Genomes and Genes
M S Sheikh
Affiliation: National Institutes of Health
- Cell cycle-independent regulation of p21Waf1/Cip1 and retinoblastoma protein during okadaic acid-induced apoptosis is coupled with induction of Bax protein in human breast carcinoma cellsM S Sheikh
Laboratory of Molecular Pharmacology, National Cancer Institute, NIH, Bethesda, Maryland 20892, USA
Cell Growth Differ 7:1599-607. 1996....
- Cloning and characterization of a human genotoxic and endoplasmic reticulum stress-inducible cDNA that encodes translation initiation factor 1(eIF1(A121/SUI1))M S Sheikh
Division of Basic Sciences, NCI, National Institutes of Health, Bethesda MD 20892, USA
J Biol Chem 274:16487-93. 1999....
- p53-dependent and -independent regulation of the death receptor KILLER/DR5 gene expression in response to genotoxic stress and tumor necrosis factor alphaM S Sheikh
Basic Research Laboratory, Division of Basic Sciences, National Cancer Institute, NIH, Bethesda, Maryland 20892, USA
Cancer Res 58:1593-8. 1998..Thus, KILLER/DR5 appears a bona fide downstream target of p53 that is also regulated in a cell type-specific, trigger-dependent, and p53-independent manner...
- Identification of several human homologs of hamster DNA damage-inducible transcripts. Cloning and characterization of a novel UV-inducible cDNA that codes for a putative RNA-binding proteinM S Sheikh
Laboratory of Molecular Pharmacology, NCI, National Institutes of Health, Bethesda, Maryland 20892, USA
J Biol Chem 272:26720-6. 1997..Thus the putative A18 hnRNP is the first hnRNP whose mRNA is specifically regulated in response to UV-induced DNA damage; accordingly, it may play some role in repair of UV-type DNA damage...
- Activation of Gadd34 by diverse apoptotic signals and suppression of its growth inhibitory effects by apoptotic inhibitorsM C Hollander
Basic Research Laboratory, Division of Basic Science, National Cancer Institute, Bethesda, Maryland 20892, USA
Int J Cancer 96:22-31. 2001..5. Thus, activation of Gadd34 is a downstream event in apoptotic signaling pathways and may directly contribute to the apoptotic process...
- The antiapoptotic decoy receptor TRID/TRAIL-R3 is a p53-regulated DNA damage-inducible gene that is overexpressed in primary tumors of the gastrointestinal tractM S Sheikh
Division of Basic Sciences, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
Oncogene 18:4153-9. 1999..It is, therefore, possible that TRID overexpressing GIT tumors may gain a selective growth advantage by escaping from TRAIL-induced apoptosis...
- Chromatin relaxation by overexpression of mutant p53, HPV16-E6, or cyclin G transgenesM L Smith
Division of Basic Science, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
Exp Cell Res 242:235-43. 1998....
- Genomic instability in Gadd45a-deficient miceM C Hollander
Gene Response Section, DBS, National Cancer Institute, Bethesda, Maryland 20892 4255, USA
Nat Genet 23:176-84. 1999..Our results indicate that Gadd45a is one component of the p53 pathway that contributes to the maintenance of genomic stability...
- The involvement of aryl hydrocarbon receptor in the activation of transforming growth factor-beta and apoptosisH Zaher
Laboratory of Metabolism, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
Mol Pharmacol 54:313-21. 1998..Taken together, these findings suggest that the phenotypic abnormalities in Ahr-/- mice could be mediated in part by abnormal levels of active TGFbeta and altered cell cycle control...
- Sulindac sulfide-induced apoptosis involves death receptor 5 and the caspase 8-dependent pathway in human colon and prostate cancer cellsY Huang
Department of Pharmacology, State University of New York, Upstate Medical University, Syracuse, New York 13210, USA
Cancer Res 61:6918-24. 2001..Thus, our results demonstrate that sulindac sulfide also engages the membrane DR pathway involving DR5 and proximal caspase 8 to induce apoptosis...
- Transcriptional upregulation of PUMA modulates endoplasmic reticulum calcium pool depletion-induced apoptosis via Bax activationX Luo
Department of Pharmacology, State University of New York, Upstate Medical University, Syracuse, NY 13210, USA
Cell Death Differ 12:1310-8. 2005..Thus, our results demonstrate that TG engages PUMA and Bax for full transduction of apoptotic signals and both PUMA and Bax appear to exist in the same TG-activated apoptotic pathway in which PUMA may reside upstream of Bax...