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{{for|the military districts under the early Caliphates|Jund}}
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{{Infobox_gene}}
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'''Transcription factor JunD''' is a [[protein]] that in humans is encoded by the ''JUND'' [[gene]].<ref name="pmid2112242">{{cite journal | vauthors = Nomura N, Ide M, Sasamoto S, Matsui M, Date T, Ishizaki R | title = Isolation of human cDNA clones of jun-related genes, jun-B and jun-D | journal = Nucleic Acids Res. | volume = 18 | issue = 10 | pages = 3047–8  | date = July 1990 | pmid = 2112242 | pmc = 330838 | doi = 10.1093/nar/18.10.3047 }}</ref><ref name="pmid1903194">{{cite journal | vauthors = Berger I, Shaul Y | title = Structure and function of human jun-D | journal = Oncogene | volume = 6 | issue = 4 | pages = 561–6  | date = June 1991 | pmid = 1903194 | pmc = | doi = }}</ref>
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<!-- The GNF_Protein_box is automatically maintained by Protein Box Bot.  See Template:PBB_Controls to Stop updates. -->
== Function ==
{{GNF_Protein_box
| image =
| image_source =
| PDB =
| Name = Jun D proto-oncogene
| HGNCid = 6206
| Symbol = JUND
| AltSymbols =;
| OMIM = 165162
| ECnumber = 
| Homologene = 3910
| MGIid = 96648
| GeneAtlas_image1 = PBB_GE_JUND_203752_s_at_tn.png
| GeneAtlas_image2 = PBB_GE_JUND_203751_x_at_tn.png
| GeneAtlas_image3 = PBB_GE_JUND_214326_x_at_tn.png
| Function = {{GNF_GO|id=GO:0003700 |text = transcription factor activity}} {{GNF_GO|id=GO:0003702 |text = RNA polymerase II transcription factor activity}} {{GNF_GO|id=GO:0043565 |text = sequence-specific DNA binding}} {{GNF_GO|id=GO:0046983 |text = protein dimerization activity}}
| Component = {{GNF_GO|id=GO:0000785 |text = chromatin}} {{GNF_GO|id=GO:0005634 |text = nucleus}}
| Process = {{GNF_GO|id=GO:0006350 |text = transcription}} {{GNF_GO|id=GO:0006357 |text = regulation of transcription from RNA polymerase II promoter}}
| Orthologs = {{GNF_Ortholog_box
    | Hs_EntrezGene = 3727
    | Hs_Ensembl = ENSG00000130522
    | Hs_RefseqProtein = NP_005345
    | Hs_RefseqmRNA = NM_005354
    | Hs_GenLoc_db = 
    | Hs_GenLoc_chr = 19
    | Hs_GenLoc_start = 18252251
    | Hs_GenLoc_end = 18253294
    | Hs_Uniprot = P17535
    | Mm_EntrezGene = 16478
    | Mm_Ensembl = 
    | Mm_RefseqmRNA = NM_010592
    | Mm_RefseqProtein = NP_034722
    | Mm_GenLoc_db = 
    | Mm_GenLoc_chr = 
    | Mm_GenLoc_start = 
    | Mm_GenLoc_end = 
    | Mm_Uniprot =
  }}
}}
'''Jun D proto-oncogene''', also known as '''JUND''', is a human [[gene]].


<!-- The PBB_Summary template is automatically maintained by Protein Box Bot.  See Template:PBB_Controls to Stop updates. -->
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.<ref name="entrez">{{cite web | title = Entrez Gene: JUND jun D proto-oncogene| url = https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=3727| accessdate = }}</ref>
{{PBB_Summary
| section_title =
| summary_text = 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.<ref name="entrez">{{cite web | title = Entrez Gene: JUND jun D proto-oncogene| url = http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=3727| accessdate = }}</ref>
}}


