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JunB is a critical regulator of IRF4-dependent regulatory T cell effector programs, highlighting important functions for AP-1 in regulatory T cell-mediated immune homeostasis.
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JunB has an essential role in IL-23-dependent pathogenicity of Th17 cells
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Data show that JunB is a nonredundant regulator of transcriptional programs that support Th17 cell identity and restrain alternative Th1 and Treg cell fates.
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the present data demonstrates for the first time that JunB plays an important role in the formation of embryonic vascular networks.
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BATF/JUN-B and BATF/C-JUN complexes play important roles in OA cartilage destruction through regulating anabolic and catabolic gene expression in chondrocytes.
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JUNB is a significant modulator of both classical and alternative macrophage activation.
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Study shows that myeloid deletion of JUNB dampens immune polarization and reshapes disease outcomes during infection with both P. berghei and N. brasiliensis by limiting type 1 and type 2 responses, respectively. Thus, JUNB is an important regulator of myeloid responses to both type 1 and type 2 infections in vivo.
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Loss of JunB expression led to increased proliferation and decreased senescence, likely owing to decreased p16(Ink4a) and p21(CIP1) in epithelial cells.
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JunB and c-Jun expression in post-mitotic oligodendrocytes is mostly dispensable for the maintainance of white matter tracts throughout adult life, even under demyelinating conditions.
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JunB controls epidermal growth, barrier formation, and proinflammatory responses through direct and indirect mechanisms, pinpointing SQSTM1 as a key mediator of JunB suppression of NF-kappaB-dependent inflammation
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our results suggest a functional cooperation between NFAT1 and JunB in mediating IL-31 gene expression in CD4(+) T cells
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an important role of the A2B receptor-dependent upregulation of JunB in VEGF production and possibly other AP-1-regulated events.
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In experimental hepatitis, the absence of JUNB in immune cells decreased IFN-gamma expression and secretion from NK & NKT cells, leading to reduced STAT1 pathway activation.
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The results show that the junb gene is organized in a nuclear chromatin loop bringing into close spatial proximity the upstream promoter region and the downstream enhancer and that this configuration permits immediate RNA Pol II release on the junb body on binding of LPS-activated NF-kappaB to the enhancer.
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Data indicate that the C-terminal JunB caspase cleavage product functions as a potent inhibitor of AP-1-dependent transcription.
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Data suggest that JunB contributes to Id2 repression and provides important input in setting the transcriptional program of the EMT and profibrotic responses to TGF-beta.
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Wwp1 induces JunB ubiquitination and degradation.
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investigation of role of JunB: growth retardation of JunB-deficient mice correlates with strongly reduced fat mass (and is also associated with high lethality); in white adipose tissue, TNFalpha is up-regulated and perilipin is down-regulated
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T cell receptor signaling together with TGF-beta/IL-2 stimulation cooperatively enhance Foxp3 gene expression by maintaining accessible chromatin structure and by actively recruiting key transcription factors JunB and c-Rel.
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JunB is important not only in dividing populations but also in adult muscle, where it is required for the maintenance of muscle size and can induce rapid hypertrophy and block atrophy.
