TBP

Initiation of transcription by RNA polymerase II requires the activities of more than 70 polypeptides. The protein that coordinates these activities is transcription factor IID (TFIID), which binds to the core promoter to position the polymerase properly, serves as the scaffold for assembly of the remainder of the transcription complex, and acts as a channel for regulatory signals. TFIID is composed of the TATA-binding protein (TBP) and a group of evolutionarily conserved proteins known as TBP-associated factors or TAFs. TAFs may participate in basal transcription, serve as coactivators, function in promoter recognition or modify general transcription factors (GTFs) to facilitate complex assembly and transcription initiation. This gene encodes TBP, the TATA-binding protein. A distinctive feature of TBP is a long string of glutamines in the N-terminus. This region of the protein modulates the DNA binding activity of the C terminus, and modulation of DNA binding affects the rate of transcription complex formation and initiation of transcription. The number of CAG repeats encoding the polyglutamine tract is usually 25-42, and expansion of the number of repeats to 45-66 increases the length of the polyglutamine string and is associated with spinocerebellar ataxia 17, a neurodegenerative disorder classified as a polyglutamine disease. Two transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2016]

TBP TATA-Box Binding Protein

The TFIID basal transcription factor complex plays a major role in the initiation of RNA polymerase II (Pol II)-dependent transcription (PubMed:33795473).
TFIID recognizes and binds promoters with or without a TATA box via its subunit TBP, a TATA-box-binding protein, and promotes assembly of the pre-initiation complex (PIC) (PubMed:33795473, PubMed:27193682, PubMed:2194289, PubMed:2363050, PubMed:2374612).
The TFIID complex consists of TBP and TBP-associated factors (TAFs), including TAF1, TAF2, TAF3, TAF4, TAF5, TAF6, TAF7, TAF8, TAF9, TAF10, TAF11, TAF12 and TAF13 (PubMed:33795473, PubMed:27007846).
The TFIID complex structure can be divided into 3 modules TFIID-A, TFIID-B, and TFIID-C (PubMed:33795473).
TBP forms the TFIID-A module together with TAF3 and TAF5 (PubMed:33795473).
TBP is a general transcription factor that functions at the core of the TFIID complex (PubMed:33795473, PubMed:27193682, PubMed:2194289, PubMed:2363050, PubMed:2374612, PubMed:9836642).
During assembly of the core PIC on the promoter, as part of TFIID, TBP binds to and also bends promoter DNA, irrespective of whether the promoter contains a TATA box (PubMed:33795473).
Component of a BRF2-containing transcription factor complex that regulates transcription mediated by RNA polymerase III (PubMed:26638071).
Component of the transcription factor SL1/TIF-IB complex, which is involved in the assembly of the PIC during RNA polymerase I-dependent transcription (PubMed:15970593).
The rate of PIC formation probably is primarily dependent on the rate of association of SL1 with the rDNA promoter (PubMed:15970593).
SL1 is involved in stabilization of nucleolar transcription factor 1/UBTF on rDNA (PubMed:15970593).

Biological Process DNA-templated transcription initiationIBA:GO_Central1 Publication
Biological Process mRNA transcription by RNA polymerase IIIDA:ComplexPortal1 Publication
Biological Process positive regulation of transcription initiation by RNA polymerase IIIDA:ComplexPortal1 Publication
Biological Process protein phosphorylationIDA:ComplexPortal1 Publication
Biological Process RNA polymerase II preinitiation complex assemblyIDA:CAFA1 Publication
Biological Process transcription by RNA polymerase IIIDA:BHF-UCL1 Publication
Biological Process transcription by RNA polymerase IIIIDA:MGI1 Publication
Biological Process transcription initiation at RNA polymerase II promoterTAS:ProtInc1 Publication

Nucleus

Spinocerebellar ataxia 17 (SCA17):
Spinocerebellar ataxia is a clinically and genetically heterogeneous group of cerebellar disorders. Patients show progressive incoordination of gait and often poor coordination of hands, speech and eye movements, due to degeneration of the cerebellum with variable involvement of the brainstem and spinal cord. SCA17 is an autosomal dominant cerebellar ataxia (ADCA) characterized by widespread cerebral and cerebellar atrophy, dementia and extrapyramidal signs. The molecular defect in SCA17 is the expansion of a CAG repeat in the coding region of TBP. Longer expansions result in earlier onset and more severe clinical manifestations of the disease.