ELMP), which occurs upstream of mitochondria and correlates with the release of cathepsins. My project is focused on determining if cytosolic acidification and cathepsin release, following heat shock-induced ELMP, is important for caspase activation and cell death following heat shock.
Grim is an endogenous inhibitor of apoptosis (IAP) antagonist in Drosophila, which induces rapid cell death upon expression. Although Grim displaces fly caspases from the fly IAP, DIAP1, recent studies indicate that Grim's IAP binding motif (IBM) is not essential for cell death. Therefore, my project is focused on understanding how Grim induces IBM-independent apoptosis.
Heat shock, also referred to as hyperthermia, is currently under consideration as an adjunct to cancer therapy, but the basic mechanisms involved in heat shock-induced apoptosis are unclear and hotly debated. In my project, I am investigating the molecular players that regulate heat shock-induced apoptosis using cells derived from various knock-out mice, as well as cancer cell lines.
My project is related to autophagy and the molecular mechanism(s) that regulate the formation and maturation of autophagosomes, with a particular emphasis on the role that p38 MAPKs play in this process.
Chu-Chiao (Crystal) Wu
The Apaf-1 apoptosome is a large caspase (cysteine protease)-activating complex activated during the mitochondrial (intrinsic) cell death pathway. My project is focused on the stoichiometry and dimerization/conformational status of caspase-9 within this complex and it's activation mechanism in vivo using a novel caspase-9 knock-in mouse model.
Intrinsic apoptosis is dependent upon the successful formation of the apoptosome and subsequent activation of caspase-9. As are most other critical cellular processes, it is subject to regulation. Pro-life kinases have been paradoxically reported to both inhibit and activate caspase-9 by phosphorylation. My projects aim to elucidate the mechanisms by which caspase-9 is affected by these modifications in vitro, in cell culture, as well as by a knock-in mouse model.
Kuei-Ting (Michelle) Yang
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a potential therapy due to its capacity to induce apoptosis
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Pharmacology & Toxicology
College of Pharmacy
The University of Texas
107 W. Dean Keeton
Austin, TX, USA
Email Address: pharmtox
"Drugs, the Brain and Behavior" is co-authored by Dr. Carlton Erickson, the college's associate dean for research and graduate studies, and Dr. John Brick, executive director of Intoxikon International.