TRIM24
Transcription intermediary factor 1-alpha
Also known as: hTIF1, RNF82, TIF1, Tif1a, TIF1A_HUMAN
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- O15164
- Gene
- TRIM24
- Ensembl
- ENSG00000122779
- Chromosome
- 7
- Canonical length
- 1050 aa
- Protein class
- Cancer-related genes, Disease related genes, Enzymes, Plasma proteins, Potential drug targets, Predicted intracellular proteins
- Subcellular location
- Nucleoplasm
OverviewNCBI Gene
The protein encoded by this gene mediates transcriptional control by interaction with the activation function 2 (AF2) region of several nuclear receptors, including the estrogen, retinoic acid, and vitamin D3 receptors. The protein localizes to nuclear bodies and is thought to associate with chromatin and heterochromatin-associated factors. The protein is a member of the tripartite motif (TRIM) family. The TRIM motif includes three zinc-binding domains - a RING, a B-box type 1 and a B-box type 2 - and a coiled-coil region. Two alternatively spliced transcript variants encoding different isoforms have been described for this gene. [provided by RefSeq, Jul 2008]
Canonical amino-acid sequenceUniProt
1050 residues, UniProt reviewed canonical sequence.
>O15164|TRIM24
1 MEVAVEKAVA AAAAASAAAS GGPSAAPSGE NEAESRQGPD SERGGEAARL NLLDTCAVCH
61 QNIQSRAPKL LPCLHSFCQR CLPAPQRYLM LPAPMLGSAE TPPPVPAPGS PVSGSSPFAT
121 QVGVIRCPVC SQECAERHII DNFFVKDTTE VPSSTVEKSN QVCTSCEDNA EANGFCVECV
181 EWLCKTCIRA HQRVKFTKDH TVRQKEEVSP EAVGVTSQRP VFCPFHKKEQ LKLYCETCDK
241 LTCRDCQLLE HKEHRYQFIE EAFQNQKVII DTLITKLMEK TKYIKFTGNQ IQNRIIEVNQ
301 NQKQVEQDIK VAIFTLMVEI NKKGKALLHQ LESLAKDHRM KLMQQQQEVA GLSKQLEHVM
361 HFSKWAVSSG SSTALLYSKR LITYRLRHLL RARCDASPVT NNTIQFHCDP SFWAQNIINL
421 GSLVIEDKES QPQMPKQNPV VEQNSQPPSG LSSNQLSKFP TQISLAQLRL QHMQQQVMAQ
481 RQQVQRRPAP VGLPNPRMQG PIQQPSISHQ QPPPRLINFQ NHSPKPNGPV LPPHPQQLRY
541 PPNQNIPRQA IKPNPLQMAF LAQQAIKQWQ ISSGQGTPST TNSTSSTPSS PTITSAAGYD
601 GKAFGSPMID LSSPVGGSYN LPSLPDIDCS STIMLDNIVR KDTNIDHGQP RPPSNRTVQS
661 PNSSVPSPGL AGPVTMTSVH PPIRSPSASS VGSRGSSGSS SKPAGADSTH KVPVVMLEPI
721 RIKQENSGPP ENYDFPVVIV KQESDEESRP QNANYPRSIL TSLLLNSSQS STSEETVLRS
781 DAPDSTGDQP GLHQDNSSNG KSEWLDPSQK SPLHVGETRK EDDPNEDWCA VCQNGGELLC
841 CEKCPKVFHL SCHVPTLTNF PSGEWICTFC RDLSKPEVEY DCDAPSHNSE KKKTEGLVKL
901 TPIDKRKCER LLLFLYCHEM SLAFQDPVPL TVPDYYKIIK NPMDLSTIKK RLQEDYSMYS
961 KPEDFVADFR LIFQNCAEFN EPDSEVANAG IKLENYFEEL LKNLYPEKRF PKPEFRNESE
1021 DNKFSDDSDD DFVQPRKKRL KSIEERQLLKLocalizationUniProt · AlphaFold · HPA
Whether an antibody against TRIM24 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)
- 0.52
- Highest tissue expression
- 26 nTPM
Expression across tissuesHPA
Tissue
- testis: 26 nTPM
- ovary: 25 nTPM
- adrenal gland: 24 nTPM
- liver: 22 nTPM
- thymus: 16 nTPM
- tongue: 15 nTPM
Single-cell type
- adrenal cortex cells: 316 nCPM
- thymocytes: 278 nCPM
- megakaryocyte progenitors: 240 nCPM
- hematopoietic stem cells: 232 nCPM
- retinal horizontal cells: 212 nCPM
- prostatic glandular cells: 202 nCPM
Immune cell
- eosinophil: 1 nTPM
- neutrophil: 0.9 nTPM
- T-reg: 0.7 nTPM
- classical monocyte: 0.6 nTPM
- intermediate monocyte: 0.6 nTPM
- NK-cell: 0.6 nTPM
Brain region
- white matter: 20 nTPM
- hypothalamus: 19 nTPM
- medulla oblongata: 17 nTPM
- basal ganglia: 16 nTPM
- midbrain: 16 nTPM
- thalamus: 15 nTPM
DiseaseUniProt · ClinVar · IEDB · PubMed
Four sources answering four different questions about TRIM24.
Disease | GeneticClinVar
1 pathogenic / likely-pathogenic of 123 ClinVar records.
