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  • 1
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    Prokaryotic regulation of epithelial responses by inhibition of IkappaB-alpha ubiquitination (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-09-01
    Description: Epithelia of the vertebrate intestinal tract characteristically maintain an inflammatory hyporesponsiveness toward the lumenal prokaryotic microflora. We report the identification of enteric organisms (nonvirulent Salmonella strains) whose direct interaction with model human epithelia attenuate synthesis of inflammatory effector molecules elicited by diverse proinflammatory stimuli. This immunosuppressive effect involves inhibition of the inhibitor kappaB/nuclear factor kappaB (IkappaB/NF-kappaB) pathway by blockade of IkappaB-alpha degradation, which prevents subsequent nuclear translocation of active NF-kappaB dimer. Although phosphorylation of IkappaB-alpha occurs, subsequent polyubiquitination necessary for regulated IkappaB-alpha degradation is completely abrogated. These data suggest that prokaryotic determinants could be responsible for the unique tolerance of the gastrointestinal mucosa to proinflammatory stimuli.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Neish, A S -- Gewirtz, A T -- Zeng, H -- Young, A N -- Hobert, M E -- Karmali, V -- Rao, A S -- Madara, J L -- DK-35932/DK/NIDDK NIH HHS/ -- DK-47662/DK/NIDDK NIH HHS/ -- DK09800/DK/NIDDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 2000 Sep 1;289(5484):1560-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Epithelial Pathobiology Unit, Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA. aneish@emory.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10968793" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Nucleus/metabolism ; Cysteine Proteinase Inhibitors/pharmacology ; Cytoskeletal Proteins/metabolism ; DNA-Binding Proteins/*metabolism ; Dimerization ; Humans ; *I-kappa B Proteins ; Inflammation Mediators/pharmacology ; Interleukin-8/genetics/metabolism ; Intestinal Mucosa/*metabolism/*microbiology ; Leupeptins/pharmacology ; Ligases/metabolism ; NF-kappa B/genetics/*metabolism ; Phosphorylation ; Salmonella/pathogenicity/*physiology ; Salmonella typhimurium/pathogenicity/physiology ; *Trans-Activators ; Transcription Factor RelA ; Tumor Cells, Cultured ; Tumor Necrosis Factor-alpha/pharmacology ; Ubiquitin-Protein Ligases ; Ubiquitins/metabolism ; beta Catenin
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Clinical resistance to STI-571 cancer therapy caused by BCR-ABL gene mutation or amplification (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-06-26
    Description: Clinical studies with the Abl tyrosine kinase inhibitor STI-571 in chronic myeloid leukemia demonstrate that many patients with advanced stage disease respond initially but then relapse. Through biochemical and molecular analysis of clinical material, we find that drug resistance is associated with the reactivation of BCR-ABL signal transduction in all cases examined. In six of nine patients, resistance was associated with a single amino acid substitution in a threonine residue of the Abl kinase domain known to form a critical hydrogen bond with the drug. This substitution of threonine with isoleucine was sufficient to confer STI-571 resistance in a reconstitution experiment. In three patients, resistance was associated with progressive BCR-ABL gene amplification. These studies provide evidence that genetically complex cancers retain dependence on an initial oncogenic event and suggest a strategy for identifying inhibitors of STI-571 resistance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gorre, M E -- Mohammed, M -- Ellwood, K -- Hsu, N -- Paquette, R -- Rao, P N -- Sawyers, C L -- GM07185/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2001 Aug 3;293(5531):876-80. Epub 2001 Jun 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Molecular Biology Institute, University of California, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11423618" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acid Substitution ; Antineoplastic Agents/metabolism/pharmacology/therapeutic use ; Base Sequence ; Benzamides ; Blast Crisis/genetics ; Cell Line ; Drug Resistance, Neoplasm/genetics ; Fusion Proteins, bcr-abl/*metabolism ; Gene Amplification ; *Genes, abl ; Humans ; Hydrogen Bonding ; Imatinib Mesylate ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/*drug therapy/*genetics ; Molecular Sequence Data ; Philadelphia Chromosome ; Phosphorylation ; Piperazines/metabolism/*pharmacology/therapeutic use ; Point Mutation ; Protein Structure, Tertiary ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-abl/antagonists & ; inhibitors/chemistry/*genetics/metabolism ; Proto-Oncogene Proteins c-crk ; Pyrimidines/metabolism/*pharmacology/therapeutic use ; Recurrence ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
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