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JUNB (jun B proto-oncogene)

Written2003-01Fei Chen
Health Effects Laboratory Division, NIOSH, 1095 Willowdale Rd, Morgantown, WV 26505, USA

(Note : for Links provided by Atlas : click)

Identity

Other aliasJUN-B
JUN protooncogene homolog B
LocusID (NCBI) 3726
Atlas_Id 178
Location 19p13.2  [Link to chromosome band 19p13]
Location_base_pair Starts at and ends at bp from pter
Fusion genes
(updated 2017)
Data from Atlas, Mitelman, Cosmic Fusion, Fusion Cancer, TCGA fusion databases with official HUGO symbols (see references in chromosomal bands)
JUNB (19p13.13) / SEC63 (6q21)JUNB (19p13.2) / CAPZB (1p36.13)JUNB (19p13.2) / SEC63 (6q21)

DNA/RNA

Description The JUNB gene maps on chromosome 19p13.2 covering 1820 bp.
Transcription It contains no confirmed intron. Therefore, no alternative splicing transcripts have been identified.

Protein

 
Description JUNB has 347 amino acids with a predicted molecular weight 35,9 kD. Structurally, JUNB is similar to JUN, which contains a JNK docking site, nuclear localization signal, basic domain for DNA binding and a leucine zipper domain for dimerization. However, JUNB does not contain a JUNK phosphorylation site. Thus, the transactivation activity of JUNB is not regulated by JNK.
Expression Ubiquitously expressed.
Localisation Nuclear
Function JUNB is a member of JUN family (JUN, JUNB and JUND) that can dimerize with one another, or with members of Fos and ATF families, to form AP-1 transcription factor. Comparing with JUN, the transactivation activity of JUNB is much weaker. Due to the small differences on the amino acid sequences in the basic DNA bindind domain, and leucine zipper domain, JUNB requires multiple AP-1 DNA binding sites for sufficient DNA binding. A number of studies demonstrated that JUNB antagonizes the functions of JUN in cell cycle regulation, proliferation and transformation by competing with JUN to form less efficient transactivating dimers. Thus, JUNB was considered as a tumor suppressor.
In gene knockout studies, mice lacking Jun gene die during embryonic day 12.5 and 13.5, whereas embryos lacking JunB die earlier, around day 9.5, owing to vascular defects in the placenta and extraembryonic tissue. Interestingly; gene knock-in experiment indicated that JUNB could partially substitute the activities of JUN in mouse development and cell proliferation. As possible explanation for this is that in presence of JUN, JUNB is a negative regulator for JUN. In contrast, in the absence of JUN, JUNB may substitute JUN and activate AP-1 target genes required for development and cell proliferation.

Implicated in

Note
  
Entity Inflammation, cancer
Oncogenesis Decreased expression of JUNB has been observed in certain human cancer. However, no mutation, rearrangement or amplification of JunB gene has been reported.
  

Bibliography

JunB can substitute for Jun in mouse development and cell proliferation.
Passegué E, Jochum W, Behrens A, Ricci R, Wagner EF
Nature genetics. 2002 ; 30 (2) : 158-166.
PMID 11818961
 
JunB is essential for mammalian placentation.
Schorpp-Kistner M, Wang ZQ, Angel P, Wagner EF
The EMBO journal. 1999 ; 18 (4) : 934-948.
PMID 10022836
 

Citation

This paper should be referenced as such :
Chen, F
JUNB (jun B proto-oncogene)
Atlas Genet Cytogenet Oncol Haematol. 2003;7(2):94-95.
Free journal version : [ pdf ]   [ DOI ]
On line version : http://AtlasGeneticsOncology.org/Genes/JUNBID178.html


Other Leukemias implicated (Data extracted from papers in the Atlas) [ 2 ]
  Mycosis fungoides/Sezary's syndrome
Primary cutaneous CD30+ anaplastic large cell lymphoma


Other Solid tumors implicated (Data extracted from papers in the Atlas) [ 1 ]
  t(6;19)(q21;p13) JUNB/SEC63


External links

Nomenclature
Cards
AtlasJUNBID178.txt
Aliases
Genomic and cartography
Gene and transcription
RefSeq transcript (Entrez)
RefSeq genomic (Entrez)
SOURCE (Princeton)Expression in : [Datasets]   [Normal Tissue Atlas]  [carcinoma Classsification]  [NCI60]
BioGPS (Tissue expression)3726
Protein : pattern, domain, 3D structure
Domain families : Pfam (Sanger)
Domain families : Pfam (NCBI)
Protein Interaction databases
Ontologies - Pathways
Clinical trials, drugs, therapy
Miscellaneous
canSAR (ICR) (select the gene name)
Probes
Litterature
REVIEW articlesautomatic search in PubMed
Last year publicationsautomatic search in PubMed


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indexed on : Thu Oct 18 17:40:32 CEST 2018

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