Affinage

JUNB

Transcription factor JunB · UniProt P17275

Length
347 aa
Mass
35.9 kDa
Annotated
2026-06-10
100 papers in source corpus 41 papers cited in narrative 39 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

JUNB is an AP-1 transcription factor that controls cell proliferation, senescence, and lineage-specific gene programs by binding AP-1 and AP-1-like elements as homodimers or heterodimers with Fos, Jun, and ATF/BATF family members (PMID:8383624, PMID:8441422). Relative to c-Jun, JunB has roughly 10-fold lower DNA-binding activity, attributable to a small number of residues in its DNA-binding and leucine-zipper domains; two destabilizing glycines in its zipper favor inactive heterodimers with c-Jun, so JunB can attenuate c-Jun-driven transcription (PMID:8383624). It enforces cell-cycle and senescence control by directly activating the CDK inhibitor p16(INK4a) to trigger premature senescence (PMID:10856241), yet also driving proliferation through direct activation of cyclin A and cyclin E1, with loss causing S-phase accumulation and impaired CDK activity (PMID:12121977, PMID:36494864); this proliferative/senescence balance underlies its tumor-suppressive role in prostate epithelium and its senescence-driven depletion of skin stem cell niches (PMID:25526087, PMID:34469740). A GSK3-primed phospho-degron targets JunB for SCF(FBXW7)-mediated degradation in G2, and disrupting this axis causes premature sister-chromatid separation via repression of the helicase DDX11 (PMID:22710716). JunB is a master regulator of adaptive and innate immunity, directing T helper fate by activating IL-4 with c-Maf in Th2 cells (PMID:9889198), specifying Th17 identity through BATF heterodimerization and activation of RORγt/RORα while repressing Foxp3 (PMID:28824171, PMID:28555647, PMID:29234109), supporting Treg effector programs via IRF4 (PMID:30559442, PMID:31285535), and protecting T cells from apoptosis by promoting IRF4 occupancy at Bcl2l11 (PMID:35837408). It is essential for vascular and developmental processes, with knockout embryos dying from defective placental vascularization (PMID:10022836), and directly activating Myl9 to control actomyosin contractility (PMID:20551518). JunB additionally governs muscle mass by blocking FoxO3-driven atrogene transcription (PMID:20921137), and acts in TGF-β/Smad signaling both as a feedback repressor of Smad3 and as a driver of EMT and invasion (PMID:11402315, PMID:22391036, PMID:29186616). Its abundance is set by an extensive post-translational and post-transcriptional network including ubiquitination by Smurf1, neddylation by Itch, deubiquitination by USP38, and m6A/ac4C-dependent mRNA regulation by METTL3 and NAT10 (PMID:20200942, PMID:27245101, PMID:30224386, PMID:36183833, PMID:39363363).

Mechanistic history

Synthesis pass · year-by-year structured walk · 38 steps
  1. 1993 High

    Established the molecular basis for JunB's weak transactivation relative to c-Jun, explaining how it can act as a dampener of AP-1 activity.

    Evidence Domain-swap mutagenesis, transactivation reporter, and dimerization analysis defining DNA-binding and leucine-zipper residue differences

    PMID:8383624

    Open questions at the time
    • Did not resolve which endogenous heterodimer partners predominate in specific cell types
    • Structural basis of zipper destabilization not solved at atomic resolution
  2. 1993 High

    Identified JunB as an inducible AP-1 component of the NFAT-1 complex in activated T cells, linking it to T-cell transcriptional programs.

    Evidence EMSA supershift with AP-1-specific antibodies, AP-1 site mutation, reporter assay

    PMID:8441422

    Open questions at the time
    • Did not establish downstream T-cell genes controlled by this complex
    • Functional consequence of JunB/Fra-1 versus other dimers at NFAT sites unaddressed
  3. 1999 High

    Defined JunB as a Th2-selective activator of IL-4 acting cooperatively with c-Maf, and tied this to JNK phosphorylation of JunB.

    Evidence EMSA, reporter assay, Thr102/104 phospho-mutagenesis, JNK kinase assay, transgenic overexpression

    PMID:9889198

    Open questions at the time
    • Did not define the structural mechanism by which phosphorylation enables cooperative DNA binding
    • Other Th2 target genes not enumerated
  4. 1999 High

    Demonstrated that JunB is essential for placental and embryonic vascularization, defining trophoblast target genes through which it acts.

    Evidence junB-null mice, trophoblast gene expression analysis, tetraploid blastocyst rescue

    PMID:10022836

    Open questions at the time
    • Direct versus indirect regulation of proliferin/MMP-9/uPA/flt-1 not fully resolved
    • Cell-autonomous mechanism in each vascular cell type undefined
  5. 2000 High

    Showed JunB directly activates p16(INK4a) to induce senescence, establishing it as an anti-proliferative AP-1 factor.

    Evidence Gain/loss of function in fibroblasts, p16 promoter reporter/deletion, cyclin D kinase assay, INK4a-null epistasis

    PMID:10856241

    Open questions at the time
    • How the same factor toggles between senescence and proliferation outputs not mechanistically resolved here
  6. 2002 High

    Resolved the in vivo specificity of JunB by showing it can substitute for c-Jun at Jun/Fos but not Jun/ATF target genes.

    Evidence Jun-locus knock-in, transgenic complementation, target-class gene expression

    PMID:11818961

    Open questions at the time
    • Molecular basis for selective rescue of Jun/Fos versus Jun/ATF targets not pinned to specific residues
  7. 2002 High

    Established a pro-proliferative arm of JunB via direct activation of cyclin A at a CRE element, driving G2/M progression.

    Evidence junB-null fibroblasts, cyclin A CRE promoter reporter, CDK assays, inducible JunB rescue

    PMID:12121977

    Open questions at the time
    • Reconciliation with JunB's senescence-promoting role left open
    • Context determining activation versus repression of cell-cycle genes undefined
  8. 2004 High

    Revealed cell-autonomous roles of JunB in both osteoblasts and osteoclasts, linking it to bone homeostasis.

    Evidence Lineage-specific conditional knockouts, differentiation assays, gene expression analysis

    PMID:14769860

    Open questions at the time
    • Direct target genes in osteoclast lineage not defined
    • Mechanism of opposing effects in two lineages unresolved
  9. 2004 Medium

    Identified phosphorylation-dependent coactivator recruitment, showing Ser-79 phosphorylation enables JunB-p300 cooperation at the DMP1 promoter.

    Evidence Co-IP, ChIP, Ser-79 phospho-mutant, DMP1 reporter

    PMID:15308641

    Open questions at the time
    • Kinase responsible for Ser-79 phosphorylation not identified
    • Single lab; reciprocal validation of p300 interaction limited
  10. 2001 Medium

    Placed JunB in a TGF-β negative feedback loop by showing it binds Smad3 off-DNA to limit Smad-driven transcription.

