JunD

Source: Wikipedia, the free encyclopedia.

JUND
Gene ontology
Molecular function
Cellular component
Biological process
Sources:Amigo / QuickGO
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

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

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

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

See also

  • AP-1 (transcription factor)

References

  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000130522Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000071076Ensembl, 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. PMID 2112242
    .
  6. .
  7. ^ "Entrez Gene: JUND jun D proto-oncogene".
  8. PMID 16776597
    .
  9. ^ . ΔFosB has been linked directly to several addiction-related behaviors ... Importantly, genetic or viral overexpression of ΔJunD, a dominant negative mutant of JunD which antagonizes ΔFosB- and other AP-1-mediated transcriptional activity, in the NAc or OFC blocks these key effects of drug exposure14,22–24. This indicates that ΔFosB is both necessary and sufficient for many of the changes wrought in the brain by chronic drug exposure. ΔFosB is also induced in D1-type NAc MSNs by chronic consumption of several natural rewards, including sucrose, high fat food, sex, wheel running, where it promotes that consumption14,26–30. This implicates ΔFosB in the regulation of natural rewards under normal conditions and perhaps during pathological addictive-like states.
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Further reading

External links


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


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