TRIP4
Activating signal cointegrator 1
Also known as: ASC-1, HsT17391, TRIP4_HUMAN, ZC2HC5
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- Q15650
- Gene
- TRIP4
- Ensembl
- ENSG00000103671
- Chromosome
- 15
- Canonical length
- 581 aa
- Protein class
- Cancer-related genes, Disease related genes, Human disease related genes, Predicted intracellular proteins
- Subcellular location
- Nucleoplasm,Nuclear bodies
OverviewNCBI Gene
This gene encodes a subunit of the tetrameric nuclear activating signal cointegrator 1 (ASC-1) complex, which associates with transcriptional coactivators, nuclear receptors and basal transcription factors to facilitate nuclear receptors-mediated transcription. This protein is localized in the nucleus and contains an E1A-type zinc finger domain, which mediates interaction with transcriptional coactivators and ligand-bound nuclear receptors, such as thyroid hormone receptor and retinoid X receptor alpha, but not glucocorticoid receptor. Mutations in this gene are associated with spinal muscular atrophy with congenital bone fractures-1 (SMABF1). [provided by RefSeq, Apr 2016]
Canonical amino-acid sequenceUniProt
581 residues, UniProt reviewed canonical sequence.
>Q15650|TRIP4
1 MAVAGAVSGE PLVHWCTQQL RKTFGLDVSE EIIQYVLSIE SAEEIREYVT DLLQGNEGKK
61 GQFIEELITK WQKNDQELIS DPLQQCFKKD EILDGQKSGD HLKRGRKKGR NRQEVPAFTE
121 PDTTAEVKTP FDLAKAQENS NSVKKKTKFV NLYTREGQDR LAVLLPGRHP CDCLGQKHKL
181 INNCLICGRI VCEQEGSGPC LFCGTLVCTH EEQDILQRDS NKSQKLLKKL MSGVENSGKV
241 DISTKDLLPH QELRIKSGLE KAIKHKDKLL EFDRTSIRRT QVIDDESDYF ASDSNQWLSK
301 LERETLQKRE EELRELRHAS RLSKKVTIDF AGRKILEEEN SLAEYHSRLD ETIQAIANGT
361 LNQPLTKLDR SSEEPLGVLV NPNMYQSPPQ WVDHTGAASQ KKAFRSSGFG LEFNSFQHQL
421 RIQDQEFQEG FDGGWCLSVH QPWASLLVRG IKRVEGRSWY TPHRGRLWIA ATAKKPSPQE
481 VSELQATYRL LRGKDVEFPN DYPSGCLLGC VDLIDCLSQK QFKEQFPDIS QESDSPFVFI
541 CKNPQEMVVK FPIKGNPKIW KLDSKIHQGA KKGLMKQNKA VLocalizationUniProt · AlphaFold · HPA
Whether an antibody against TRIP4 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)
- 0.46
- Highest tissue expression
- 26 nTPM
Expression across tissuesHPA
Tissue
- kidney: 26 nTPM
- thyroid gland: 24 nTPM
- esophagus: 19 nTPM
- parathyroid gland: 19 nTPM
- thymus: 19 nTPM
- rectum: 18 nTPM
Single-cell type
- proximal tubule cells: 95 nCPM
- neutrophils: 72 nCPM
- neutrophil progenitors: 72 nCPM
- esophageal apical cells: 65 nCPM
- fibro-adipogenic progenitors: 65 nCPM
- endometrial ciliated cells: 61 nCPM
Immune cell
- basophil: 70 nTPM
- eosinophil: 54 nTPM
- non-classical monocyte: 43 nTPM
- neutrophil: 31 nTPM
- intermediate monocyte: 29 nTPM
- T-reg: 23 nTPM
Brain region
- white matter: 13 nTPM
- choroid plexus: 12 nTPM
- medulla oblongata: 11 nTPM
- thalamus: 11 nTPM
- basal ganglia: 11 nTPM
- pons: 10 nTPM
DiseaseUniProt · ClinVar · IEDB · PubMed
Four sources answering four different questions about TRIP4.
Disease | AllUniProt
Conditions TRIP4 is implicated in, by any mechanism.
- Spinal muscular atrophy with congenital bone fractures 1 (SMABF1) MIM:616866
- Muscular dystrophy, congenital, Davignon-Chauveau type (MDCDC) MIM:617066
Disease | GeneticClinVar
32 pathogenic / likely-pathogenic of 349 ClinVar records.
Conditions with pathogenic or likely-pathogenic variants.
- Spinal muscular atrophy with congenital bone fractures 1
- TRIP4-related disorder
- Congenital muscular dystrophy-respiratory failure-skin abnormalities-joint hyperlaxity syndrome
- Centronuclear myopathy
- Gastric cancer
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)
- 0.67
- gnomAD pLI
- 0
- gnomAD missense Z
- 0.57
- DepMap mean gene effect
- -0.17
- DepMap dependency class
- selective
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
- estrogen receptor signaling pathway
- positive regulation of DNA-templated transcription
- regulation of DNA-templated transcription
- regulation of myoblast differentiation
- rescue of stalled ribosome
- ribosome disassembly
- ribosome-associated ubiquitin-dependent protein catabolic process
Molecular functions
- histone acetyltransferase binding
- nuclear estrogen receptor binding
- nuclear receptor binding
- protease binding
- protein kinase binding
- transcription coactivator activity
- ubiquitin-like protein ligase binding
- zinc ion binding
Cellular components
Protein domainsUniProt · Pfam · InterPro
- ASCH domain
- PUA-like superfamily
- TRIP4/RQT4, C2HC5-type zinc finger
- Activating signal cointegrator 1-like
- Activating signal cointegrator 1, third domain
- Activating signal cointegrator 1, N-terminal
- ASCH domain
- Putative zinc finger motif, C2HC5-type
- TRIP4, third domain
- TRI4 N-terminal domain
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of TRIP4 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 TRIP4 as an antibody target. Whether an autoantibody or antibody against TRIP4 could matter depends on whether native TRIP4 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
TRIP4 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 TRIP4 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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