    Evidence Smad3-JunB co-IP, reporter assays in junB-null versus WT MEFs with rescue

    PMID:11402315

    Open questions at the time
    • Single lab; reciprocal/structural validation of the Smad3 interaction lacking
    • Later work shows context-dependent pro-EMT role, leaving the dual function partly unreconciled
  11. 2006 Medium

    Showed dimer-composition switching (JunB homodimer to JunB/FosB) at the MMP-2 promoter drives oxidant-stress-induced transcription during cardiac I/R injury.

    Evidence ChIP of endogenous MMP-2 AP-1 site, IHC, qPCR, radical-scavenger inhibition

    PMID:16699069

    Open questions at the time
    • Single lab; functional consequence of dimer switch on cardiac outcome correlative
    • Signal linking oxidant stress to FosB induction not defined
  12. 2007 Medium

    Demonstrated dual transcriptional and translational control of JUNB downstream of NPM-ALK via ERK and mTOR in ALCL.

    Evidence NPM-ALK expression, ERK/mTOR inhibition, knockdown, polysome fractionation

    PMID:17690253

    Open questions at the time
    • Single lab; direct ERK/mTOR effectors on the JUNB locus/mRNA not identified
    • Generalizability beyond ALCL untested here
  13. 2008 High

    Defined JunB as a direct repressor of G-CSF in keratinocytes mediating skin-to-bone-marrow signaling, with genetic epistasis confirming the target.

    Evidence Epidermal-specific conditional KO, G-CSF double-mutant rescue, promoter studies

    PMID:18641637

    Open questions at the time
    • Bone loss phenotype is G-CSF-independent, leaving its mediator undefined
  14. 2010 High

    Identified Myl9 as a direct JunB target controlling actomyosin contractility, motility, and arterial function.

    Evidence Conditional KO in vascular cells, Myl9 rescue, contractility/stress-fiber assays, ChIP

    PMID:20551518

    Open questions at the time
    • Additional cytoskeletal targets not mapped genome-wide here
  15. 2010 High

    Established JunB as a regulator of muscle mass that opposes FoxO3-driven atrogene transcription independently of Akt/mTOR.

    Evidence In vivo muscle electroporation OE/KD, ChIP of FoxO3 at atrogin-1/MuRF-1, protein synthesis, denervation model

    PMID:20921137

    Open questions at the time
    • Mechanism by which JunB blocks FoxO3 promoter binding (competition versus complex) not resolved
  16. 2010 High

    Identified Smurf1 as an E3 ligase that destabilizes JunB, coupling JunB turnover to mesenchymal proliferation and osteoblast differentiation.

    Evidence Co-IP via PY motif, ubiquitination assay, cyclin D1 reporter, knockdown rescue in Smurf1-null cells

    PMID:20200942

    Open questions at the time
    • Signals controlling Smurf1-JunB engagement in vivo not defined
  17. 2012 High

    Defined a GSK3-FBXW7 phospho-degron controlling JunB degradation in G2 and linked its failure to chromosome cohesion defects via DDX11 repression.

    Evidence Phospho-degron mutagenesis, co-IP with GSK3/FBXW7, ubiquitylation assay, chromatid cohesion readout

    PMID:22710716

    Open questions at the time
    • Whether JunB-DDX11 repression contributes to genomic instability in cancer not tested in vivo
  18. 2012 Medium

    Showed JunB stability is controlled downstream of CARMA1 signaling, linking TCR signaling to JunB-dependent Th2 differentiation.

    Evidence CARMA1-deficient T cells, JunB ubiquitination/stability assays, Th2 differentiation

    PMID:22371397

    Open questions at the time
    • Single lab; the E3 ligase acting downstream of CARMA1 not identified
  19. 2012 Medium

    Implicated JunB in TGF-β-induced EMT, including Smad-mediated Id2 repression via ATF3 and induction of mesenchymal/fibrotic genes.

    Evidence siRNA, JunB-ATF3 co-IP, ChIP, junction/actin imaging, reporter

    PMID:22391036

    Open questions at the time
    • Single lab; direct versus indirect target assignment for each mesenchymal gene incomplete
  20. 2013 High

    Established IFN-γ (Ifng) as a direct JUNB target in NK/NKT cells driving STAT1-dependent hepatitis.

    Evidence Conditional immune KO, ChIP at Ifng promoter, cytokine ELISA, IFN-γ/IRF1 rescue

    PMID:24200694

    Open questions at the time
    • Dimer partner controlling Ifng activation in NK/NKT cells not specified
  21. 2014 Medium

    Linked JunB to ER-stress survival signaling by showing it activates XBP1 via C/EBPδ to sustain AKT and suppress BAD-driven apoptosis in β-cells.

    Evidence siRNA/overexpression, BAD and AKT phosphorylation assays, C/EBPδ reporter, XBP1s rescue

    PMID:24786832

    Open questions at the time
    • Single lab; directness of JunB regulation of the XBP1 axis not fully resolved
  22. 2014 Medium

    Showed JunB is required for both classical and alternative macrophage activation programs.

    Evidence siRNA knockdown in macrophages, LPS/IL-4 stimulation, expression profiling with network modeling

    PMID:25472994

    Open questions at the time
    • Single lab; direct macrophage target genes not defined by ChIP
  23. 2014 Medium

    Defined a tumor-suppressive role for JunB in prostate, where its loss reduces p16/p21 and senescence to cooperate with Pten loss in invasive cancer.

    Evidence Prostate-specific Junb/Pten double KO, histology, senescence/proliferation immunostaining

    PMID:25526087

    Open questions at the time
    • Single lab; mechanism of stromal osteopontin/S100A8/9 induction not resolved
  24. 2017 High

    Established JunB as essential for Th17 identity through BATF heterodimerization, RORγt/RORα activation, and Foxp3 repression, with replication across labs.

    Evidence Conditional Junb T cells, ATAC-seq/ChIP-seq of BATF at Rorc, RNA-seq, EAE/colitis models

    PMID:28555647 PMID:28824171 PMID:29234109

    Open questions at the time
    • Distinction between pathogenic versus non-pathogenic Th17 control only partly mechanistically explained
  25. 2018 High

    Showed JunB enables effector Treg programs by facilitating IRF4 chromatin occupancy at Icos/Ctla4 loci, preventing autoimmunity.

    Evidence Treg-specific KO, IRF4 ChIP-seq with/without JunB, flow cytometry

    PMID:30559442

    Open questions at the time
    • BATF-independent arm of JunB action not mechanistically defined
  26. 2018 High

    Identified USP38 as a deubiquitinase stabilizing JunB downstream of TCR signaling to support Th2 development.

    Evidence USP38-JunB co-IP, K48-specific deubiquitination assay, USP38 KO mice, asthma models

    PMID:30224386

    Open questions at the time
    • Counteracting E3 ligase for TCR-induced JunB turnover not identified here
  27. 2018 Medium

    Placed JUNB in a TGF-β feed-forward network driving late invasion genes WNT7A/7B in breast cancer.

