Gene Ontology annotation through association of InterPro records with GO terms
Gene Ontology annotation based on Enzyme Commission mapping
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Gene Ontology annotation based on curation of immunofluorescence data
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Combined Automated Annotation using Multiple IEA Methods
The xeroderma pigmentosum group C protein complex XPC-HR23B plays an important role in the recruitment of transcription factor IIH to damaged DNA.
Distinct regions of MAT1 regulate cdk7 kinase and TFIIH transcription activities.
Trichothiodystrophy, a transcription syndrome.
A new, tenth subunit of TFIIH is responsible for the DNA repair syndrome trichothiodystrophy group A.
Dynamic interaction of TTDA with TFIIH is stabilized by nucleotide excision repair in living cells.
The role of XPB in cell apoptosis and viability and its relationship with p53, p21(waf1/cip1) and c-myc in hepatoma cells.
DNA nucleotide excision repair-dependent signaling to checkpoint activation.
Detection and identification of transcription factors as interaction partners of alien in vivo.
Distinct roles for the XPB/p52 and XPD/p44 subcomplexes of TFIIH in damaged DNA opening during nucleotide excision repair.
Influence of XPB helicase on recruitment and redistribution of nucleotide excision repair proteins at sites of UV-induced DNA damage.
Genetic susceptibility of newborn daughters to oxidative stress.
Structural basis for group A trichothiodystrophy.
Both XPD alleles contribute to the phenotype of compound heterozygote xeroderma pigmentosum patients.
A presumed DNA helicase encoded by ERCC-3 is involved in the human repair disorders xeroderma pigmentosum and Cockayne's syndrome.
Toward an understanding of the protein interaction network of the human liver.
TFIIH: when transcription met DNA repair.
A proteome-scale map of the human interactome network.
A human interactome in three quantitative dimensions organized by stoichiometries and abundances.
Near-atomic resolution visualization of human transcription promoter opening.
Architecture of the human interactome defines protein communities and disease networks.
Extensive disruption of protein interactions by genetic variants across the allele frequency spectrum in human populations.
A reference map of the human binary protein interactome.
Dual proteome-scale networks reveal cell-specific remodeling of the human interactome.
A protein network map of head and neck cancer reveals PIK3CA mutant drug sensitivity.
p53 modulation of TFIIH-associated nucleotide excision repair activity.
Transcription factor IIE binds preferentially to RNA polymerase IIa and recruits TFIIH: a model for promoter clearance.
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.
A 3' --> 5' XPB helicase defect in repair/transcription factor TFIIH of xeroderma pigmentosum group B affects both DNA repair and transcription.
The XPB and XPD DNA helicases are components of the p53-mediated apoptosis pathway.
Isolation and characterization of two human transcription factor IIH (TFIIH)-related complexes: ERCC2/CAK and TFIIH.
Human cyclin-dependent kinase-activating kinase exists in three distinct complexes.
The XPB subunit of repair/transcription factor TFIIH directly interacts with SUG1, a subunit of the 26S proteasome and putative transcription factor.
Immunoaffinity purification and functional characterization of human transcription factor IIH and RNA polymerase II from clonal cell lines that conditionally express epitope-tagged subunits of the multiprotein complexes.