==See also==
=={{anchor|Delta JunD}}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 (transcription factor)|AP-1]]-mediated transcriptional activity.<ref name="Nestler, Hyman, and Malenka 2">{{cite journal | vauthors = Hyman SE, Malenka RC, Nestler EJ | title = Neural mechanisms of addiction: the role of reward-related learning and memory | journal = Annu. Rev. Neurosci. | volume = 29 | issue =  | pages = 565–98 | year = 2006 | pmid = 16776597 | doi = 10.1146/annurev.neuro.29.051605.113009 }}</ref><ref name="Nestler">{{cite journal | vauthors = Robison AJ, Nestler EJ | title = Transcriptional and epigenetic mechanisms of addiction | journal = Nat. Rev. Neurosci. | volume = 12 | issue = 11 | pages = 623–37  | date = November 2011 | pmid = 21989194 | pmc = 3272277 | doi = 10.1038/nrn3111 | quote = ΔFosB has been linked directly to several addiction-related behaviors&nbsp;...  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. }}</ref><ref name="Genetic sex addiction">{{cite journal | vauthors = Pitchers KK, Frohmader KS, Vialou V, Mouzon E, Nestler EJ, Lehman MN, Coolen LM | title = ΔFosB in the nucleus accumbens is critical for reinforcing effects of sexual reward | journal = Genes Brain Behav. | volume = 9 | issue = 7 | pages = 831–40  | date = October 2010 | pmid = 20618447 | pmc = 2970635 | doi = 10.1111/j.1601-183X.2010.00621.x }}</ref>  In the [[nucleus accumbens]], ΔJunD directly opposes many of the neurological changes that occur in [[addiction]] (i.e., those induced by ΔFosB).<ref name="Nestler" /><ref name="Genetic sex addiction" /> ΔFosB inhibitors (drugs that oppose its action) may be an effective treatment for addiction and addictive disorders.<ref name="Malenka_2009_04">{{cite book |vauthors=Malenka RC, Nestler EJ, Hyman SE |veditors=Sydor A, Brown RY | title = Molecular Neuropharmacology: A Foundation for Clinical Neuroscience | year = 2009 | publisher = McGraw-Hill Medical | location = New York | isbn = 9780071481274 | pages = 384–385 | edition = 2nd | chapter = Chapter 15: Reinforcement and addictive disorders }}</ref>
 
== Interactions ==
 
JunD has been shown to [[Protein-protein interaction|interact]] with [[ATF3]],<ref name=pmid8152431>{{cite journal | vauthors = Chu HM, Tan Y, Kobierski LA, Balsam LB, Comb MJ | title = Activating transcription factor-3 stimulates 3',5'-cyclic adenosine monophosphate-dependent gene expression | journal = Mol. Endocrinol. | volume = 8 | issue = 1 | pages = 59–68  | date = January 1994 | pmid = 8152431 | doi = 10.1210/mend.8.1.8152431 }}</ref> [[MEN1]],<ref name=pmid9989505>{{cite journal | vauthors = Agarwal SK, Guru SC, Heppner C, Erdos MR, Collins RM, Park SY, Saggar S, Chandrasekharappa SC, Collins FS, Spiegel AM, Marx SJ, Burns AL | title = Menin interacts with the AP1 transcription factor JunD and represses JunD-activated transcription | journal = Cell | volume = 96 | issue = 1 | pages = 143–52  | date = January 1999 | pmid = 9989505 | doi = 10.1016/S0092-8674(00)80967-8 }}</ref> [[DNA damage-inducible transcript 3]]<ref name=pmid10523647>{{cite journal | vauthors = Ubeda M, Vallejo M, Habener JF | title = CHOP enhancement of gene transcription by interactions with Jun/Fos AP-1 complex proteins | journal = Mol. Cell. Biol. | volume = 19 | issue = 11 | pages = 7589–99  | date = November 1999 | pmid = 10523647 | pmc = 84780 }}</ref> and [[BRCA1]].<ref name=pmid12080089>{{cite journal | vauthors = Hu YF, Li R | title = JunB potentiates function of BRCA1 activation domain 1 (AD1) through a coiled-coil-mediated interaction | journal = Genes Dev. | volume = 16 | issue = 12 | pages = 1509–17  | date = June 2002 | pmid = 12080089 | pmc = 186344 | doi = 10.1101/gad.995502 }}</ref>
 
== See also ==
* [[AP-1 (transcription factor)]]
* [[AP-1 (transcription factor)]]