    Evidence SMAD2/3 ChIP-seq, JUNB knockdown, motif analysis, invasion assays, WNT manipulation

    PMID:29186616

    Open questions at the time
    • Single lab; direct JUNB binding at WNT7A/7B loci not fully established
  28. 2019 Medium

    Demonstrated JunB is required for Treg development by enabling IL-2 production and CD25 expression, with a cell-intrinsic defect rescuable by IL-2.

    Evidence Cd4-Cre conditional KO, in vitro Treg ±IL-2, mixed bone marrow chimera, IL-2 complex rescue, DSS colitis

    PMID:31285535

    Open questions at the time
    • Single lab; direct target through which JunB controls IL-2/CD25 not defined
  29. 2021 Medium

    Showed persistent JunB drives fibroblast senescence (p16 up, IGF-1 down) that depletes skin stem cell niches.

    Evidence Fibroblast-specific OE/silencing in vivo, p16/IGF-1 analysis, stem cell quantification

    PMID:34469740

    Open questions at the time
    • Single lab; directness of IGF-1 repression by JunB not fully established
  30. 2021 Medium

    Defined a JUNB-FBXO21-ERK axis in chondrocytes that inhibits autophagy and promotes osteoarthritic cartilage degeneration.

    Evidence ChIP of JunB at FBXO21 promoter, FBXO21-ERK co-IP/MS, siRNA, OA model

    PMID:33450132

    Open questions at the time
    • Single lab; mechanism by which FBXO21 phosphorylates ERK requires deeper validation
  31. 2021 Medium

    Identified JUNB as essential for hemogenic endothelium specialization and endothelial-to-hematopoietic transition in human hematopoiesis.

    Evidence ATAC-seq, H3K4me3/H3K27me3 ChIP-seq, RNA-seq, single-cell analysis with JUNB loss-of-function

    PMID:35668082

    Open questions at the time
    • Single lab; direct JUNB target genes driving the transition not pinpointed
  32. 2022 Medium

    Showed JUNB promotes cell-cycle progression via cyclin E1 induction and switches TGF-β2 from anti-proliferative to pro-invasive output.

    Evidence Transcriptomics, ChIP-seq, cyclin E1 reporter, polysome profiling, xenograft/metastasis

    PMID:36494864

    Open questions at the time
    • Single lab; threshold mechanism for the TGF-β2 response switch undefined
  33. 2022 Medium

    Established m6A control of JUNB mRNA stability by METTL3 and 3'UTR reader proteins during TGF-β-induced EMT.

    Evidence METTL3 KD, 3'UTR m6A site mutagenesis, reader knockdown, RNA stability assays

    PMID:36183833

    Open questions at the time
    • Single lab; identity and division of labor among readers only partly resolved
  34. 2022 Medium

    Showed JunB protects T helper cells from apoptosis by promoting IRF4 binding at Bcl2l11 and is required for clonal expansion.

    Evidence Conditional KO, apoptosis/proliferation flow cytometry, IRF4 ChIP at Bcl2l11, immunization

    PMID:35837408

    Open questions at the time
    • Single lab; how JunB enhances IRF4 occupancy mechanistically unresolved
  35. 2023 Medium

    Linked the circadian clock to JunB by showing Bmal1 directly drives Junb transcription to gate diurnal macrophage inflammation.

    Evidence Myeloid Bmal1/Junb conditional KO/KD, Bmal1 ChIP at Junb promoter, AKT/ERK assays, ConA hepatitis

    PMID:37791375

    Open questions at the time
    • Single lab; direct macrophage targets of JunB in this circuit undefined
  36. 2023 Medium

    Defined a VCAM-1-JunB-IL-8/CXCL1 axis controlling retinal endothelial sprouting and pathological neovascularization.

    Evidence siRNA, IL-8 promoter reporter, RNA-seq, intravitreal siRNA, OIR model

    PMID:37179352

    Open questions at the time
    • Single lab; signaling connecting VCAM-1 to JunB activation not detailed
  37. 2024 Medium

    Showed NAT10-mediated ac4C of JUNB mRNA elevates JunB, which activates LDHA to promote glycolysis and immunosuppression in TNBC.

    Evidence NAT10 KO/OE, ac4C-seq, ChIP/reporter for LDHA, in vivo tumor models, T-cell assays

    PMID:39363363

    Open questions at the time
    • Single lab; relative contribution of ac4C versus other JunB regulation in TNBC unclear
  38. 2024 Medium

    Demonstrated that MEK-driven JunB programs promote CAR-T exhaustion, and that JunB overexpression reverses the protective effect of MEK inhibition.

    Evidence MEKi, JunB/c-Fos overexpression, JunB Cut-and-Tag, single-cell transcriptomics, tumor efficacy

    PMID:39438476

    Open questions at the time
    • Single lab; specific exhaustion target genes mediating the effect not isolated

Open questions

Synthesis pass · forward-looking unresolved questions
  • How JunB's dimer partner identity and post-translational state are integrated to dictate its opposing outputs (proliferation versus senescence, activation versus repression, pro- versus anti-inflammatory) within a single cell remains unresolved.
  • No unifying model linking dimer composition, phosphorylation, and degradation to context-specific gene selection
  • Structural basis of partner-dependent target choice not solved
  • Genome-wide direct target maps across cell types not integrated

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 10 GO:0003677 DNA binding 5
Localization
GO:0005634 nucleus 2 GO:0005654 nucleoplasm 2
Pathway
R-HSA-168256 Immune System 7 R-HSA-74160 Gene expression (Transcription) 6 R-HSA-162582 Signal Transduction 5 R-HSA-1640170 Cell Cycle 4 R-HSA-392499 Metabolism of proteins 4 R-HSA-8953897 Cellular responses to stimuli 3
Partners
ATF3BATFEP300FOSIRF4JUNMAFSMAD3
Complex memberships
AP-1 transcription factor

