Seroatlas · Human Serome Atlas

TBP

TATA-box-binding protein

Also known as: GTF2D1, SCA17, TBP_HUMAN, TBP1, TFIID

Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene

Protein identityUniProt · HPA

UniProt accession: P20226
Gene: TBP
Ensembl: ENSG00000112592
Chromosome: 6
Canonical length: 339 aa
Protein class: Disease related genes, Human disease related genes, Predicted intracellular proteins, Transcription factors
Subcellular location: Nucleoplasm,Cytosol

OverviewNCBI Gene

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]

Canonical amino-acid sequenceUniProt

339 residues, UniProt reviewed canonical sequence.

>P20226|TBP
     1  MDQNNSLPPY AQGLASPQGA MTPGIPIFSP MMPYGTGLTP QPIQNTNSLS ILEEQQRQQQ
    61  QQQQQQQQQQ QQQQQQQQQQ QQQQQQQQQQ QQQQQAVAAA AVQQSTSQQA TQGTSGQAPQ
   121  LFHSQTLTTA PLPGTTPLYP SPMTPMTPIT PATPASESSG IVPQLQNIVS TVNLGCKLDL
   181  KTIALRARNA EYNPKRFAAV IMRIREPRTT ALIFSSGKMV CTGAKSEEQS RLAARKYARV
   241  VQKLGFPAKF LDFKIQNMVG SCDVKFPIRL EGLVLTHQQF SSYEPELFPG LIYRMIKPRI
   301  VLLIFVSGKV VLTGAKVRAE IYEAFENIYP ILKGFRKTT

LocalizationUniProt · AlphaFold · HPA

Whether an antibody against TBP can act on the native protein depends on physical access: surface and secreted proteins are reachable by circulating antibodies, intracellular proteins usually are not.

Antibody reachability: Intracellular
Secreted: No
Transmembrane segments: 0
Mean surface accessibility (rSASA): 0.48
Highest tissue expression: 32 nTPM

Expression across tissuesHPA

Tissue

testis: 32 nTPM
bone marrow: 15 nTPM
spleen: 15 nTPM
cerebellum: 13 nTPM
lymph node: 13 nTPM
ovary: 12 nTPM

Single-cell type

late primary spermatocytes: 153 nCPM
early primary spermatocytes: 49 nCPM
tuft cells: 35 nCPM
parietal cells: 34 nCPM
oocytes: 32 nCPM
differentiating spermatogonia: 31 nCPM

Immune cell

basophil: 68 nTPM
memory B-cell: 53 nTPM
naive B-cell: 50 nTPM
naive CD4 T-cell: 47 nTPM
non-classical monocyte: 46 nTPM
neutrophil: 45 nTPM

Brain region

white matter: 18 nTPM
cerebral cortex: 18 nTPM
hypothalamus: 17 nTPM
cerebellum: 16 nTPM
medulla oblongata: 15 nTPM
midbrain: 15 nTPM

DiseaseUniProt · ClinVar · IEDB · PubMed

Four sources answering four different questions about TBP.

Disease | AllUniProt

Conditions TBP is implicated in, by any mechanism.

Spinocerebellar ataxia 17 (SCA17) MIM:607136

Disease | GeneticClinVar

4 pathogenic / likely-pathogenic of 97 ClinVar records.

Conditions with pathogenic or likely-pathogenic variants.

Spinocerebellar ataxia type 17
Parkinson disease, late-onset

ReferencesPubMed · IEDB

Publications for TBP from three distinct lines of evidence, kept separate because they answer different questions: whether antibodies are directed at the protein, whether a B-cell epitope has been mapped on it, and whether a T-cell epitope has. Each is labelled with its source.

Reference: AutoantibodyPubMed

1 publication

Over-expression of TATA binding protein (TBP) and p53 and autoantibodies to these antigens are features of systemic sclerosis, systemic lupus erythematosus and overlap syndromes.
2004 · Clin Exp Immunol · RCR 0.4 · 24 citations

Sources: PubMed — antigen-level antibody evidence from a custom retrieval. Records matching a controlled set of autoantibody terms (the MeSH descriptors Autoantibodies and Autoantigens, with title and abstract term variants) were obtained through NCBI E-utilities, and their titles and abstracts parsed for constructions that direct an antibody at a named protein rather than for co-occurrence. Captured names were resolved against UniProt nomenclature and each antigen adjudicated individually against the source text. Bibliographic records from PubMed and MeSH, U.S. National Library of Medicine; citation metrics from NIH iCite (Hutchins et al., PLoS Biology 2016). Titles link to PubMed; abstracts are not reproduced here. The NLM does not endorse this analysis.

Genetic constraint and essentialitygnomAD · DepMap

Does the body need this protein intact? Low LOEUF or a strong DepMap dependency means loss or blockade of the protein is likely to be felt.

gnomAD LOEUF (loss-of-function intolerance): 0.62
gnomAD pLI: 0.02
gnomAD missense Z: 2.61
DepMap mean gene effect: -0.8
DepMap dependency class: common

Cancer expressionTCGA

Across TCGA tumor cohorts, this protein is over-expressed in roughly 5% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).

OntologyGO

Biological processes

Molecular functions

Cellular components

Protein domainsUniProt · Pfam · InterPro

KeywordsUniProt

InteractionsUniProt · HPA

Protein binding partners of TBP in the human serome: UniProt-annotated complex subunits plus reported interactors. Each links to its own Seroatlas record.

Antibody and autoantibody relevanceSeroatlas analysis

Seroatlas reads TBP as an antibody target. Whether an autoantibody or antibody against TBP could matter depends on whether native TBP is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.

TBP is annotated as predominantly intracellular. Intracellular proteins are common autoantibody markers, becoming visible to the immune system after cell injury or altered processing, but are usually markers of disease rather than direct drivers.

Annotation status

The present source text does not explicitly label TBP as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.

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