ATAD2

ATAD2
Identifiers
AliasesATAD2, ANCCA, CT137, PRO2000, ATPase family, AAA domain containing 2, ATPase family AAA domain containing 2
External IDsOMIM: 611941; MGI: 1917722; GeneCards: ATAD2
Available structures
PDBOrtholog search: PDBe RCSB
Orthologs
DatabasesNCBI: entry; OMA: entry
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_014109

NM_027435
NM_153199

RefSeq (protein)

NP_054828

NP_081711
NP_001391691
NP_001391693
NP_001391694
NP_001391695

Location (UCSC)Chr 8: 123.32 – 123.42 MbChr 15: 57.96 – 58 Mb
PubMed search
Wikidata
View/Edit HumanView/Edit Mouse

ATPase family AAA domain containing 2 is a protein that in humans is encoded by the ATAD2 gene.

The protein encoded by this gene contains two AAA domains and a bromodomain. It acts as a coactivator of transcription factors. Overexpression of ATAD2 promotes cellular proliferation and is associated with poorer outcomes in several types of cancer. ATAD2 has therefore been investigated as both a prognostic biomarker and a potential drug target for cancer treatment.

Structure

ATAD2 is a nuclear protein of 1,390 amino acids containing an acidic N-terminal region, two tandem AAA+ ATPase domains, a bromodomain and a C-terminal domain. Its ATPase domain supports ATP-dependent activity and oligomerization, while its bromodomain forms a four-helix bundle that recognizes acetylated lysine residues on histone tails, promoting association with chromatin.

Function

ATAD2 participates in chromatin organization, DNA replication and transcriptional regulation. It acts as a transcriptional coactivator for estrogen and androgen receptors, MYC and E2F transcription factors.

Clinical significance

Cancer

ATAD2 promotes the expression of genes involved in cell proliferation and survival. It is frequently overexpressed in cancers, where increased expression is associated with tumor progression and poorer prognosis.

Biomarker

ATAD2 has been proposed as a prognostic biomarker in several cancers. A meta-analysis of 13 studies involving 2,689 patients associated high ATAD2 expression with shorter overall survival and poorer recurrence-related outcomes.

As a drug target

ATAD2 is being investigated as a cancer drug target because experimental inhibition or depletion can suppress cancer cell growth. Its acetyllysine-binding bromodomain provides a binding site for small-molecule inhibitors.

References

  1. 1 2 3 GRCh38: Ensembl release 89: ENSG00000156802 – Ensembl, May 2017
  2. 1 2 3 GRCm38: Ensembl release 89: ENSMUSG00000022360 – Ensembl, May 2017
  3. ↑ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ↑ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. ↑ Biju T, Venkatesh C, Honnasiddappa DB, Sajjan M, Mahadeva NK, Dinesh BG, et al. (June 2025). "ATAD2 bromodomain in cancer therapy: current status and future perspectives". International Journal of Biological Macromolecules. 311 (Pt 3) 143948. doi:10.1016/j.ijbiomac.2025.143948. PMID 40334884.
  6. ↑ "ATAD2". Reference Sequence Collection; National Center for Biotechnology Information (NCBI). U.S. National Library of Medicine (NLM).
  7. 1 2 3 4 Fu J, Zhang J, Chen X, Liu Z, Yang X, He Z, et al. (2023). "ATPase family AAA domain-containing protein 2 (ATAD2): From an epigenetic modulator to cancer therapeutic target". Theranostics. 13 (2): 787–809. doi:10.7150/thno.78840. PMC 9830439. PMID 36632213.
  8. ↑ Garain T, Rai P, Li W, Banerjee S (October 2025). "ATAD2 as a Cancer Target: Insights into Its Structure, Functions, Mechanisms, and Drug Development". Cancers. 17 (20). Basel: 3337. doi:10.3390/cancers17203337. PMC 12563300. PMID 41154392.
  9. ↑ Han HJ, Huang QY, Huang LJ, Chang F, Diao QZ (September 2019). "Prognostic value of ATPase family, AAA+ domain containing 2 expression in human cancers: A systematic review and meta-analysis". Medicine. 98 (39) e17180. Baltimore. doi:10.1097/MD.0000000000017180. PMC 6775384. PMID 31574824.

Further reading

This article incorporates text from the United States National Library of Medicine, which is in the public domain.