Defective interplay of activators and repressors with TFIH in xeroderma pigmentosum - Test2 - elhamkhani - TriplyDB

Defective interplay of activators and repressors with TFIH in xeroderma pigmentosum

Defective interplay of activators and repressors with TFIH in xeroderma pigmentosum

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The FUSE binding proteins FBP1 and FBP3 are potential c-myc regulators in renal, but not in prostate and bladder cancer JTV1 co-activates FBP to induce USP29 transcription and stabilize p53 in response to oxidative stress The FUSE/FBP/FIR/TFIIH system is a molecular machine programming a pulse of c-myc expression True lies: the double life of the nucleotide excision repair factors in transcription and DNA repair U2AF homology motifs: protein recognition in the RRM world Molecular basis of sequence-specific single-stranded DNA recognition by KH domains: solution structure of a complex between hnRNP K KH3 and single-stranded DNA Dimerization of FIR upon FUSE DNA binding suggests a mechanism of c-myc inhibition Functional interaction of p53 and BLM DNA helicase in apoptosis The dynamic response of upstream DNA to transcription-generated torsional stress Transcriptional activators control splicing and 3'-end cleavage levels Persistence of repair proteins at unrepaired DNA damage distinguishes diseases with ERCC2 (XPD) mutations: cancer-prone xeroderma pigmentosum vs. non-cancer-prone trichothiodystrophy.TFIIH operates through an expanded proximal promoter to fine-tune c-myc expression.Identification of candidate growth promoting genes in ovarian cancer through integrated copy number and expression analysis.Controlling the Master: Chromatin Dynamics at the MYC Promoter Integrate Developmental Signaling Alternative splicing of FBP-interacting repressor coordinates c-Myc, P27Kip1/cyclinE and Ku86/XRCC5 expression as a molecular sensor for bleomycin-induced DNA damage pathway.XPB induces C1D expression to counteract UV-induced apoptosis.On the traces of XPD: cell cycle matters - untangling the genotype-phenotype relationship of XPD mutations Molecular basis of FIR-mediated c-myc transcriptional control.Blinded by the UV light: how the focus on transcription-coupled NER has distracted from understanding the mechanisms of Cockayne syndrome neurologic disease An 8 nt RNA triggers a rate-limiting shift of RNA polymerase II complexes into elongation.UBF activates RNA polymerase I transcription by stimulating promoter escape.Regulation of BRCA1 transcription by specific single-stranded DNA binding factors FBPs are calibrated molecular tools to adjust gene expression Far upstream element binding protein 1 activates translation of p27Kip1 mRNA through its internal ribosomal entry site Far upstream element binding protein 1 binds the internal ribosomal entry site of enterovirus 71 and enhances viral translation and viral growth.Inactivated RNA polymerase II open complexes can be reactivated with TFIIE.Haploinsufficiency of the c-myc transcriptional repressor FIR, as a dominant negative-alternative splicing model, promoted p53-dependent T-cell acute lymphoblastic leukemia progression by activating Notch1.Overexpression of the far upstream element binding protein 1 in hepatocellular carcinoma is required for tumor growth.Human U2 snRNA genes exhibit a persistently open transcriptional state and promoter disassembly at metaphase Far Upstream Element Binding Protein Plays a Crucial Role in Embryonic Development, Hematopoiesis, and Stabilizing Myc Expression Levels.Hierarchical mechanisms build the DNA-binding specificity of FUSE binding protein.Far upstream element binding protein 1: a commander of transcription, translation and beyond Cellular MYCro economics: Balancing MYC function with MYC expression.Defining the essential function of FBP/KSRP proteins: Drosophila Psi interacts with the mediator complex to modulate MYC transcription and tissue growth Anti-FIRs (PUF60) auto-antibodies are detected in the sera of early-stage colon cancer patients.Phosphorylation of XPB helicase regulates TFIIH nucleotide excision repair activity.Non-transmissible Sendai virus vector encoding c-myc suppressor FBP-interacting repressor for cancer therapy Characterization of STAT6 target genes in human B cells and lung epithelial cells.Adenovirus-mediated FIR demonstrated TP53-independent cell-killing effect and enhanced antitumor activity of carbon-ion beams.Concomitant expression of far upstream element (FUSE) binding protein (FBP) interacting repressor (FIR) and its splice variants induce migration and invasion of non-small cell lung cancer (NSCLC) cells.

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Defective interplay of activators and repressors with TFIH in xeroderma pigmentosum

http://www.wikidata.org/entity/Q28203672

description

2001 nî lūn-bûn

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2001 թուականի Փետրուարին հրատարակուած գիտական յօդուած

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2001 թվականի փետրվարին հրատարակված գիտական հոդված

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2001年の論文

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2001年论文

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name

Defective interplay of activators and repressors with TFIH in xeroderma pigmentosum

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Defective interplay of activators and repressors with TFIH in xeroderma pigmentosum

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Defective interplay of activators and repressors with TFIH in xeroderma pigmentosum

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Defective interplay of activators and repressors with TFIH in xeroderma pigmentosum

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Defective interplay of activators and repressors with TFIH in xeroderma pigmentosum

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Defective interplay of activators and repressors with TFIH in xeroderma pigmentosum

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Defective interplay of activators and repressors with TFIH in xeroderma pigmentosum

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Defective interplay of activators and repressors with TFIH in xeroderma pigmentosum

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Defective interplay of activators and repressors with TFIH in xeroderma pigmentosum

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