JUNB: Difference between revisions

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*{{cite journal |vauthors=Chen P, Flory E, Avots A, Jordan BW, Kirchhoff F, Ludwig S, Rapp UR | title = Transactivation of naturally occurring HIV-1 long terminal repeats by the JNK signaling pathway. The most frequent naturally occurring length polymorphism sequence introduces a novel binding site for AP-1 factors | journal = J. Biol. Chem. | volume = 275 | issue = 27 | pages = 20382–20390 | year = 2000 | pmid = 10764760 | doi = 10.1074/jbc.M001149200 }}
*{{cite journal |vauthors=Chen P, Flory E, Avots A, Jordan BW, Kirchhoff F, Ludwig S, Rapp UR | title = Transactivation of naturally occurring HIV-1 long terminal repeats by the JNK signaling pathway. The most frequent naturally occurring length polymorphism sequence introduces a novel binding site for AP-1 factors | journal = J. Biol. Chem. | volume = 275 | issue = 27 | pages = 20382–20390 | year = 2000 | pmid = 10764760 | doi = 10.1074/jbc.M001149200 }}
*{{cite journal |vauthors=Echlin DR, Tae HJ, Mitin N, Taparowsky EJ | title = B-ATF functions as a negative regulator of AP-1 mediated transcription and blocks cellular transformation by Ras and Fos | journal = Oncogene | volume = 19 | issue = 14 | pages = 1752–1763 | year = 2000 | pmid = 10777209 | doi = 10.1038/sj.onc.1203491 }}
*{{cite journal |vauthors=Echlin DR, Tae HJ, Mitin N, Taparowsky EJ | title = B-ATF functions as a negative regulator of AP-1 mediated transcription and blocks cellular transformation by Ras and Fos | journal = Oncogene | volume = 19 | issue = 14 | pages = 1752–1763 | year = 2000 | pmid = 10777209 | doi = 10.1038/sj.onc.1203491 }}
*{{cite journal |vauthors=Verrecchia F, Pessah M, Atfi A, Mauviel A | title = Tumor necrosis factor-alpha inhibits transforming growth factor-beta /Smad signaling in human dermal fibroblasts via AP-1 activation | journal = J. Biol. Chem. | volume = 275 | issue = 39 | pages = 30226–30231 | year = 2000 | pmid = 10903323 | doi = 10.1074/jbc.M005310200 }}
*{{cite journal |vauthors=Verrecchia F, Pessah M, Atfi A, Mauviel A | title = Tumor necrosis factor-alpha inhibits transforming growth factor-beta /Smad signaling in human dermal fibroblasts via AP-1 activation | journal = J. Biol. Chem. | volume = 275 | issue = 39 | pages = 30226–30231 | year = 2000 | pmid = 10903323 | doi = 10.1074/jbc.M005310200 | url = http://www.hal.inserm.fr/inserm-00150046 }}
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Latest revision as of 12:40, 4 November 2018

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Identifiers
Aliases
External IDsGeneCards: [1]
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

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RefSeq (protein)

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Location (UCSC)n/an/a
PubMed searchn/an/a
Wikidata
View/Edit Human

Transcription factor jun-B is a protein that in humans is encoded by the JUNB gene.[1][2] Transcription factor jun-B is a transcription factor involved in regulating gene activity following the primary growth factor response. It binds to the DNA sequence 5'-TGA[CG]TCA-3'.

Interactions

JUNB has been shown to interact with

See also

References

  1. Schütte J, Viallet J, Nau M, Segal S, Fedorko J, Minna J (Feb 1990). "jun-B inhibits and c-fos stimulates the transforming and trans-activating activities of c-jun". Cell. 59 (6): 987–997. doi:10.1016/0092-8674(89)90755-1. PMID 2513129.
  2. "Entrez Gene: JUNB jun B proto-oncogene".
  3. Hu YF, Li R (Jun 2002). "JunB potentiates function of BRCA1 activation domain 1 (AD1) through a coiled-coil-mediated interaction". Genes Dev. 16 (12): 1509–17. doi:10.1101/gad.995502. PMC 186344. PMID 12080089.
  4. Liberati NT, Datto MB, Frederick JP, Shen X, Wong C, Rougier-Chapman EM, Wang XF (Apr 1999). "Smads bind directly to the Jun family of AP-1 transcription factors". Proc. Natl. Acad. Sci. U.S.A. 96 (9): 4844–9. doi:10.1073/pnas.96.9.4844. PMC 21779. PMID 10220381.

Further reading

External links

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