Evidence

Reading pass · 39 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1993 JunB has ~10-fold lower DNA-binding activity than c-Jun due to a small number of amino acid differences in its DNA-binding and dimerization domains. Substituting four amino acids in JunB's DNA-binding/dimerization motifs with the corresponding c-Jun sequences converts JunB into a c-Jun-like activator. JunB attenuates c-Jun trans-activation via its leucine zipper; two glycine residues in the JunB leucine zipper decrease zipper stability, reducing homodimerization and increasing heterodimerization with c-Jun to form inactive heterodimers. Domain-swap mutagenesis, transactivation reporter assays, dimerization analysis Genes & development High 8383624
1993 The NFAT-1 DNA-binding complex in activated T cells contains JunB and Fra-1 as its inducible nuclear AP-1 component, binding a variant AP-1 site at the 3' end of the NFAT-1 sequence. Mutation of this AP-1 site inhibits both NFAT-1 binding and NFAT-1-driven reporter expression. Antibody supershift experiments identified JunB and Fra-1 specifically within the complex. EMSA supershift with AP-1 family-specific antibodies, site-directed mutation of AP-1 site, reporter assay Molecular and cellular biology High 8441422
1999 JunB is selectively induced in Th2 (not Th1) cells during differentiation and binds directly to the P1 AP-1 site of the IL-4 promoter, synergizing with c-Maf to activate IL-4 transcription. This synergy requires phosphorylation of JunB at Thr102 and Thr104 by JNK MAP kinase, which facilitates cooperative DNA binding between JunB and c-Maf. Elevated JunB in transgenic mice increased Th2 cytokine expression in developing Th1 cells. EMSA, reporter gene assay, site-directed mutagenesis (Thr102/104), JNK kinase assay, transgenic mouse overexpression The EMBO journal High 9889198
1999 JunB-deficient embryos die between E8.5–E10.0 due to failure to establish proper vascular interactions with maternal circulation. In trophoblasts, loss of JunB causes deregulation of proliferin, MMP-9, and uPA expression, resulting in defective decidual neovascularization. Downregulation of VEGF-receptor 1 (flt-1) leads to dilated yolk sac vessels. Tetraploid rescue (injection of junB−/− ES cells into WT blastocysts) rescued fetal growth retardation and placental labyrinth defects. Genetic knockout (junB−/− mice), gene expression analysis of trophoblast targets, tetraploid blastocyst complementation rescue The EMBO journal High 10022836
2000 JunB directly activates transcription of the cyclin-dependent kinase inhibitor p16(INK4a) through three AP-1-like binding sites in the p16 promoter. Increased JunB expression induces premature senescence in primary cells and reduces proliferation in 3T3 cells by abolishing cyclin D-associated kinase activity and reducing pRb hyperphosphorylation. The anti-proliferative effect of JunB is p16-dependent (absent in INK4a−/− cells). Gain/loss-of-function in mouse fibroblasts, p16 promoter reporter and deletion analysis, cyclin D kinase assay, pRb phosphorylation assay, INK4a−/− epistasis The EMBO journal High 10856241
2001 JunB (and c-Jun) interact physically with Smad3 off-DNA, reducing Smad3/DNA interactions and thereby suppressing TGF-β/Smad3-driven transcription. Conversely, junB−/− fibroblasts show significantly higher Smad-specific promoter transactivation, and rescue of junB expression normalizes this. Thus, TGF-β-induced JunB expression constitutes a negative feedback loop on early Smad-driven gene activation. Co-immunoprecipitation (Smad3–JunB interaction), reporter assay in junB−/− vs. wild-type MEFs, JunB rescue experiment Oncogene Medium 11402315
2002 JunB can functionally substitute for c-Jun during mouse development in a gene-dosage-dependent manner when knocked into the Jun locus. JunB rescues Jun/Fos-regulated gene expression but not Jun/ATF-regulated gene expression, thereby rescuing liver and cardiac defects of Jun-null mice in vivo and in primary fibroblasts and fetal hepatoblasts in vitro. Knock-in strategy, transgenic complementation, gene expression analysis of Jun/Fos vs Jun/ATF targets Nature genetics High 11818961
2002 JunB directly activates cyclin A transcription by binding to the CRE element in the cyclin A promoter, driving G2/M cell cycle progression. junB−/− fibroblasts show impaired cyclin A-CDK2 and cyclin B-CDC2 kinase activities and accumulate in S-phase. Re-introduction of inducible JunB-ER(TM) restores cyclin A expression and normal cell cycle distribution. junB−/− fibroblasts, cyclin A promoter reporter (CRE binding), kinase activity assays, inducible JunB rescue The Journal of biological chemistry High 12121977
2004 Conditional deletion of JunB in osteoblasts and osteoclasts reveals cell-autonomous roles: mutant osteoblasts show elevated p16(INK4a) but decreased cyclin D1 and cyclin A, reduced osteocalcin and bone sialoprotein, and transiently increased Runx2; macrophage-lineage-specific JunB deletion causes osteopetrosis-like phenotype with reduced osteoclast numbers, indicating JunB is a positive regulator of osteoclast activity. Conditional (Cre-lox) knockout in osteoblast and macrophage-osteoclast lineages, in vivo and in vitro differentiation assays, gene expression analysis The Journal of cell biology High 14769860
2006 During cardiac ischemia-reperfusion (I/R) injury, JunB and FosB accumulate in nuclei of cardiomyocytes, fibroblasts, and endothelial cells. ChIP of the MMP-2 promoter AP-1 site shows JunB homodimers occupying it under control conditions, switching to JunB/FosB heterodimers after I/R, driving enhanced MMP-2 transcription and translation. This induction is blocked by the hydroxyl radical scavenger MPG, implicating oxidant stress. Chromatin immunoprecipitation (ChIP) of AP-1 site in MMP-2 promoter, immunohistochemistry, real-time PCR, Western blot, pharmacological inhibition American journal of physiology. Heart and circulatory physiology Medium 16699069
2007 In NPM-ALK-positive ALCL, ERK1/2 activation downstream of NPM-ALK transcriptionally upregulates JUNB mRNA, while active mTOR pathway promotes JUNB mRNA translation (shifting it from monosomes/RNPs to large polysomes). JunB knockdown decreases proliferation; mTOR inhibition downregulates JunB protein by shifting its mRNA to monosomes/RNPs. NPM-ALK expression, pharmacological ERK/mTOR inhibition, siRNA/shRNA knockdown, polysome fractionation, cell cycle analysis Blood Medium 17690253
2008 JunB directly represses G-CSF (Csf3) transcription in epidermal keratinocytes. Loss of epidermal JunB causes elevated systemic G-CSF, leading to myeloproliferative disease and low bone mass. Genetic ablation of G-CSF in JunB epidermal-KO mice prevents myeloproliferative disease but not bone loss, establishing G-CSF as a direct JunB transcriptional target mediating skin-to-hematopoietic organ signaling. Epidermal-specific conditional JunB knockout, G-CSF genetic rescue (double mutant), in vitro keratinocyte analysis, promoter studies Nature cell biology High 18641637
