Activation of p53 or loss of the Cockayne syndrome group B repair protein causes metaphase fragility of human U1, U2, and 5S genes

Molecular Cell

Volumn 5, Issue 5, 2000, Pages 801-810

  Yu, Adong ^a   Fan, Hua Ying ^a   Liao, Daiqing ^a   Bailey, Arnold D ^a   Weiner, Alan M ^a  

^a YALE UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ELONGATION FACTOR; MESSENGER RNA; PROTEIN P53; RNA;

ADENOVIRUS; ARTICLE; CARBOXY TERMINAL SEQUENCE; CHROMATIN CONDENSATION; CHROMOSOME FRAGILITY; CLINICAL FEATURE; COCKAYNE SYNDROME; CONTROLLED STUDY; GENE ACTIVATION; GENE EXPRESSION; GENE LOCUS; GENE MUTATION; GENE OVEREXPRESSION; GENETIC TRANSFECTION; HUMAN; HUMAN CELL; METAPHASE; NONHUMAN; PROTEIN INTERACTION; RNA TRANSCRIPTION; RNA TRANSLATION; TANDEM REPEAT;

ADENOVIRIDAE; HUMAN ADENOVIRUS TYPE 12;

EID: 0033634972     PISSN: 10972765     EISSN: None     Source Type: Journal    
DOI: 10.1016/S1097-2765(00)80320-2     Document Type: Article

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14. The gene cluster for human U2 RNA is located on chromosome 17q21
15. The Cockayne syndrome group A gene encodes a WD repeat protein that interacts with CSB protein and a subunit of RNA polymerase II TFIIH
16. Interactions involving the human RNA polymerase II transcription/nucleotide excision repair complex TFIIH, the nucleotide excision repair protein XPG, and Cockayne syndrome group B (CSB) protein
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33. Several hydrophobic amino acids in the p53 amino-terminal domain are required for transcriptional activation, binding to mdm-2 and the adenovirus 5 E1B 55-kD protein
34. DNA excision repair pathways
35. Human genes for U2 small nuclear RNA map to a major Adenovirus 12 modification site on chromosome 17
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37. Genomic organization of human 5S rDNA and sequence of one tandem repeat
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39. Cloning and characterization of p52, the fifth subunit of the core of the transcription/DNA repair factor TFIIH
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41. Displacement of sequence-specific transcription factors from mitotic chromatin
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55. Progression of the cell cycle through mitosis leads to abortion of nascent transcripts
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