==References==
== References ==
{{reflist|2}}
{{reflist}}


==Further reading==
== Further reading ==
{{refbegin | 2}}
{{refbegin | 2}}
{{PBB_Further_reading
* {{cite journal | vauthors = Mollinedo F, Vaquerizo MJ, Naranjo JR | title = Expression of c-jun, jun B and jun D proto-oncogenes in human peripheral-blood granulocytes | journal = Biochem. J. | volume = 273(Pt 2) | issue =  | pages = 477–9 | year = 1991 | pmid = 1899335 | pmc = 1149869 | doi =  }}
| citations =
* {{cite journal | vauthors = Franklin CC, McCulloch AV, Kraft AS | title = In vitro association between the Jun protein family and the general transcription factors, TBP and TFIIB | journal = Biochem. J. | volume = 305 | issue = 3 | pages = 967–74 | year = 1995 | pmid = 7848298 | pmc = 1136352 | doi =  10.1042/bj3050967}}
*{{cite journal | author=Mollinedo F, Vaquerizo MJ, Naranjo JR |title=Expression of c-jun, jun B and jun D proto-oncogenes in human peripheral-blood granulocytes. |journal=Biochem. J. |volume=273(Pt 2) |issue=  |pages= 477-9 |year= 1991 |pmid= 1899335 |doi=  }}
* {{cite journal | vauthors = Maruyama K, Sugano S | title = Oligo-capping: a simple method to replace the cap structure of eukaryotic mRNAs with oligoribonucleotides | journal = Gene | volume = 138 | issue = 1–2 | pages = 171–4 | year = 1994 | pmid = 8125298 | doi = 10.1016/0378-1119(94)90802-8 }}
*{{cite journal | author=Berger I, Shaul Y |title=Structure and function of human jun-D. |journal=Oncogene |volume=6 |issue= 4 |pages= 561-6 |year= 1991 |pmid= 1903194 |doi=  }}
* {{cite journal | vauthors = Chu HM, Tan Y, Kobierski LA, Balsam LB, Comb MJ | title = Activating transcription factor-3 stimulates 3',5'-cyclic adenosine monophosphate-dependent gene expression | journal = Mol. Endocrinol. | volume = 8 | issue = 1 | pages = 59–68 | year = 1994 | pmid = 8152431 | doi = 10.1210/mend.8.1.8152431 }}
*{{cite journal | author=Nomura N, Ide M, Sasamoto S, ''et al.'' |title=Isolation of human cDNA clones of jun-related genes, jun-B and jun-D. |journal=Nucleic Acids Res. |volume=18 |issue= 10 |pages= 3047-8 |year= 1990 |pmid= 2112242 |doi= }}
* {{cite journal | vauthors = Trask B, Fertitta A, Christensen M, Youngblom J, Bergmann A, Copeland A, de Jong P, Mohrenweiser H, Olsen A, Carrano A | title = Fluorescence in situ hybridization mapping of human chromosome 19: cytogenetic band location of 540 cosmids and 70 genes or DNA markers | journal = Genomics | volume = 15 | issue = 1 | pages = 133–45 | year = 1993 | pmid = 8432525 | doi = 10.1006/geno.1993.1021 }}
*{{cite journal | author=Franklin CC, McCulloch AV, Kraft AS |title=In vitro association between the Jun protein family and the general transcription factors, TBP and TFIIB. |journal=Biochem. J. |volume=305 ( Pt 3) |issue= |pages= 967-74 |year= 1995 |pmid= 7848298 |doi= }}
* {{cite journal | vauthors = Dorsey MJ, Tae HJ, Sollenberger KG, Mascarenhas NT, Johansen LM, Taparowsky EJ | title = B-ATF: a novel human bZIP protein that associates with members of the AP-1 transcription factor family | journal = Oncogene | volume = 11 | issue = 11 | pages = 2255–65 | year = 1995 | pmid = 8570175 | doi =  }}
*{{cite journal | author=Maruyama K, Sugano S |title=Oligo-capping: a simple method to replace the cap structure of eukaryotic mRNAs with oligoribonucleotides. |journal=Gene |volume=138 |issue= 1-2 |pages= 171-4 |year= 1994 |pmid= 8125298 |doi= }}
* {{cite journal | vauthors = Claret FX, Hibi M, Dhut S, Toda T, Karin M | title = A new group of conserved coactivators that increase the specificity of AP-1 transcription factors | journal = Nature | volume = 383 | issue = 6599 | pages = 453–7 | year = 1996 | pmid = 8837781 | doi = 10.1038/383453a0 }}
*{{cite journal | author=Chu HM, Tan Y, Kobierski LA, ''et al.'' |title=Activating transcription factor-3 stimulates 3',5'-cyclic adenosine monophosphate-dependent gene expression. |journal=Mol. Endocrinol. |volume=8 |issue= 1 |pages= 59-68 |year= 1994 |pmid= 8152431 |doi=  }}
