Jerry E. Chipuk

The androgen receptor represses transforming growth factor-beta signaling through interaction with Smad3.

Identification and characterization of a novel rat ov-serpin family member, trespin.

p53's believe it or not: lessons on transcription-independent death.

Pharmacologic activation of p53 elicits Bax-dependent apoptosis in the absence of transcription.

Direct activation of Bax by p53 mediates mitochondrial membrane permeabilization and apoptosis.

Cytoplasmic p53: bax and forward.

Do inducers of apoptosis trigger caspase-independent cell death?

BH3 domains of BH3-only proteins differentially regulate Bax-mediated mitochondrial membrane permeabilization both directly and indirectly.

PUMA couples the nuclear and cytoplasmic proapoptotic function of p53.

p53 and metabolism: Inside the TIGAR.

Chemical inhibition of the mitochondrial division dynamin reveals its role in Bax/Bak-dependent mitochondrial outer membrane permeabilization.

How do BCL-2 proteins induce mitochondrial outer membrane permeabilization?

Apoptosis: Stabbed in the BAX.

Mechanism of apoptosis induction by inhibition of the anti-apoptotic BCL-2 proteins.

Mitochondrial outer membrane proteins assist Bid in Bax-mediated lipidic pore formation.

PUMA cooperates with direct activator proteins to promote mitochondrial outer membrane permeabilization and apoptosis.

The BCL-2 family reunion.

PB1-F2 proteins from H5N1 and 20 century pandemic influenza viruses cause immunopathology.

BH3 domains other than Bim and Bid can directly activate Bax/Bak.

The Role of BH3-Only Proteins in Tumor Cell Development, Signaling, and Treatment.

Born to be alive: a role for the BCL-2 family in melanoma tumor cell survival, apoptosis, and treatment.

Sphingolipid metabolism cooperates with BAK and BAX to promote the mitochondrial pathway of apoptosis.

GM-CSF controls nonlymphoid tissue dendritic cell homeostasis but is dispensable for the differentiation of inflammatory dendritic cells.