A5005652280- Cell death mechanisms and regulation
- RNA Interference and Gene Delivery
- Cancer-related Molecular Pathways
- Signaling Pathways in Disease
- Neuroblastoma Research and Treatments
- Myasthenia Gravis and Thymoma
- Peripheral Neuropathies and Disorders
- Autoimmune Neurological Disorders and Treatments
- Monoclonal and Polyclonal Antibodies Research
- Aging, Elder Care, and Social Issues
- Cardiac electrophysiology and arrhythmias
- Computational Drug Discovery Methods
- Reproductive biology and impacts on aquatic species
- Cardiac Fibrosis and Remodeling
- Animal Genetics and Reproduction
- Cancer Research and Treatments
- Enzyme Structure and Function
- Aquaculture Nutrition and Growth
- Molecular Biology Techniques and Applications
- Viral Infections and Immunology Research
- Toxin Mechanisms and Immunotoxins
- Protein Structure and Dynamics
Sanford Burnham Prebys Medical Discovery Institute
1996-2001
Discovery Institute
1996-2001
Inserm
1999
National Foundation for Cancer Research
1995-1996
Cancer Research Center
1996
Centre National de la Recherche Scientifique
1995
Most members of the Bcl-2 protein family apoptosis regulating proteins contain two evolutionarily conserved domains, termed BH1 and BH2. Both BH2 in are required for its function as an inhibitor cell death heterodimerization with proapoptotic Bax. In this report, we mapped region Bax homodimerization Bax, using yeast two-hybrid vitro protein-protein interaction assays. Neither nor domain was binding to wild-type proteins. Moreover, (ΔBH1) (ΔBH2) mutant bound efficiently themselves each...
The BCL-2 gene was first discovered because of its involvement in the t(14;18) chromosomal translocations commonly found lymphomas, which result deregulation expression and cause inappropriately high levels Bcl-2 protein production. Expression can also become altered human cancers through other mechanisms, including loss p53 tumor suppressor normally functions as a repressor some tissues. is blocker programmed cell death apoptosis that contributes to neoplastic expansion by preventing...
The Bcl-2 protein is a suppressor of programmed cell death that homodimerizes with itself and forms heterodimers homologous Bax, promoter death. Expression Bax in Saccharomyces cerevisiae as membrane-bound fusion results lethal phenotype suppressible by co-expression Bcl-2. Functional analysis deletion mutants human yeast demonstrated the presence at least three conserved domains are required to suppress Bax-mediated cytotoxicity, termed A (amino acids 11-33), B 138-154), C 188-196). In...
Bcl-2 is a critical suppressor of apoptosis that overproduced in many types cancer. Phosphorylation the protein induced on serine residues tumor cells arrested by microtubule-targeting drugs (paclitaxel, vincristine, nocodazole) and has been associated with inactivation antiapoptotic function through an unknown mechanism. Comparison variety pharmacological inhibitors serinel threonine-specific kinases demonstrated cyclin-dependent kinase inhibitor, flavopiridol, selectively blocks...
We show here that the anti-apoptosis protein Bcl-2 potently inhibits p53-dependent transcriptional activation of various p53-responsive promoters in reporter gene co-transfection assays human embryonic kidney 293 and MCF7 cells, without affecting nuclear accumulation p53 protein. In contrast, Bcl-2(Δtransmembrane (TM)), which lacks a hydrophobic membrane-anchoring domain, had no effect on activity. Similarly, cells stably expressing either or Bcl-2(ΔTM), levels were up-regulated upon...
The BCL-2 gene was first discovered because of its involvement in the t(14;18) chromosomal translocations commonly found lymphomas, which result deregulation expression and cause inappropriately high levels Bcl-2 protein production. Expression can also become altered human cancers through other mechanisms, including loss p53 tumor suppressor normally functions as a repressor some tissues. is blocker programmed cell death apoptosis that contributes to neoplastic expansion by preventing...