Formation of the closed pre-initiation complex
Addition of nucleotides between position +11 and +30
Recruitment of elongation factors to form elongation complex
Hypophosphorylation of RNA Pol II CTD by FCP1P protein
Addition of nucleotides leads to transcript elongation
Extrusion of 5'-end of 30 nt long transcript through the pore in Pol II complex
Formation of the pre-incision complex in GG-NER
Recruitment of XPA and release of CAK
DNA polymerases delta, epsilon or kappa bind the GG-NER site
3'-incision of DNA by ERCC5 (XPG) in GG-NER
5'- incision of DNA by ERCC1:ERCC4 in GG-NER
Binding of ERCC1:ERCC4 (ERCC1:XPF) to pre-incision complex in GG-NER
ERCC2 and ERCC3 DNA helicases form an open bubble structure in damaged DNA
TFIIH binds GG-NER site to form a verification complex
CHD1L is recruited to GG-NER site
RNA Pol II initiates transcription from damaged DNA template
Active RNA Pol II complex transcribes lesion-containing DNA template
Transcription-Coupled Nucleotide Excision Repair (TC-NER)
ERCC8 (CSA) binds stalled RNA Pol II
ERCC6 binds stalled RNA Pol II
ERCC8:DDB1:CUL4:RBX1 ubiquitinates ERCC6 and RNA Pol II
Assembly of the pre-incision complex in TC-NER
UVSSA:USP7 deubiquitinates ERCC6
ERCC2-facilitated RNA Pol II backtracking in TC-NER
ERCC5 and RPA bind TC-NER site
Binding of ERCC1:ERCC4 (ERCC1:XPF) to pre-incision complex in TC-NER
5' incision of damaged DNA strand by ERCC1:ERCC4 in TC-NER
Repair DNA synthesis of ~27-30 bases long patch by POLD, POLE or POLK in TC-NER
DNA polymerases delta, epsilon or kappa bind the TC-NER site
3' incision by ERCC5 (XPG) in TC-NER
Ligation of newly synthesized repair patch to incised DNA in TC-NER
Recovery of RNA synthesis after TC-NER
RNF111 ubiquitinates SUMOylated XPC
CDK12 phosphorylates RNA Pol II CTD at DNA repair genes
CCNK:CDK12 binds RNA Pol II at DNA repair genes
Recruitment of Active RNA Polymerase I to SL1:phos.UBF-1:rDNA Promoter
Loss of Rrn3 from RNA Polymerase I promoter escape complex
RNA Polymerase II Promoter Escape
RNA Polymerase II Transcription
Abortive initiation after formation of the first phosphodiester bond
Elongation of pre-rRNA transcript
Dissociation of PTRF:Polymerase I/Nascent Pre rRNA Complex:TTF-I:Sal Box
PTRF Binds the Polymerase I Transcription Complex/Nascent Pre rRNA Complex paused at the TTF-I:Sal Box
Polymerase I Transcription Complex/Nascent Pre rRNA Complex pauses at the TTF-I:Sal Box
Addition of the third nucleotide on the nascent transcript
Abortive Initiation Before Second Transition
NTP Binds Active Site of RNA Polymerase II
Fall Back to Closed Pre-initiation Complex
Newly Formed Phosphodiester Bond Stabilized and PPi Released
Nucleophillic Attack by 3'-hydroxyl Oxygen of nascent transcript on the Alpha Phosphate of NTP
Addition of the fourth nucleotide on the Nascent Transcript: Second Transition
Addition of Nucleotides 5 through 9 on the growing Transcript
Abortive Initiation After Second Transition
RNA Polymerase II Promoter Opening: First Transition
Addition of nucleotides 10 and 11 on the growing transcript: Third Transition
RNA Polymerase II CTD (phosphorylated) binds to CE
Phosphorylation (Ser5) of RNA pol II CTD
SPT5 subunit of Pol II binds the RNA triphosphatase (RTP)
Capping complex formation
Hydrolysis of the 5'-end of the nascent transcript by the capping enzyme
Formation of the CE:GMP intermediate complex
Transfer of GMP from the capping enzyme GT site to 5'-end of mRNA
Dissociation of transcript with 5'-GMP from GT
Methylation of GMP-cap by RNA Methyltransferase
Unwinding of DNA for the Nascent Transcript: Second Transition
Unwinding DNA for the nascent transcript
ERCC3-facilitated RNA Pol II backtracking in TC-NER
Pre-incision structures reveal principles of DNA nucleotide excision repair.
Differential dependencies of human RNA polymerase II promoters on TBP, TAF1, TFIIBÂ and XPB.
ERCC3 primary-source and database evidence guide
Transcription factor TFIIH and DNA endonuclease Rad2 constitute yeast nucleotide excision repair factor 3: implications for nucleotide excision repair and Cockayne syndrome.
Architecture of the RNA polymerase II preinitiation complex and mechanism of ATP-dependent promoter opening.
Defective transcription initiation causes postnatal growth failure in a mouse model of nucleotide excision repair (NER) progeria.
Nucleotide excision repair gene expression in the rat conceptus during organogenesis.
Mutations in TFIIH causing trichothiodystrophy are responsible for defects in ribosomal RNA production and processing.
Toward an understanding of the protein interaction network of the human liver.