Preparing your results

Our searching services are busy right now. Your search will reload in five seconds.

X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

The proapoptotic activity of the Bcl-2 family member Bim is regulated by interaction with the dynein motor complex.

Molecular cell | Mar 26, 1999

http://www.ncbi.nlm.nih.gov/pubmed/10198631

Bcl-2 family members that have only a single Bcl-2 homology domain, BH3, are potent inducers of apoptosis, and some appear to play a critical role in developmentally programmed cell death. We examined the regulation of the proapoptotic activity of the BH3-only protein Bim. In healthy cells, most Bim molecules were bound to LC8 cytoplasmic dynein light chain and thereby sequestered to the microtubule-associated dynein motor complex. Certain apoptotic stimuli disrupted the interaction between LC8 and the dynein motor complex. This freed Bim to translocate together with LC8 to Bcl-2 and to neutralize its antiapoptotic activity. This process did not require caspase activity and therefore constitutes an initiating event in apoptosis signaling.

Pubmed ID: 10198631 RIS Download

Mesh terms: Amino Acid Sequence | Animals | Apoptosis | Apoptosis Regulatory Proteins | Binding Sites | Carrier Proteins | Caspase Inhibitors | Caspases | Cell Line | Dimerization | Drosophila Proteins | Dyneins | Gene Library | Humans | Membrane Proteins | Mice | Microtubules | Molecular Motor Proteins | Molecular Sequence Data | Mutation | Precipitin Tests | Protein Binding | Protein Isoforms | Proto-Oncogene Proteins | Proto-Oncogene Proteins c-bcl-2 | Saccharomyces cerevisiae

Research resources used in this publication

None found

Research tools detected in this publication

None found

Data used in this publication

None found

Associated grants

  • Agency: NIGMS NIH HHS, Id: GM51293

BioGRID (Data, Interactions)

Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.