Transcription factor JunD is a protein that in humans is encoded by the JUND gene.[5][6]

JUND
Available structures
PDBOrtholog search: PDBe RCSB
Identifiers
AliasesJUND, AP-1, JunD, JunD proto-oncogene, AP-1 transcription factor subunit
External IDsOMIM: 165162; MGI: 96648; HomoloGene: 3910; GeneCards: JUND; OMA:JUND - orthologs
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_005354
NM_001286968

NM_001286944
NM_010592

RefSeq (protein)

NP_001273897
NP_005345

NP_001273873
NP_034722

Location (UCSC)Chr 19: 18.28 – 18.28 MbChr 8: 71.15 – 71.15 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Function

The protein encoded by this intronless gene is a member of the JUN family, and a functional component of the AP1 transcription factor complex. It has been proposed to protect cells from p53-dependent senescence and apoptosis. Alternate translation initiation site usage results in the production of different isoforms.[7]

ΔJunD

The dominant negative mutant variant of JunD, known as ΔJunD or Delta JunD, is a potent antagonist of the ΔFosB transcript, as well as other forms of AP-1-mediated transcriptional activity.[8][9][10] In the nucleus accumbens, ΔJunD directly opposes many of the neurological changes that occur in addiction (i.e., those induced by ΔFosB).[9][10] ΔFosB inhibitors (drugs that oppose its action) may be an effective treatment for addiction and addictive disorders.[11] Being an unnatural genetic variant, deltaJunD has not been observed in humans.

Interactions

JunD has been shown to interact with ATF3,[12] MEN1,[13] DNA damage-inducible transcript 3[14] and BRCA1.[15]

See also

References

Further reading

External links


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