Conditions with pathogenic or likely-pathogenic variants.
Disease | AutoantibodyPubMed
Conditions in which antibodies against TRIM24 are reported. Each links to that disease's full target list.
ReferencesPubMed · IEDB
Publications for TRIM24 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
16 publications
- Recent advances in dermatomyositis-specific autoantibodies.
2016 · Curr Opin Rheumatol · RCR 5 · 112 citations - Focused HLA analysis in Caucasians with myositis identifies significant associations with autoantibody subgroups.
2019 · Ann Rheum Dis · RCR 4.9 · 99 citations - The temporal relationship between cancer and adult onset anti-transcriptional intermediary factor 1 antibody-positive dermatomyositis.
2019 · Rheumatology (Oxford) · RCR 4.1 · 83 citations - Anti-MDA5 autoantibodies associated with juvenile dermatomyositis constitute a distinct phenotype in North America.
2021 · Rheumatology (Oxford) · RCR 3.9 · 45 citations - Pathogenic mechanisms of disease in idiopathic inflammatory myopathies: autoantibodies as clues.
2024 · Front Immunol · RCR 3.9 · 17 citations
Show 11 more
- Clinical features of dermatomyositis patients with anti-TIF1 antibodies: A case based comprehensive review.
2023 · Autoimmun Rev · RCR 3.5 · 21 citations - Expression of interferon-regulated genes in juvenile dermatomyositis versus Mendelian autoinflammatory interferonopathies.
2020 · Arthritis Res Ther · RCR 3.5 · 57 citations - Longitudinal changes in nailfold videocapillaroscopy findings differ by myositis-specific autoantibody in idiopathic inflammatory myopathy.
2023 · Rheumatology (Oxford) · RCR 2 · 9 citations - Autoantibodies Recognizing Specificity Protein 4 Co-occur With Anti-Transcription Intermediary Factor 1 and Are Associated With Distinct Clinical Features and Immunogenetic Risk Factors in Juvenile Myositis.
2023 · Arthritis Rheumatol · RCR 1.9 · 11 citations - Clinical features of anti-TIF1-α antibody-positive dermatomyositis patients are closely associated with coexistent dermatomyositis-specific autoantibodies and anti-TIF1-γ or anti-Mi-2 autoantibodies.
2012 · Rheumatology (Oxford) · RCR 1.4 · 43 citations - Genetics of idiopathic inflammatory myopathies: insights into disease pathogenesis.
2019 · Curr Opin Rheumatol · RCR 1 · 19 citations - A case of juvenile amyopathic dermatomyositis with anti-transcription intermediary factor 1-α antibody showing negative anti-TIF1-γ ELISA results: Comment on "Case of pembrolizumab-induced dermatomyositis with anti-transcription intermediary factor 1-γ antibody".
2023 · J Dermatol · RCR 0.7 · 2 citations - Environmental factors associated with juvenile idiopathic inflammatory myopathy clinical and serologic phenotypes.
2022 · Pediatr Rheumatol Online J · RCR 0.7 · 7 citations - Autoantibody to transcriptional intermediary factor-1β as a myositis-specific antibody: clinical correlation with clinically amyopathic dermatomyositis or dermatomyositis with mild myopathy.
2019 · Br J Dermatol · RCR 0.7 · 10 citations - Anti-TIF-1α/γ Antibody-Positive Dermatomyositis Associated With Metastatic Prostatic Adenocarcinoma.
2021 · J Clin Neuromuscul Dis · RCR 0.1 · 1 citations - A rare intersection: squamous cell carcinoma of the tonsil and the anti-TIF1 syndrome masquerade.
2025 · BMC Rheumatol
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)
- 0.12
- gnomAD pLI
- 1
- gnomAD missense Z
- 3.43
- DepMap mean gene effect
- 0.06
- DepMap dependency class
- selective
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 7% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
- calcium ion homeostasis
- cellular response to estrogen stimulus
- epithelial cell proliferation
- negative regulation of DNA-templated transcription
- negative regulation of epithelial cell proliferation
- positive regulation of gene expression
- protein catabolic process
- protein ubiquitination
- regulation of apoptotic process
- regulation of protein stability
- regulation of signal transduction by p53 class mediator
- regulation of vitamin D receptor signaling pathway
- response to peptide hormone
- transcription by RNA polymerase II
Molecular functions
- chromatin binding
- estrogen response element binding
- nuclear receptor binding
- p53 binding
- protein kinase activity
- signaling receptor binding
- transcription coactivator activity
- ubiquitin protein ligase activity
- zinc ion binding
- histone H3K23ac reader activity
Cellular components
Protein domainsUniProt · Pfam · InterPro
- B-box-type zinc finger
- Bromodomain
- Zinc finger, RING-type
- Zinc finger, PHD-type
- B-box, C-terminal
- Zinc finger, FYVE/PHD-type
- Zinc finger, RING/FYVE/PHD-type
- Zinc finger, RING-type, conserved site
- Bromodomain, conserved site
- Zinc finger, PHD-type, conserved site
- Zinc finger, PHD-finger
- Bromodomain-like superfamily
- Bromodomain
- PHD-finger
- B-box zinc finger
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of TRIM24 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 TRIM24 as an antibody target. Whether an autoantibody or antibody against TRIM24 could matter depends on whether native TRIM24 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
TRIM24 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 TRIM24 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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