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Transcription factor involved in regulating gene activity following the primary growth factor response. Additionally we are shipping JUNB Antibodies (246) and JUNB Proteins (8) and many more products for this protein.
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Results suggested that JunB could play an important role in promoting cell invasion, migration and distant metastasis in head and neck squamous cell carcinoma via pathways other than epithelial-to-mesenchymal transition.
Highly recurrent mutation of JUNB is associated with nodular lymphocyte predominant Hodgkin lymphoma.
ETS2 (show ETS2 ELISA Kits), HNF4A (show HNF4A ELISA Kits) and JUNB are synergistic master regulators of epithelial-to-mesenchymal transition in cancer.
CARMA1 (show CARD11 ELISA Kits)- and MyD88 (show MYD88 ELISA Kits)-dependent activation of Jun (show JUN ELISA Kits)/ATF-type AP-1 (show FOSB ELISA Kits) complexes is a hallmark of ABC (show ABCB6 ELISA Kits) diffuse large B-cell lymphomas.
PDK1 (show PDK1 ELISA Kits) functions as a tumor promoter in human gallbladder cancer by upregulating JunB, promoting epithelial mesenchymal transformation, and cell migration.
Our findings demonstrate that miRNA-149* may serve as an oncogenic regulator in T-cell acute lymphoblastic leukemia by negatively regulating JunB
The MAPK (show MAPK1 ELISA Kits) pathway plays a primary role in the control of JUNB gene expression.
JunB is likely to be a key target of c-Abl (show ABL1 ELISA Kits) in expression of p21 (show CDKN1A ELISA Kits) in Adriamycin-induced DDR (show DDR1 ELISA Kits).
Caveolin 2 (show CAV2 ELISA Kits) disengages repressed Egr-1 (show EGR1 ELISA Kits) and JunB promoters from lamin A/C (show LMNA ELISA Kits) through disassembly of H3K9me3 in the inner nuclear membrane.
JunB expression was significantly increased while cyclin-D1 (show CCND1 ELISA Kits) expression was significantly down-regulated in pre-eclampsia relative to control placental mesenchymal stromal cells.
The present data indicate that bovine dialyzable leukocyte extract can block the AP-1 (show JUN ELISA Kits) DNA-binding activity and expression of several transcriptions factors in breast cancer cells.
Data demonstrate for the first time an essential role of JunB-CBFbeta (show CBFB ELISA Kits) signaling for maintaining sarcomere architecture and function.
JUNB is a significant modulator of both classical and alternative macrophage activation.
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.
Loss of JunB expression led to increased proliferation and decreased senescence, likely owing to decreased p16(Ink4a) and p21(CIP1 (show CDKN1A ELISA Kits)) in epithelial cells.
JunB and c-Jun (show JUN ELISA Kits) expression in post-mitotic oligodendrocytes is mostly dispensable for the maintainance of white matter tracts throughout adult life, even under demyelinating conditions.
JunB controls epidermal growth, barrier formation, and proinflammatory responses through direct and indirect mechanisms, pinpointing SQSTM1 (show SQSTM1 ELISA Kits) as a key mediator of JunB suppression of NF-kappaB (show NFKB1 ELISA Kits)-dependent inflammation
our results suggest a functional cooperation between NFAT1 (show NFAT1 ELISA Kits) and JunB in mediating IL-31 (show IL31 ELISA Kits) gene expression in CD4 (show CD4 ELISA Kits)(+) T cells
an important role of the A2B (show ADORA2B ELISA Kits) receptor-dependent upregulation of JunB in VEGF (show VEGFA ELISA Kits) production and possibly other AP-1 (show JUN ELISA Kits)-regulated events.
In experimental hepatitis, the absence of JUNB in immune cells decreased IFN-gamma (show IFNG ELISA Kits) expression and secretion from NK & NKT (show CTSL1 ELISA Kits) cells, leading to reduced STAT1 (show STAT1 ELISA Kits) pathway activation.
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 (show POLR2F ELISA Kits) release on the junb body on binding of LPS (show TLR4 ELISA Kits)-activated NF-kappaB (show NFKB1 ELISA Kits) to the enhancer.
Data indicate that the C-terminal JunB caspase (show CASP3 ELISA Kits) cleavage product functions as a potent inhibitor of AP-1 (show JUN ELISA Kits)-dependent transcription.
Transcription factor involved in regulating gene activity following the primary growth factor response. Binds to the DNA sequence 5'-TGATCA-3'.
jun B proto-oncogene
, jun-B proto-oncogene
, activator protein 1
, transcription factor jun-B
, Jun-B oncogene