2010 JunB directly activates transcription of myosin regulatory light chain 9 (Myl9), which controls actomyosin contractility and stress fiber assembly. Conditional ablation of Junb impairs arterial contractility, stress fiber formation, and cellular motility in VSMCs, MEFs, and endothelial cells. Re-expression of either Junb or Myl9 in Junb-deficient cells restores stress fiber formation, motility, and contractile capacity. Conditional Junb knockout in vascular cells, Myl9 rescue experiment, vascular contractility assays, stress fiber imaging, ChIP/promoter analysis The Journal of clinical investigation High 20551518
2010 JunB overexpression induces skeletal muscle hypertrophy independently of the Akt/mTOR pathway and prevents denervation atrophy. JunB blocks FoxO3 binding to the atrogin-1 and MuRF-1 promoters, thereby reducing protein breakdown. RNAi-mediated JunB knockdown in adult muscles causes atrophy; nuclear exclusion of JunB is observed in atrophying myotubes. Electroporation-based OE/KD in adult mouse muscles, ChIP (FoxO3 binding to atrogin-1/MuRF-1 promoters), protein synthesis measurement, denervation model The Journal of cell biology High 20921137
2010 Smurf1 ubiquitin E3 ligase interacts with JunB through its PY motif, ubiquitinates JunB, and targets it for proteasomal degradation. Smurf1-deficient mesenchymal stem cells have elevated JunB protein, increased cyclin D1 (a JunB transcriptional target), and enhanced proliferation and osteoblast differentiation. JunB knockdown in Smurf1−/− cells restores osteogenic potential to wild-type level. Co-immunoprecipitation, ubiquitination assay, cyclin D1 promoter reporter, JunB knockdown rescue in Smurf1−/− cells Journal of bone and mineral research High 20200942
2012 JunB undergoes phosphorylation-dependent ubiquitylation during the G2 phase of the cell cycle. GSK3 phosphorylates a consensus phospho-degron on JunB, and the E3 ubiquitin ligase SCF(FBXW7) mediates JunB ubiquitylation and degradation in G2. Inactivation of this GSK3-FBXW7-JunB axis causes JunB accumulation in G2/M, transcriptional repression of the DNA helicase DDX11, and premature sister chromatid separation. Phospho-degron mutagenesis, co-immunoprecipitation with GSK3/FBXW7, ubiquitylation assay, pharmacological/genetic GSK3 inhibition, chromatid cohesion assay Oncogene High 22710716
2012 JunB is required for TGF-β-induced epithelial-mesenchymal transition (EMT). JunB depletion by siRNA abrogates TGF-β-induced disruption of cell-cell junctions, actin fiber formation, focal adhesions, and expression of fibrotic proteins. JunB contributes to Smad-mediated repression of inhibitor of differentiation 2 (Id2) through interaction with transcriptional repressor ATF3, and mediates TGF-β induction of fibronectin, fibulin-2, tropomyosin (Tpm1), and integrin-β3. siRNA knockdown, co-immunoprecipitation (JunB–ATF3), ChIP, actin/junction immunofluorescence, reporter assay The Journal of cell biology Medium 22391036
2013 JUNB in NK and NKT cells directly activates Ifng transcription (IFN-γ is a direct transcriptional target of JUNB). Targeted deletion of Junb in immune cells decreases IFN-γ expression and secretion from NK/NKT cells, reducing STAT1 pathway activation and protecting against concanavalin A-induced hepatitis. Systemic IFN-γ treatment or adenoviral IRF1 delivery restores hepatotoxicity in Junb-deficient mice. Conditional immune-cell Junb knockout, ChIP (JUNB at Ifng promoter), cytokine ELISA, STAT1 activation assay, IFN-γ rescue experiment The Journal of clinical investigation High 24200694
2014 JunB is required for full LPS-induced expression of Il1b and other pro-inflammatory genes in macrophages, and also modulates alternative macrophage activation markers induced by IL-4. Junb knockdown in macrophages reduces both classical (M1) and alternative (M2) activation gene expression. siRNA knockdown in macrophages, LPS/IL-4 stimulation, gene expression analysis, network modeling validation Journal of immunology Medium 25472994
2014 JUNB loss-of-function in prostate epithelium combined with Pten loss promotes invasive cancer. JunB deficiency leads to decreased p16(Ink4a) and p21(CIP1) in epithelial cells, increased proliferation, and decreased senescence. Tumor stroma shows increased osteopontin and S100A8/9 expression. Prostate epithelium-specific conditional Junb/Pten double knockout, topical Cre delivery, histology, immunostaining for senescence/proliferation markers Cell death and differentiation Medium 25526087
2016 Itch is a HECT-type neddylation E3 ligase that neddylates JunB, attenuating its transcriptional activity. Itch-mediated neddylation of JunB also promotes its ubiquitination-dependent proteasomal degradation. Neddylation assay in cells, co-immunoprecipitation (Itch–JunB), reporter assay of JunB transcriptional activity, ubiquitination assay Cellular signalling Medium 27245101
2017 JunB is required for Th17 cell identity: it directly activates expression of RORγt and RORα (Th17 lineage-specifying receptors) and represses Foxp3. JunB forms a heterodimer with BATF to activate Th17 signature genes; JunB facilitates BATF DNA binding at the Rorc locus. JunB expression is induced by IL-6, is required for IL-23 receptor expression and IL-23-dependent pathogenic Th17 differentiation, but is dispensable for TGF-β1-dependent non-pathogenic Th17 cells. Conditional Junb-deficient T cells, ATAC-seq/ChIP-seq (BATF binding at Rorc locus), RNA-seq, EAE and colitis models, cytokine stimulation (IL-6, IL-23, TGF-β1) Nature communications / Scientific reports High 28555647 28824171 29234109
2018 JunB in effector Treg cells promotes an IRF4-dependent transcriptional program by facilitating the accumulation of IRF4 at a subset of its target sites, including loci near Icos and Ctla4. JunB promotes Treg effector molecule expression (ICOS, CTLA4) in BATF-dependent and BATF-independent manners. Mice lacking JunB in Treg cells develop multi-organ autoimmunity. Treg-specific Junb conditional KO, ChIP-seq (IRF4 binding at Icos/Ctla4 loci with/without JunB), flow cytometry, in vitro Treg differentiation Nature communications High 30559442
2018 USP38 is a deubiquitinase that directly associates with JunB, removes Lys-48-linked poly-ubiquitin chains from JunB, and thereby blocks TCR-induced JunB proteasomal turnover. USP38 is required for TCR-induced JunB protein stabilization, Th2 cytokine production, and Th2 development in vitro and in vivo. Co-immunoprecipitation (USP38–JunB), deubiquitination assay (K48-specific), USP38 KO mice, Th2 differentiation assay, OVA/HDM asthma model The Journal of experimental medicine High 30224386
2018 JUNB governs a TGFβ feed-forward regulatory network in breast cancer: prolonged TGFβ stimulation alters the genome-wide SMAD2/3 binding landscape and induces JUNB expression; JUNB is required for expression of late invasion-mediating genes, including WNT7A and WNT7B. WNT7A/7B overexpression enhances TGFβ-induced invasion, while WNT pathway inhibition reduces it. ChIP-seq (SMAD2/3 binding), siRNA knockdown of JUNB, de novo motif analysis, invasion assays, WNT pathway manipulation Nucleic acids research Medium 29186616
