Atlas of Genetics and Cytogenetics in Oncology and Haematology

Home   Genes   Leukemias   Solid Tumors   Cancer-Prone   Deep Insight   Case Reports   Journals  Portal   Teaching   

X Y 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 NA

JUN (V-Jun sarcoma virus 17 oncogene homolog (avian))

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

(Note : for Links provided by Atlas : click)


Other aliasc-jun
Activator Protein-1
LocusID (NCBI) 3725
Atlas_Id 151
Location 1p32.1  [Link to chromosome band 1p32]
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)
ADCY1 (7p12.3) / JUN (1p32.1)JUN (1p32.1) / GMPR2 (14q12)JUN (1p32.1) / LARP4B (10p15.3)
JUN (1p32.1) / MPV17 (2p23.3)JUN (1p32.1) / SLC25A1 (22q11.21)MAGI1 (3p14.1) / JUN (1p32.1)
PIGY (4q22.1) / JUN (1p32.1)SLC25A1 (22q11.21) / JUN (1p32.1)


Description The Jun gene maps on chromosome 1p32-p31 spanning 333799bp. The study by Hattori et al suggested that the Jun gene has no introns.
Transcription Due to 5' and 3' heterogeneities, several transcripts of Jun mRNA has been identified. The predicted molecular weight of JUN protein is 41.9 kD.


Description The JUN protein was originally identified as an oncoprotein encoded by a cellular insert in the genome of avian sarcoma virus 17. Following studies demonstrated that JUN is a critical component of AP-1 transcription factor that recognizes the palindromic DNA sequence TGAC/GTCA, the so-called TPA response element (TRE), in the promoter or intron region of a number of genes. JUN can stably associate with itself or Fos protein to form AP-1 complex. JUN can also interact with some activating transcription factor (ATF) members, such as ATF2, ATF3 and ATF4, to form heterodimers that bind to the cAMP-responsive element (CRE) DNA sequence, TGACGTCA. All JUN proteins from different species contain a N-terminal JNK docking domain (delta domain) adjacent to the JNK phosphorylating site Ser63/73. In the C-terminal, there is a basic domain for DNA binding, followed by a nuclear localization signal (NLS) and a leucine zipper motif for dimerization with partner proteins.
Expression Ubiquitously expressed.
Localisation Nuclear and mitochondria.
Function JUN is the most important component of AP-1 transcription factors, and its transcriptional activity is possibly attenuated by JUNB or JUND. It has been well accepted that JUN regulates cell proliferation, apoptosis and transformation. JUN promotes cell cycle transition from G1 phase to S phase by up-regulating cyclin D1 expression and antagonizing the function of p53and p21. The JUN protein is involved in both the induction and prevention of apoptosis, possibly dependent on the types and development stages of cells. JUN-dependent induction of pro-apoptotic protein FasL and Bim has been demonstrated in several experimental systems. However, evidence indicating an anti-apoptotic activity of JUN has also been provided by the fact that deficiency of Jun gene causes massive hepatocyte apoptosis. The potential oncogenic transformation of JUN has been revealed by overexpression experiments. This effect of JUN may partially through the induction of certain JUN targeting genes, such as heparin-bind epidermal growth factor-like growth factor (HB-EGF), proliferin and Jun-activated gene in chicken embryo fibroblasts (JAC).

Implicated in

Entity Inflammation
Entity cancer
Oncogenesis Overexpression of JUN has been observed in certain human cancer. However, no mutation, rearrangement or amplification of Jun gene has been reported.


Structure and chromosomal localization of the functional intronless human JUN protooncogene.
Hattori K, Angel P, Le Beau MM, Karin M
Proceedings of the National Academy of Sciences of the United States of America. 1988 ; 85 (23) : 9148-9152.
PMID 3194415
AP-1 as a regulator of cell life and death.
Shaulian E, Karin M
Nature cell biology. 2002 ; 4 (5) : E131-E136.
PMID 11988758
Fortuitous convergences: the beginnings of JUN.
Vogt PK
Nature reviews. Cancer. 2002 ; 2 (6) : 465-469.
PMID 12189388


This paper should be referenced as such :
Chen, F
JUN (v-Jun sarcoma virus 17 oncogene homolog (avian))
Atlas Genet Cytogenet Oncol Haematol. 2003;7(2):98-99.
Free journal version : [ pdf ]   [ DOI ]
On line version :

Other Leukemias implicated (Data extracted from papers in the Atlas) [ 5 ]
  t(1;5)(p32;q31) without TAL1 rearrangement
t(2;11)(p21;q24) MIR125B1/?
t(5;7)(q35;q21) TLX3/CDK6
t(9;13)(p12;q21) PAX5/DACH1
t(10;16)(q22;p13) KAT6B/CREBBP

Other Solid tumors implicated (Data extracted from papers in the Atlas) [ 1 ]
  Soft tissue tumors: an overview

External links

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)3725
Protein : pattern, domain, 3D structure
Domain families : Pfam (Sanger)
Domain families : Pfam (NCBI)
Protein Interaction databases
Ontologies - Pathways
Clinical trials, drugs, therapy
canSAR (ICR) (select the gene name)
REVIEW articlesautomatic search in PubMed
Last year publicationsautomatic search in PubMed

© Atlas of Genetics and Cytogenetics in Oncology and Haematology
indexed on : Thu Oct 18 17:40:35 CEST 2018

Home   Genes   Leukemias   Solid Tumors   Cancer-Prone   Deep Insight   Case Reports   Journals  Portal   Teaching   

For comments and suggestions or contributions, please contact us