Jun B proto-oncogene, also known as JUNB, is a human gene. [cite web | title = Entrez Gene: JUNB jun B proto-oncogene | url = http://www.ncbi.nlm.nih.gov/sites/entrez?db=gene&cmd=retrieve&dopt=default&list_uids=3726&rn=1| accessdate = ]

section_title =
summary_text =

ee also

* AP-1 (transcription factor)


Further reading

citations =
*cite journal | author=Hsu JC, Bravo R, Taub R |title=Interactions among LRF-1, JunB, c-Jun, and c-Fos define a regulatory program in the G1 phase of liver regeneration. |journal=Mol. Cell. Biol. |volume=12 |issue= 10 |pages= 4654–65 |year= 1992 |pmid= 1406655 |doi=
*cite journal | author=Zafarullah M, Martel-Pelletier J, Cloutier JM, "et al." |title=Expression of c-fos, c-jun, jun-B, metallothionein and metalloproteinase genes in human chondrocyte. |journal=FEBS Lett. |volume=306 |issue= 2-3 |pages= 169–72 |year= 1992 |pmid= 1633872 |doi=
*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 | 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 | author=Schütte J, Viallet J, Nau M, "et al." |title=jun-B inhibits and c-fos stimulates the transforming and trans-activating activities of c-jun. |journal=Cell |volume=59 |issue= 6 |pages= 987–97 |year= 1990 |pmid= 2513129 |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 | 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 | author=Phinney DG, Tseng SW, Ryder K |title=Complex genetic organization of junB: multiple blocks of flanking evolutionarily conserved sequence at the murine and human junB loci. |journal=Genomics |volume=28 |issue= 2 |pages= 228–34 |year= 1996 |pmid= 8530030 |doi= 10.1006/geno.1995.1135
*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 | author=Neyns B, Katesuwanasing , Vermeij J, "et al." |title=Expression of the jun family of genes in human ovarian cancer and normal ovarian surface epithelium. |journal=Oncogene |volume=12 |issue= 6 |pages= 1247–57 |year= 1996 |pmid= 8649827 |doi=
*cite journal | author=Mendelson KG, Contois LR, Tevosian SG, "et al." |title=Independent regulation of JNK/p38 mitogen-activated protein kinases by metabolic oxidative stress in the liver. |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=93 |issue= 23 |pages= 12908–13 |year= 1996 |pmid= 8917518 |doi=
*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 | 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 | author=Fuchs SY, Xie B, Adler V, "et al." |title=c-Jun NH2-terminal kinases target the ubiquitination of their associated transcription factors. |journal=J. Biol. Chem. |volume=272 |issue= 51 |pages= 32163–8 |year= 1998 |pmid= 9405416 |doi=
*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 | author=Li B, Tournier C, Davis RJ, Flavell RA |title=Regulation of IL-4 expression by the transcription factor JunB during T helper cell differentiation. |journal=EMBO J. |volume=18 |issue= 2 |pages= 420–32 |year= 1999 |pmid= 9889198 |doi= 10.1093/emboj/18.2.420
*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 | author=Chen P, Flory E, Avots A, "et al." |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= 20382–90 |year= 2000 |pmid= 10764760 |doi= 10.1074/jbc.M001149200
*cite journal | author=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= 1752–63 |year= 2000 |pmid= 10777209 |doi= 10.1038/sj.onc.1203491
*cite journal | author=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= 30226–31 |year= 2000 |pmid= 10903323 |doi= 10.1074/jbc.M005310200

External links


update_page = yes
require_manual_inspection = no
update_protein_box = yes
update_summary = yes
update_citations = yes

Wikimedia Foundation. 2010.

Look at other dictionaries:

  • FOSB — FBJ murine osteosarcoma viral oncogene homolog B Identifiers Symbols FOSB; AP 1; DKFZp686C0818; G0S3; GOS3; GOSB; MGC42291 External IDs …   Wikipedia

  • FOSL1 — FOS like antigen 1, also known as FOSL1, is a human gene.cite web | title = Entrez Gene: FOSL1 FOS like antigen 1| url = http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene Cmd=ShowDetailView TermToSearch=8061| accessdate = ] PBB Summary section… …   Wikipedia

  • Receptor (biochemistry) — For other uses, see Receptor (disambiguation). In biochemistry, a receptor is a molecule found on the surface of a cell, which receives specific chemical signals from neighbouring cells or the wider environment within an organism. These signals… …   Wikipedia

  • CREB — redirects here. For other uses, see Clean Renewable Energy Bonds. CREB (top) is a transcription factor capable of binding DNA (bottom) and regulating gene expression. CREB (cAMP response element binding) is a cellular transcription factor. It… …   Wikipedia

  • MyoD — Myogenic differentiation 1 PDB rendering based on 1mdy …   Wikipedia

  • Oct-4 — POU class 5 homeobox 1 Identifiers Symbols POU5F1; MGC22487; OCT3; OCT4; OTF 3; OTF3; OTF4; Oct 3; Oct 4 External IDs …   Wikipedia

  • Estrogen receptor — 1 (ER alpha) A dimer of the ligand binding region of ERα (PDB rendering based on 3erd). Identifi …   Wikipedia

  • Progesterone receptor — PDB rendering based on 1a28 …   Wikipedia

  • Androgen receptor — Structure of the ligand binding domain of the androgen receptor (rainbow cartoon) complexed with testosterone (white sticks).[1] …   Wikipedia

  • NF-κB — Mechanism of NF κB action. In this figure, the NF κB heterodimer between Rel and p50 proteins is used as an example. While in an inactivated state, NF κB is located in the cytosol complexed with the inhibitory protein IκBα. Through the… …   Wikipedia

Share the article and excerpts

Direct link
Do a right-click on the link above
and select “Copy Link”

We are using cookies for the best presentation of our site. Continuing to use this site, you agree with this.