2021 Persistent JunB activation in fibroblasts drives senescence through concomitant upregulation of p16INK4A and repression of IGF-1. This fibroblast senescence disrupts the stem cell niche, depleting skin stem cell pools. Fibroblast-specific JunB silencing restores IGF-1 and p16 levels and rescues skin stem cell pools and tissue integrity. Fibroblast-specific JunB overexpression/silencing in vivo, p16/IGF-1 expression analysis, skin stem cell quantification, niche interaction assays Cell reports Medium 34469740
2021 JunB directly activates FBXO21 promoter expression in chondrocytes. The JUNB-FBXO21-ERK axis promotes cartilage degeneration in osteoarthritis: FBXO21 inhibits autophagy by interacting with and phosphorylating ERK. JUNB knockdown reduces FBXO21 expression and attenuates OA-related cartilage degeneration. ChIP (JunB at FBXO21 promoter), co-immunoprecipitation (FBXO21–ERK), mass spectrometry, siRNA knockdown, in vivo OA model Aging cell Medium 33450132
2021 JUNB is an essential regulator of hemogenic endothelium specialization and endothelial-to-hematopoietic transition during human hematopoiesis in vitro, as identified by integrative chromatin accessibility (ATAC-seq), H3K4me3/H3K27me3 ChIP-seq, and transcriptomic profiling with JUNB loss-of-function. ATAC-seq, H3K4me3/H3K27me3 ChIP-seq, RNA-seq, single-cell analysis, JUNB loss-of-function during hPSC-to-HPC differentiation Nature communications Medium 35668082
2022 JUNB promotes cell cycle progression by inducing cyclin E1 expression and repressing TGF-β2 gene transcription. High JUNB levels switch TGF-β2 stimulation from an anti-proliferative to a pro-invasive response and promote TGF-β2 mRNA translation. These functions were established by combined transcriptomic, genomic, and functional studies. Transcriptomics, ChIP-seq, siRNA/overexpression, cyclin E1 promoter reporter, polysome profiling, in vivo xenograft/metastasis model Genome biology Medium 36494864
2022 m6A methylation by METTL3 regulates JUNB expression at the level of mRNA stability (not translation): specific m6A motifs in the JUNB 3'UTR are recognized by distinct m6A reader proteins that control JUNB mRNA stability during TGF-β-induced EMT. JUNB knockdown impairs expression of specific mesenchymal target genes during EMT. METTL3 KD, m6A site mutagenesis in 3'UTR, m6A reader protein knockdown, RNA stability assays, siRNA knockdown of JUNB The Journal of biological chemistry Medium 36183833
2004 JunB cooperates with the transcriptional coactivator p300 to activate DMP1 (dentin matrix protein 1) transcription during osteoblast differentiation. Phosphorylation of JunB at Ser-79 is required for its interaction with p300. Immunoprecipitation and ChIP confirmed the in vivo interaction of JunB and p300 at the DMP1 promoter. Co-immunoprecipitation (JunB–p300), ChIP, Ser-79 phospho-mutant, DMP1 promoter reporter assay The Journal of biological chemistry Medium 15308641
2014 JunB stimulates XBP1 expression via the transcription factor C/EBPδ during ER stress, and this JunB–XBP1 axis activates AKT signaling. JunB silencing inhibits AKT activation and activates the pro-apoptotic Bcl-2 protein BAD via dephosphorylation; forced XBP1s expression rescues viability of JunB-deficient β-cells. XBP1 knockdown also reduces AKT phosphorylation, linking JunB to AKT through XBP1. siRNA knockdown (JunB, XBP1), adenoviral overexpression, BAD phosphorylation assay, AKT phosphorylation assay, C/EBPδ reporter assay, GLP-1 agonist treatment Cell death and differentiation Medium 24786832
2019 JunB plays a crucial role in Treg cell development by facilitating IL-2 production and CD25 (high-affinity IL-2 receptor subunit) expression in CD4+ T cells. Junb-deficient CD4+ T cells fail to differentiate into Treg cells in vitro unless exogenous IL-2 is supplied; a cell-intrinsic defect confirmed by mixed bone marrow transfer. IL-2/anti-IL-2 complex injection rescued Treg expansion and alleviated DSS colitis in Junbfl/flCd4-Cre mice. Conditional Junb KO (Cd4-Cre), in vitro Treg differentiation ±IL-2, mixed bone marrow chimera, IL-2 complex rescue, DSS colitis model Mucosal immunology Medium 31285535
2022 JunB directly inhibits expression of apoptosis-promoting genes, including Bcl2l11 (encoding Bim), in T helper cells by promoting IRF4 DNA binding at the Bcl2l11 locus. JunB is required for clonal expansion of Th1, Th2, and Th17 cells; TCR-stimulated Junb-deficient CD4+ T cells are more sensitive to apoptosis. Conditional Junb KO, flow cytometry (apoptosis, proliferation), ChIP (IRF4 at Bcl2l11 locus in the presence/absence of JunB), immunization models Frontiers in immunology Medium 35837408
2012 CARMA1 deficiency reduces JunB protein stability by enhancing its ubiquitination and degradation, impairing TCR-induced Th2 cytokine production and differentiation. JunB stability is regulated downstream of CARMA1 signaling. CARMA1-deficient T cells, ubiquitination assay of JunB, JunB protein stability measurement, Th2 differentiation assay Journal of immunology Medium 22371397
2023 Bmal1 (core circadian clock gene) directly regulates Junb transcription in macrophages, controlling diurnal variation in ConA-induced hepatitis. JunB in macrophages promotes inflammation by regulating AKT and ERK signaling pathways. Macrophage-specific Junb knockdown blunts the time-of-day-dependent effect of ConA-induced liver injury. Myeloid-specific Bmal1 and Junb conditional KO/KD, ChIP (Bmal1 at Junb promoter), AKT/ERK signaling assays, ConA hepatitis model JHEP reports Medium 37791375
2023 VCAM-1 regulates JunB-mediated IL-8 promoter activity and expression in human retinal endothelial cells. JunB-driven IL-8/CXCL1 signaling downstream of VCAM-1 controls retinal endothelial cell sprouting and pathological neovascularization. Intravitreal VCAM-1 siRNA decreases VCAM-1–JunB–CXCL1 signaling and reduces OIR-induced retinal neovascularization. siRNA knockdown (VCAM-1, JunB), IL-8 promoter reporter assay, RNA-seq, intravitreal siRNA injection, OIR mouse model Communications biology Medium 37179352
2024 NAT10-mediated ac4C modification of JUNB mRNA increases its expression in TNBC. JunB then upregulates LDHA transcription, promoting glycolysis and immunosuppression. Loss of NAT10 inhibits JunB expression and TNBC tumor progression; the combination of NAT10 inhibitor remodelin and CTLA-4 antibody synergistically activates T cells. NAT10 KO/overexpression, ac4C sequencing, ChIP/reporter for JunB-driven LDHA, in vitro and in vivo tumor models, T cell functional assays Journal of experimental & clinical cancer research Medium 39363363
2024 MEK inhibition prevents CAR-T cell exhaustion and terminal differentiation by downregulating c-Fos and JunB. Overexpression of JunB in CAR-T cells counteracts MEK inhibition effects. Cut-and-Tag assay shows that MEK inhibition reduces JunB-driven gene programs associated with exhaustion, differentiation, anergy, glycolysis, and apoptosis in CAR-T cells. MEKi treatment, JunB/c-Fos overexpression in CAR-T cells, Cut-and-Tag (JunB ChIP-seq), single-cell transcriptomics, tumor efficacy assays Signal transduction and targeted therapy Medium 39438476