* {{cite journal | vauthors = Kallunki T, Deng T, Hibi M, Karin M | title = c-Jun can recruit JNK to phosphorylate dimerization partners via specific docking interactions | journal = Cell | volume = 87 | issue = 5 | pages = 929–39 | year = 1996 | pmid = 8945519 | doi = 10.1016/S0092-8674(00)81999-6 }}
*{{cite journal | author=Trask B, Fertitta A, Christensen M, ''et al.'' |title=Fluorescence in situ hybridization mapping of human chromosome 19: cytogenetic band location of 540 cosmids and 70 genes or DNA markers. |journal=Genomics |volume=15 |issue= 1 |pages= 133-45 |year= 1993 |pmid= 8432525 |doi= }}
* {{cite journal | vauthors = Aronheim A, Zandi E, Hennemann H, Elledge SJ, Karin M | title = Isolation of an AP-1 repressor by a novel method for detecting protein-protein interactions | journal = Mol. Cell. Biol. | volume = 17 | issue = 6 | pages = 3094–102 | year = 1997 | pmid = 9154808 | pmc = 232162 | doi = 10.1128/mcb.17.6.3094}}
*{{cite journal | author=Dorsey MJ, Tae HJ, Sollenberger KG, ''et al.'' |title=B-ATF: a novel human bZIP protein that associates with members of the AP-1 transcription factor family. |journal=Oncogene |volume=11 |issue= 11 |pages= 2255-65 |year= 1996 |pmid= 8570175 |doi= }}
* {{cite journal | vauthors = Suzuki Y, Yoshitomo-Nakagawa K, Maruyama K, Suyama A, Sugano S | title = Construction and characterization of a full length-enriched and a 5'-end-enriched cDNA library | journal = Gene | volume = 200 | issue = 1–2 | pages = 149–56 | year = 1997 | pmid = 9373149 | doi = 10.1016/S0378-1119(97)00411-3 }}
*{{cite journal | author=Claret FX, Hibi M, Dhut S, ''et al.'' |title=A new group of conserved coactivators that increase the specificity of AP-1 transcription factors. |journal=Nature |volume=383 |issue= 6599 |pages= 453-7 |year= 1996 |pmid= 8837781 |doi= 10.1038/383453a0 }}
* {{cite journal | vauthors = Labudova O, Krapfenbauer K, Moenkemann H, Rink H, Kitzmüller E, Cairns N, Lubec G | title = Decreased transcription factor junD in brains of patients with Down syndrome | journal = Neurosci. Lett. | volume = 252 | issue = 3 | pages = 159–62 | year = 1998 | pmid = 9739985 | doi = 10.1016/S0304-3940(98)00569-2 }}
*{{cite journal | author=Kallunki T, Deng T, Hibi M, Karin M |title=c-Jun can recruit JNK to phosphorylate dimerization partners via specific docking interactions. |journal=Cell |volume=87 |issue= 5 |pages= 929-39 |year= 1997 |pmid= 8945519 |doi= }}
* {{cite journal | vauthors = Venugopal R, Jaiswal AK | title = Nrf2 and Nrf1 in association with Jun proteins regulate antioxidant response element-mediated expression and coordinated induction of genes encoding detoxifying enzymes | journal = Oncogene | volume = 17 | issue = 24 | pages = 3145–56 | year = 1998 | pmid = 9872330 | doi = 10.1038/sj.onc.1202237 }}
*{{cite journal | author=Aronheim A, Zandi E, Hennemann H, ''et al.'' |title=Isolation of an AP-1 repressor by a novel method for detecting protein-protein interactions. |journal=Mol. Cell. Biol. |volume=17 |issue= 6 |pages= 3094-102 |year= 1997 |pmid= 9154808 |doi= }}
* {{cite journal | vauthors = Agarwal SK, Guru SC, Heppner C, Erdos MR, Collins RM, Park SY, Saggar S, Chandrasekharappa SC, Collins FS, Spiegel AM, Marx SJ, Burns AL | title = Menin interacts with the AP1 transcription factor JunD and represses JunD-activated transcription | journal = Cell | volume = 96 | issue = 1 | pages = 143–52 | year = 1999 | pmid = 9989505 | doi = 10.1016/S0092-8674(00)80967-8 }}
*{{cite journal | author=Suzuki Y, Yoshitomo-Nakagawa K, Maruyama K, ''et al.'' |title=Construction and characterization of a full length-enriched and a 5'-end-enriched cDNA library. |journal=Gene |volume=200 |issue= 1-2 |pages= 149-56 |year= 1997 |pmid= 9373149 |doi= }}
* {{cite journal | vauthors = Liberati NT, Datto MB, Frederick JP, Shen X, Wong C, Rougier-Chapman EM, Wang XF | title = Smads bind directly to the Jun family of AP-1 transcription factors | journal = Proc. Natl. Acad. Sci. U.S.A. | volume = 96 | issue = 9 | pages = 4844–9 | year = 1999 | pmid = 10220381 | pmc = 21779 | doi = 10.1073/pnas.96.9.4844 }}
