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Transcription factor involved in regulating gene activity following the primary growth factor response.
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It has been shown that the AP-1 (show FOSB ELISA Kits) family member JunB and retinoic acid receptor alpha (RARa (show RARA ELISA Kits)) mediate catalase (show CAT ELISA Kits) transcriptional activation and repression, respectively, by controlling chromatin remodeling through a histone deacetylases-dependent mechanism.
JunB neddylation mediated by Itch promotes its ubiquitination-dependent degradation.
a specific role for AP-1/JunB in multiple myeloma cell proliferation, survival and drug resistance.
BATF/JUN (show JUN ELISA Kits)-B and BATF/C-JUN (show JUN ELISA Kits) complexes play important roles in OA cartilage destruction through regulating anabolic and catabolic gene expression in chondrocytes.
VEGF (show VEGFA ELISA Kits)-induced endothelial migration is mediated primarily by induction of JunB whereas the promotion of endothelial proliferation by VEGF (show VEGFA ELISA Kits) is mediated by JunB-independent AP-1 (show FOSB ELISA Kits) family members.
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- 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.
Data demonstrate for the first time an essential role of JunB-CBFbeta signaling for maintaining sarcomere architecture and function.
JunB is a regulator of tail organization possibly through integration of several morphogen (show SHH ELISA Kits) signaling pathways.
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 show that JunB is a nonredundant regulator of transcriptional programs that support Th17 cell identity and restrain alternative Th1 (show HAND1 ELISA Kits) and Treg cell fates.
the present data demonstrates for the first time that JunB plays an important role in the formation of embryonic vascular networks.
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.
Transcription factor involved in regulating gene activity following the primary growth factor response. Binds to the DNA sequence 5'-TGATCA-3'.
activator protein 1
, transcription factor jun-B
, Jun-B oncogene
, jun B proto-oncogene
, jun-B proto-oncogene