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1993 JunB differs from c-Jun in its DNA-binding and dimerization domains, and represses c-Jun by formation of inactive heterodimers. Genes & development 309 8383624
1999 Regulation of IL-4 expression by the transcription factor JunB during T helper cell differentiation. The EMBO journal 302 9889198
2000 JunB suppresses cell proliferation by transcriptional activation of p16(INK4a) expression. The EMBO journal 268 10856241
1993 The NFAT-1 DNA binding complex in activated T cells contains Fra-1 and JunB. Molecular and cellular biology 221 8441422
1999 JunB is essential for mammalian placentation. The EMBO journal 209 10022836
1992 Regulation of jun-B messenger RNA and AP-1 activity by light and a circadian clock. Science (New York, N.Y.) 202 1549784
1989 Tissue-specific expression of c-jun and junB during organogenesis in the mouse. Development (Cambridge, England) 191 2480878
1994 Morphine induces c-fos and junB in striatum and nucleus accumbens via D1 and N-methyl-D-aspartate receptors. Proceedings of the National Academy of Sciences of the United States of America 176 8078918
2004 Mice lacking JunB are osteopenic due to cell-autonomous osteoblast and osteoclast defects. The Journal of cell biology 172 14769860
1991 Interleukin-6 signals activating junB and TIS11 gene transcription in a B-cell hybridoma. Molecular and cellular biology 164 1705005
1991 Overexpression of c-jun, junB, or junD affects cell growth differently. Proceedings of the National Academy of Sciences of the United States of America 156 1924349
1991 cAMP-dependent regulation of proenkephalin by JunD and JunB: positive and negative effects of AP-1 proteins. Proceedings of the National Academy of Sciences of the United States of America 153 1719551
2002 Amplification and overexpression of JUNB is associated with primary cutaneous T-cell lymphomas. Blood 139 12393503
2002 JunB can substitute for Jun in mouse development and cell proliferation. Nature genetics 132 11818961
2010 JunB transcription factor maintains skeletal muscle mass and promotes hypertrophy. The Journal of cell biology 130 20921137
2002 Th2 cell-specific cytokine expression and allergen-induced airway inflammation depend on JunB. The EMBO journal 121 12456639
2017 JunB promotes Th17 cell identity and restrains alternative CD4+ T-cell programs during inflammation. Nature communications 118 28824171
1991 Activation of junB by PKC and PKA signal transduction through a novel cis-acting element. Nucleic acids research 101 1708123
2018 JunB regulates homeostasis and suppressive functions of effector regulatory T cells. Nature communications 98 30559442
2014 JUNB is a key transcriptional modulator of macrophage activation. Journal of immunology (Baltimore, Md. : 1950) 97 25472994
2018 JUNB governs a feed-forward network of TGFβ signaling that aggravates breast cancer invasion. Nucleic acids research 93 29186616
2001 Induction of the AP-1 members c-Jun and JunB by TGF-beta/Smad suppresses early Smad-driven gene activation. Oncogene 87 11402315
2017 JunB is essential for IL-23-dependent pathogenicity of Th17 cells. Nature communications 85 28555647
2006 Cardiac ischemia-reperfusion injury induces matrix metalloproteinase-2 expression through the AP-1 components FosB and JunB. American journal of physiology. Heart and circulatory physiology 85 16699069
2021 JUNB-FBXO21-ERK axis promotes cartilage degeneration in osteoarthritis by inhibiting autophagy. Aging cell 84 33450132
2007 The oncoprotein NPM-ALK of anaplastic large-cell lymphoma induces JUNB transcription via ERK1/2 and JunB translation via mTOR signaling. Blood 83 17690253
2012 JunB contributes to Id2 repression and the epithelial-mesenchymal transition in response to transforming growth factor-β. The Journal of cell biology 82 22391036
2010 Smurf1 inhibits mesenchymal stem cell proliferation and differentiation into osteoblasts through JunB degradation. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 82 20200942
2002 Cell cycle promoting activity of JunB through cyclin A activation. The Journal of biological chemistry 76 12121977
1992 Transcription factors junB and c-jun are selectively up-regulated and functionally implicated in fibrosarcoma development. Genes & development 74 1459456
2008 Regulation and function of JunB in cell proliferation. Biochemical Society transactions 71 18793152
2015 Highly recurrent mutations of SGK1, DUSP2 and JUNB in nodular lymphocyte predominant Hodgkin lymphoma. Leukemia 70 26658840
2003 JunB inhibits proliferation and transformation in B-lymphoid cells. Blood 68 12907453
2023 JunB: a paradigm for Jun family in immune response and cancer. Frontiers in cellular and infection microbiology 63 37731821
2017 The AP-1 transcription factor JunB is required for Th17 cell differentiation. Scientific reports 61 29234109
2008 JunB Inhibits ER Stress and Apoptosis in Pancreatic Beta Cells. PloS one 59 18716665
2005 JunB expression is a common feature of CD30+ lymphomas and lymphomatoid papulosis. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 57 15920551
2016 JunB promotes cell invasion, migration and distant metastasis of head and neck squamous cell carcinoma. Journal of experimental & clinical cancer research : CR 56 26754630
1993 Transcriptional regulatory elements downstream of the JunB gene. Proceedings of the National Academy of Sciences of the United States of America 54 8265655
2015 miRNA-149* promotes cell proliferation and suppresses apoptosis by mediating JunB in T-cell acute lymphoblastic leukemia. Leukemia research 53 26725775
1991 Expression of c-jun, jun-B, and c-fos proto-oncogenes in human primary melanocytes and metastatic melanomas. The Journal of investigative dermatology 50 1712822
2018 JUNB, DUSP2, SGK1, SOCS1 and CREBBP are frequently mutated in T-cell/histiocyte-rich large B-cell lymphoma. Haematologica 49 30213827
2011 JunB promotes cell invasion and angiogenesis in VHL-defective renal cell carcinoma. Oncogene 49 22020339
2021 Regulation of T cell differentiation by the AP-1 transcription factor JunB. Immunological medicine 48 33470914
2021 Emerging Role of AP-1 Transcription Factor JunB in Angiogenesis and Vascular Development. International journal of molecular sciences 47 33802099
2010 Junb regulates arterial contraction capacity, cellular contractility, and motility via its target Myl9 in mice. The Journal of clinical investigation 47 20551518
1992 Regulation of the junB gene by v-src. Molecular and cellular biology 47 1630451
2013 JUNB/AP-1 controls IFN-γ during inflammatory liver disease. The Journal of clinical investigation 46 24200694
1991 Expression of the jun-B gene during induction of monocytic differentiation. Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research 46 2007095
2018 LINC00657 played oncogenic roles in esophageal squamous cell carcinoma by targeting miR-615-3p and JunB. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 45 30227324
2014 JunB protects β-cells from lipotoxicity via the XBP1-AKT pathway. Cell death and differentiation 45 24786832