*{{cite journal | author=Labudova O, Krapfenbauer K, Moenkemann H, ''et al.'' |title=Decreased transcription factor junD in brains of patients with Down syndrome. |journal=Neurosci. Lett. |volume=252 |issue= 3 |pages= 159-62 |year= 1998 |pmid= 9739985 |doi= }}
* {{cite journal | vauthors = Gobl AE, Berg M, Lopez-Egido JR, Oberg K, Skogseid B, Westin G | title = Menin represses JunD-activated transcription by a histone deacetylase-dependent mechanism | journal = Biochim. Biophys. Acta | volume = 1447 | issue = 1 | pages = 51–6 | year = 1999 | pmid = 10500243 | doi = 10.1016/S0167-4781(99)00132-3 }}
*{{cite journal | author=Venugopal R, Jaiswal AK |title=Nrf2 and Nrf1 in association with Jun proteins regulate antioxidant response element-mediated expression and coordinated induction of genes encoding detoxifying enzymes. |journal=Oncogene |volume=17 |issue= 24 |pages= 3145-56 |year= 1999 |pmid= 9872330 |doi= 10.1038/sj.onc.1202237 }}
* {{cite journal | vauthors = Ubeda M, Vallejo M, Habener JF | title = CHOP enhancement of gene transcription by interactions with Jun/Fos AP-1 complex proteins | journal = Mol. Cell. Biol. | volume = 19 | issue = 11 | pages = 7589–99 | year = 1999 | pmid = 10523647 | pmc = 84780 | doi =  }}
*{{cite journal | author=Agarwal SK, Guru SC, Heppner C, ''et al.'' |title=Menin interacts with the AP1 transcription factor JunD and represses JunD-activated transcription. |journal=Cell |volume=96 |issue= 1 |pages= 143-52 |year= 1999 |pmid= 9989505 |doi= }}
* {{cite journal | vauthors = Miyamoto NG, Medberry PS, Hesselgesser J, Boehlk S, Nelson PJ, Krensky AM, Perez HD | title = Interleukin-1beta induction of the chemokine RANTES promoter in the human astrocytoma line CH235 requires both constitutive and inducible transcription factors | journal = J. Neuroimmunol. | volume = 105 | issue = 1 | pages = 78–90 | year = 2000 | pmid = 10713367 | doi = 10.1016/S0165-5728(00)00195-8 }}
*{{cite journal | author=Liberati NT, Datto MB, Frederick JP, ''et al.'' |title=Smads bind directly to the Jun family of AP-1 transcription factors. |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=96 |issue= 9 |pages= 4844-9 |year= 1999 |pmid= 10220381 |doi=  }}
* {{cite journal | vauthors = Sharma SC, Richards JS | title = Regulation of AP1 (Jun/Fos) factor expression and activation in ovarian granulosa cells. Relation of JunD and Fra2 to terminal differentiation | journal = J. Biol. Chem. | volume = 275 | issue = 43 | pages = 33718–28 | year = 2000 | pmid = 10934195 | doi = 10.1074/jbc.M003555200 }}
*{{cite journal | author=Gobl AE, Berg M, Lopez-Egido JR, ''et al.'' |title=Menin represses JunD-activated transcription by a histone deacetylase-dependent mechanism. |journal=Biochim. Biophys. Acta |volume=1447 |issue= 1 |pages= 51-6 |year= 1999 |pmid= 10500243 |doi= }}
*{{cite journal  | author=Ubeda M, Vallejo M, Habener JF |title=CHOP enhancement of gene transcription by interactions with Jun/Fos AP-1 complex proteins. |journal=Mol. Cell. Biol. |volume=19 |issue= 11 |pages= 7589-99 |year= 1999 |pmid= 10523647 |doi=  }}
*{{cite journal  | author=Miyamoto NG, Medberry PS, Hesselgesser J, ''et al.'' |title=Interleukin-1beta induction of the chemokine RANTES promoter in the human astrocytoma line CH235 requires both constitutive and inducible transcription factors. |journal=J. Neuroimmunol. |volume=105 |issue= 1 |pages= 78-90 |year= 2000 |pmid= 10713367 |doi=  }}
*{{cite journal | author=Sharma SC, Richards JS |title=Regulation of AP1 (Jun/Fos) factor expression and activation in ovarian granulosa cells. Relation of JunD and Fra2 to terminal differentiation. |journal=J. Biol. Chem. |volume=275 |issue= 43 |pages= 33718-28 |year= 2000 |pmid= 10934195 |doi= 10.1074/jbc.M003555200 }}
}}
{{refend}}
{{refend}}


