Selected-GenAtlas references	SOURCE	GeneCards	NCBI Gene	Swiss-Prot	Ensembl
	HGNC	UniGene	Nucleotide	OMIM	UCSC

Home Page

FLASH GENE

Symbol

JUNB

contributors: mct/shn - updated : 20-12-2018

HGNC name	jun B proto-oncogene
HGNC id	6205

FLASH GENE DNA RNA EXPRESSION PROTEIN DISORDER ANIMAL & CELL MODELS

DNA

TYPE	functioning gene
STRUCTURE	1.82 kb     1 Exon(s)

10 Kb 5' upstream gene genomic sequence study

MAPPING

cloned

Y

linked

N

status

confirmed

Map	pter - D19S1165 - D19S221 - JUNB - D19S914 - D19S840 - cen

regionally located

localized in the psoriasis susceptibility region PSORS6

RNA

TRANSCRIPTS	type	messenger

identification nb exons type bp product Protein kDa AA specific expression Year Pubmed NM_002229 1 - 1832 NP_002220 - 347 - 2008 18628455

EXPRESSION

Type	ubiquitous

expressed in	(based on citations)
organ(s)	System Organ level 1 Organ level 2 Organ level 3 Organ level 4 Level Pubmed Species Stage Rna symbol Cardiovascular heart         Digestive liver       highly Nervous brain       highly   nerve cranial nerve     highly   spinal cord         Reproductive female system uterus cervix   highly Respiratory lung       highly Urinary kidney       highly

tissue

System Tissue Tissue level 1 Tissue level 2 Level Pubmed Species Stage Rna symbol Blood / Hematopoietic bone marrow       Connective adipose     highly Connective bone       Muscular striatum cardiac     Nervous central

cell lineage	erythroid
cell lines
fluid/secretion

at STAGE

PROTEIN

PHYSICAL PROPERTIES		basic
STRUCTURE

motifs/domains

basic leucine zipper (bZIP) domain

conjugated

ubiquitinated

mono polymer

heteromer , dimer

HOMOLOGY

interspecies	ortholog to Junb, Mus musculus
	ortholog to Junb, Rattus norvegicus
	ortholog to JUNB, Pan troglodytes

Homologene

FAMILY	AP-1 family
	BZIP family
	JUN subfamily

CATEGORY

transcription factor , protooncogene

SUBCELLULAR LOCALIZATION	intracellular
	intracellular,nucleus,chromatin/chromosome
	intracellular,nucleus,nucleolus

basic FUNCTION	repressor of CCND1 promoter
	regulator of erythroid differentiation
	hypoxia-responsive transcription factor, absolutely required for VEGF regulation in a cell-type-independent manner
	a key transcriptional regulator of myelopoiesis and a potential tumor suppressor gene
	a positive regulator controlling primarily osteoblast as well as osteoclast activity
	critical regulator of intrinsic mast cell functions including cross-talk with endothelial cells
	essential upstream regulator of p16 and contributes to maintain cell senescence that blocks malignant transformation of transient amplifying cells
	apparently plays an important role in controlling prostate carcinogenesis
	critical regulator of T cell function and a transcriptional activator of various cytokine genes, such as IL2, IL4, and IL10
	REL and JUNB cooperatively regulate FOXP3 expression by modulating the chromatin architecture of FOXP3 promoter region
	GRN growth factor, JUNB, and MYOD1 transcription factor form a regulatory loop and act in concert in the course of myogenesis
	a critical role in the epithelial-mesenchymal transition and profibrotic responses to TGF-beta
	provides important input in setting the transcriptional program of the epithelial-mesenchymal transition and profibrotic responses to TGF-beta

CELLULAR PROCESS	cell life, differentiation
	nucleotide, transcription

PHYSIOLOGICAL PROCESS

circadian

PATHWAY

metabolism

signaling

a component	forming heterodimers with JUN, JUND, FOS, FOSB to form the transcription factor AP1 major target of mitogen-activated signal transduction pathway
	REL and JUNB cooperatively enhance FOXP3 expression during induced regulatory T cell differentiation
	BATF forms a heterodimeric complex with JUNB and JUN, induced upregulation of matrix-degrading enzymes and downregulation of cartilage matrix molecules in chondrocytes

INTERACTION

DNA

RNA

small molecule

conjugated with small ubiquitin-like modifier (SUMO) on lysine 237

protein	B-ATF
	c-Jun NH2-terminal kinase, JNK
	Nrf2 and Nrf1
	Smad3 and Smad4
	estrogen receptor alpha, ERalpha
	BRCA1
	BCL-6
	c-Fos and LRF-1
	c-Jun
	NFATC2 and JUNB cooperatively regulate IL31 gene expression in CD4+ T cells in health and disease
	BATF/JUNB and BATF/JUN complexes play important roles in osteoarthritic cartilage destruction through regulating anabolic and catabolic gene expression in chondrocytes
	N4BP1 controls the proper function of keratinocytes and neutrophils by negatively regulating JUNB, FOSB, and CXCL1, respectively, and that is critical for psoriasis prevention

cell & other

REGULATION

activated by	erythropoietin induced
	hypoxia-induced NFKB

induced by	ligand induced
		light in the suprachiasmatic nucleus
		in response to hypoxia and required for VEGF expression

Other	phosphorylated and inactivated by CDC2, in mitotic and early G1 cells
	sumoylation of JUNB regulates its ability to induce cytokine gene transcription and likely plays a critical role in T cell activation

ASSOCIATED DISORDERS

corresponding disease(s)

Other morbid association(s)

Type Gene Modification Chromosome rearrangement Protein expression Protein Function tumoral     --over   with JUN in Hodgkin lymphoma cells constitutional     --low   in epidermal keratinocytes of psoriatic lesions constitutional         affects VEGF expression resulting in impaired neovascularization (in tumor) tumoral     --low   in patients with chronic myelogenous leukemia, due aberrant DNA methylation of its promoter, but downregulated in advanced phase CML through a mechanism independent from DNA methylation

Susceptibility

Variant & Polymorphism

Candidate gene
Marker
Therapy target
	System Type Disorder Pubmed cancer angiogenesis   for anti-angiogenic tumor therapies cancer     new target for cancer prevention and therapy

ANIMAL & CELL MODELS

	Transgenic mice specifically lacking JunB expression in the myeloid lineage develop a transplantable myeloproliferative disease eventually progressing to blast crisis and mice reconstituted with ES cell-derived junB-/- fetal liver cells also develop a myeloproliferative disease
	JunBDelta/Delta mice are viable, but develop severe low turnover osteopenia caused by apparent cell-autonomous osteoblast and osteoclast defects before a chronic myeloid leukemia-like disease
	mice with specific inactivation of Junb in the macrophage-osteoclast lineage develop an osteopetrosis-like phenotype with increased bone mass and reduced numbers of osteoclasts
	inducible epidermal deletion of JunB and c-Jun in adult mice leads to a phenotype resembling the histological and molecular hallmarks of psoriasis, including arthritic lesions
	Depletion of JunB by siRNA abrogates TGF-&
	946;-induced disruption of cell-cell junctions, formation of actin fibers, focal adhesions, and expression of fibrotic proteins