M S Sheikh

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. ncbi request reprint 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 cells
    M S Sheikh
    Laboratory of Molecular Pharmacology, National Cancer Institute, NIH, Bethesda, Maryland 20892, USA
    Cell Growth Differ 7:1599-607. 1996
  2. ncbi request reprint 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
  3. ncbi request reprint p53-dependent and -independent regulation of the death receptor KILLER/DR5 gene expression in response to genotoxic stress and tumor necrosis factor alpha
    M S Sheikh
    Basic Research Laboratory, Division of Basic Sciences, National Cancer Institute, NIH, Bethesda, Maryland 20892, USA
    Cancer Res 58:1593-8. 1998
  4. ncbi request reprint 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 protein
    M S Sheikh
    Laboratory of Molecular Pharmacology, NCI, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Biol Chem 272:26720-6. 1997
  5. ncbi request reprint Activation of Gadd34 by diverse apoptotic signals and suppression of its growth inhibitory effects by apoptotic inhibitors
    M C Hollander
    Basic Research Laboratory, Division of Basic Science, National Cancer Institute, Bethesda, Maryland 20892, USA
    Int J Cancer 96:22-31. 2001
  6. ncbi request reprint The antiapoptotic decoy receptor TRID/TRAIL-R3 is a p53-regulated DNA damage-inducible gene that is overexpressed in primary tumors of the gastrointestinal tract
    M S Sheikh
    Division of Basic Sciences, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    Oncogene 18:4153-9. 1999
  7. ncbi request reprint Chromatin relaxation by overexpression of mutant p53, HPV16-E6, or cyclin G transgenes
    M L Smith
    Division of Basic Science, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    Exp Cell Res 242:235-43. 1998
  8. ncbi request reprint Genomic instability in Gadd45a-deficient mice
    M C Hollander
    Gene Response Section, DBS, National Cancer Institute, Bethesda, Maryland 20892 4255, USA
    Nat Genet 23:176-84. 1999
  9. ncbi request reprint The involvement of aryl hydrocarbon receptor in the activation of transforming growth factor-beta and apoptosis
    H Zaher
    Laboratory of Metabolism, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    Mol Pharmacol 54:313-21. 1998
  10. ncbi request reprint Sulindac sulfide-induced apoptosis involves death receptor 5 and the caspase 8-dependent pathway in human colon and prostate cancer cells
    Y Huang
    Department of Pharmacology, State University of New York, Upstate Medical University, Syracuse, New York 13210, USA
    Cancer Res 61:6918-24. 2001

Collaborators

Detail Information

Publications11

  1. ncbi request reprint 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 cells
    M S Sheikh
    Laboratory of Molecular Pharmacology, National Cancer Institute, NIH, Bethesda, Maryland 20892, USA
    Cell Growth Differ 7:1599-607. 1996
    ....
  2. ncbi request reprint 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
    ....
  3. ncbi request reprint p53-dependent and -independent regulation of the death receptor KILLER/DR5 gene expression in response to genotoxic stress and tumor necrosis factor alpha
    M 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...
  4. ncbi request reprint 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 protein
    M 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...
  5. ncbi request reprint Activation of Gadd34 by diverse apoptotic signals and suppression of its growth inhibitory effects by apoptotic inhibitors
    M 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...
  6. ncbi request reprint The antiapoptotic decoy receptor TRID/TRAIL-R3 is a p53-regulated DNA damage-inducible gene that is overexpressed in primary tumors of the gastrointestinal tract
    M 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...
  7. ncbi request reprint Chromatin relaxation by overexpression of mutant p53, HPV16-E6, or cyclin G transgenes
    M L Smith
    Division of Basic Science, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    Exp Cell Res 242:235-43. 1998
    ....
  8. ncbi request reprint Genomic instability in Gadd45a-deficient mice
    M 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...
  9. ncbi request reprint The involvement of aryl hydrocarbon receptor in the activation of transforming growth factor-beta and apoptosis
    H 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...
  10. ncbi request reprint Sulindac sulfide-induced apoptosis involves death receptor 5 and the caspase 8-dependent pathway in human colon and prostate cancer cells
    Y 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...
  11. ncbi request reprint Transcriptional upregulation of PUMA modulates endoplasmic reticulum calcium pool depletion-induced apoptosis via Bax activation
    X 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...