2018 USP38 critically promotes asthmatic pathogenesis by stabilizing JunB protein. The Journal of experimental medicine 44 30224386
2012 GSK3-SCF(FBXW7) targets JunB for degradation in G2 to preserve chromatid cohesion before anaphase. Oncogene 44 22710716
2004 BCL2 and JUNB abnormalities in primary cutaneous lymphomas. The British journal of dermatology 44 15377339
2023 Vascular cell-adhesion molecule 1 (VCAM-1) regulates JunB-mediated IL-8/CXCL1 expression and pathological neovascularization. Communications biology 43 37179352
2021 Persistent JunB activation in fibroblasts disrupts stem cell niche interactions enforcing skin aging. Cell reports 43 34469740
2008 Epidermal JunB represses G-CSF transcription and affects haematopoiesis and bone formation. Nature cell biology 43 18641637
2024 NAT10/ac4C/JunB facilitates TNBC malignant progression and immunosuppression by driving glycolysis addiction. Journal of experimental & clinical cancer research : CR 42 39363363
2014 Loss of JUNB/AP-1 promotes invasive prostate cancer. Cell death and differentiation 42 25526087
2007 Targeting c-Jun and JunB proteins as potential anticancer cell therapy. Oncogene 41 17667939
2008 Function of JunB in transient amplifying cell senescence and progression of human prostate cancer. Clinical cancer research : an official journal of the American Association for Cancer Research 40 18628455
2021 The AP-1 transcription factors c-Jun and JunB are essential for CD8α conventional dendritic cell identity. Cell death and differentiation 38 33758366
1993 Estrogen induces expression of c-jun and jun-B protooncogenes in specific rat uterine cells. Endocrinology 38 8319568
2021 JunB is a key regulator of multiple myeloma bone marrow angiogenesis. Leukemia 37 34007044
2018 JunB defines functional and structural integrity of the epidermo-pilosebaceous unit in the skin. Nature communications 36 30143626
2018 MicroRNA 199a-5p induces apoptosis by targeting JunB. Scientific reports 35 29703907
1999 Expression of c-fos, junB, c-jun, MKP-1 and hsp72 following traumatic neocortical lesions in rats--relation to spreading depression. Neuroscience 34 10197778
1995 NMDA and D1 receptors mediate induction of c-fos and junB genes in striatum following morphine administration: implications for studies of memory. Behavioural brain research 34 7755894
2012 CARMA1 controls Th2 cell-specific cytokine expression through regulating JunB and GATA3 transcription factors. Journal of immunology (Baltimore, Md. : 1950) 32 22371397
2024 MEK inhibition prevents CAR-T cell exhaustion and differentiation via downregulation of c-Fos and JunB. Signal transduction and targeted therapy 31 39438476
2019 JunB plays a crucial role in development of regulatory T cells by promoting IL-2 signaling. Mucosal immunology 31 31285535
2004 Transcriptional regulation of dentin matrix protein 1 by JunB and p300 during osteoblast differentiation. The Journal of biological chemistry 31 15308641
2022 m6A RNA methylation regulates the transcription factors JUN and JUNB in TGF-β-induced epithelial-mesenchymal transition of lung cancer cells. The Journal of biological chemistry 30 36183833
2022 New roles for AP-1/JUNB in cell cycle control and tumorigenic cell invasion via regulation of cyclin E1 and TGF-β2. Genome biology 30 36494864
2018 Abnormally expressed JunB transactivated by IL-6/STAT3 signaling promotes uveal melanoma aggressiveness via epithelial-mesenchymal transition. Bioscience reports 30 29899166
2016 Itch promotes the neddylation of JunB and regulates JunB-dependent transcription. Cellular signalling 30 27245101
2009 Expression and clinical significance of p53, JunB and KAI1/CD82 in human hepatocellular carcinoma. Hepatobiliary & pancreatic diseases international : HBPD INT 30 19666408
2005 MEKK1 regulates the AP-1 dimer repertoire via control of JunB transcription and Fra-2 protein stability. Oncogene 30 15558021
2001 Role of JunB in erythroid differentiation. The Journal of biological chemistry 30 11726656
2013 Role of JunB in adenosine A2B receptor-mediated vascular endothelial growth factor production. Molecular pharmacology 29 24136993
2015 PDK1 induces JunB, EMT, cell migration and invasion in human gallbladder cancer. Oncotarget 28 26318166
2015 Junb controls lymphatic vascular development in zebrafish via miR-182. Scientific reports 26 26458334
2014 The oncogenic JUNB/CD30 axis contributes to cell cycle deregulation in ALK+ anaplastic large cell lymphoma. British journal of haematology 25 25145835
2009 Downregulation of SRF-FOS-JUNB pathway in fumarate hydratase deficiency and in uterine leiomyomas. Oncogene 24 19151755
2023 Circadian control of ConA-induced acute liver injury and inflammatory response via Bmal1 regulation of Junb. JHEP reports : innovation in hepatology 23 37791375
2014 RNA-Seq and ChIP-Seq reveal SQSTM1/p62 as a key mediator of JunB suppression of NF-κB-dependent inflammation. The Journal of investigative dermatology 23 25501661
2011 Ets-1 activates overexpression of JunB and CD30 in Hodgkin's lymphoma and anaplastic large-cell lymphoma. The American journal of pathology 23 22107829
1997 Induction of c-fos and junB mRNA following in vivo brain irradiation. Brain research. Molecular brain research 23 9332719
2022 Integrative epigenomic and transcriptomic analysis reveals the requirement of JUNB for hematopoietic fate induction. Nature communications 22 35668082
2018 RAC2 promotes abnormal proliferation of quiescent cells by enhanced JUNB expression via the MAL-SRF pathway. Cell cycle (Georgetown, Tex.) 22 29895215
2017 JunB regulates angiogenesis and neurovascular parallel alignment in mouse embryonic skin. Journal of cell science 22 28096474
2014 JunB/cyclin-D1 imbalance in placental mesenchymal stromal cells derived from preeclamptic pregnancies with fetal-placental compromise. Placenta 22 24780198
2001 JunB negatively regulates AP-1 activity and cell proliferation of malignant mouse keratinocytes. Journal of cancer research and clinical oncology 22 11862466
1994 c-Fos- and JunB-immunoreactivities in the enteric nervous system of the guinea-pig ileum. Neuroreport 22 7819542
2022 JunB Is Critical for Survival of T Helper Cells. Frontiers in immunology 21 35837408
2021 Circular RNA PUM1 (CircPUM1) attenuates trophoblast cell dysfunction and inflammation in recurrent spontaneous abortion via the MicroRNA-30a-5p (miR-30a-5p)/JUNB axis. Bioengineered 21 34519628
2005 JunB as a downstream mediator of PTHrP actions in cementoblasts. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 21 16418780
2023 TGFβ1-Induced EMT in the MCF10A Mammary Epithelial Cell Line Model Is Executed Independently of SNAIL1 and ZEB1 but Relies on JUNB-Coordinated Transcriptional Regulation. Cancers 20 36672507
2009 c-Jun-NH2 terminal kinase (JNK)-mediates AP-1 activation by thioredoxin: phosphorylation of cJun, JunB, and Fra-1. Molecular and cellular biochemistry 20 19859790
2022 FGF7/FGFR2-JunB signalling counteracts the effect of progesterone in luminal breast cancer. Molecular oncology 19 35726195

Missed literature

Know a paper Affinage missed for JUNB? Flag it for the maintainers and the community.

No submissions yet.