== External links ==
== External links ==
* {{MeshName|JUND+protein,+human}}
* {{MeshName|JUND+protein,+human}}
* {{FactorBook|JunD}}
{{NLM content}}
{{Transcription factors|g1}}


{{NLM content}}
{{gene-19-stub}}
{{Transcription factors}}
[[Category:Transcription factors]]
[[Category:Transcription factors]]
{{WikiDoc Sources}}

Latest revision as of 05:10, 2 September 2017

For the military districts under the early Caliphates, see Jund.

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Identifiers
Aliases
External IDsGeneCards: [1]
Orthologs
SpeciesHumanMouse
Entrez

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Ensembl

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UniProt

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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 JunD is a protein that in humans is encoded by the JUND gene.[1][2]

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.[3]

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.[4][5][6] In the nucleus accumbens, ΔJunD directly opposes many of the neurological changes that occur in addiction (i.e., those induced by ΔFosB).[5][6] ΔFosB inhibitors (drugs that oppose its action) may be an effective treatment for addiction and addictive disorders.[7]

Interactions

JunD has been shown to interact with ATF3,[8] MEN1,[9] DNA damage-inducible transcript 3[10] and BRCA1.[11]

See also

References

  1. ↑ Nomura N, Ide M, Sasamoto S, Matsui M, Date T, Ishizaki R (July 1990). "Isolation of human cDNA clones of jun-related genes, jun-B and jun-D". Nucleic Acids Res. 18 (10): 3047–8. doi:10.1093/nar/18.10.3047. PMC 330838. PMID 2112242.
  2. ↑ Berger I, Shaul Y (June 1991). "Structure and function of human jun-D". Oncogene. 6 (4): 561–6. PMID 1903194.
  3. ↑ "Entrez Gene: JUND jun D proto-oncogene".
  4. ↑ Hyman SE, Malenka RC, Nestler EJ (2006). "Neural mechanisms of addiction: the role of reward-related learning and memory". Annu. Rev. Neurosci. 29: 565–98. doi:10.1146/annurev.neuro.29.051605.113009. PMID 16776597.
  5. ↑ 5.0 5.1 Robison AJ, Nestler EJ (November 2011). "Transcriptional and epigenetic mechanisms of addiction". Nat. Rev. Neurosci. 12 (11): 623–37. doi:10.1038/nrn3111. PMC 3272277. PMID 21989194. 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.
  6. ↑ 6.0 6.1 Pitchers KK, Frohmader KS, Vialou V, Mouzon E, Nestler EJ, Lehman MN, Coolen LM (October 2010). "ΔFosB in the nucleus accumbens is critical for reinforcing effects of sexual reward". Genes Brain Behav. 9 (7): 831–40. doi:10.1111/j.1601-183X.2010.00621.x. PMC 2970635. PMID 20618447.
  7. ↑ Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 15: Reinforcement and addictive disorders". In Sydor A, Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 384–385. ISBN 9780071481274.
  8. ↑ Chu HM, Tan Y, Kobierski LA, Balsam LB, Comb MJ (January 1994). "Activating transcription factor-3 stimulates 3',5'-cyclic adenosine monophosphate-dependent gene expression". Mol. Endocrinol. 8 (1): 59–68. doi:10.1210/mend.8.1.8152431. PMID 8152431.
  9. ↑ Agarwal SK, Guru SC, Heppner C, Erdos MR, Collins RM, Park SY, Saggar S, Chandrasekharappa SC, Collins FS, Spiegel AM, Marx SJ, Burns AL (January 1999). "Menin interacts with the AP1 transcription factor JunD and represses JunD-activated transcription". Cell. 96 (1): 143–52. doi:10.1016/S0092-8674(00)80967-8. PMID 9989505.
  10. ↑ Ubeda M, Vallejo M, Habener JF (November 1999). "CHOP enhancement of gene transcription by interactions with Jun/Fos AP-1 complex proteins". Mol. Cell. Biol. 19 (11): 7589–99. PMC 84780. PMID 10523647.
  11. ↑ Hu YF, Li R (June 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.

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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