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Transcription factor involved in regulating gene activity following the primary growth factor response. Additionally we are shipping JUNB Kits (12) and JUNB Proteins (10) and many more products for this protein.
Showing 10 out of 273 products:
Human Polyclonal JUNB Primary Antibody for IF, IHC - ABIN361924
Narayanan, Srinivas, Peterson, Ramachandran, Hao, Thimmapaya, Scherer, George: Transcriptional regulation of dentin matrix protein 1 by JunB and p300 during osteoblast differentiation. in The Journal of biological chemistry 2004
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Human Polyclonal JUNB Primary Antibody for IHC, WB - ABIN361926
Beausoleil, Jedrychowski, Schwartz, Elias, Villén, Li, Cohn, Cantley, Gygi: Large-scale characterization of HeLa cell nuclear phosphoproteins. in Proceedings of the National Academy of Sciences of the United States of America 2004
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Cow (Bovine) Polyclonal JUNB Primary Antibody for IHC, WB - ABIN2780413
Trøen, Nygaard, Jenssen, Ikonomou, Tierens, Matutes, Gruszka-Westwood, Catovsky, Myklebost, Lauritzsen, Hovig, Delabie: Constitutive expression of the AP-1 transcription factors c-jun, junD, junB, and c-fos and the marginal zone B-cell transcription factor Notch2 in splenic marginal zone lymphoma. in The Journal of molecular diagnostics : JMD 2004
Human Polyclonal JUNB Primary Antibody for IF, IHC (p) - ABIN197138
Bockmeyer, Kern, Forstmeier, Lovric, Modde, Agustian, Steffens, Birschmann, Traeder, Dämmrich, Schwarz, Kreipe, Bröcker, Becker: Arteriolar vascular smooth muscle cell differentiation in benign nephrosclerosis. in Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association 2012
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It has been shown that the AP-1 (show FOSB Antibodies) family member JunB and retinoic acid receptor alpha (RARa (show RARA Antibodies)) mediate catalase (show CAT Antibodies) 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 Antibodies)-B and BATF/C-JUN (show JUN Antibodies) complexes play important roles in OA cartilage destruction through regulating anabolic and catabolic gene expression in chondrocytes.
VEGF (show VEGFA Antibodies)-induced endothelial migration is mediated primarily by induction of JunB whereas the promotion of endothelial proliferation by VEGF (show VEGFA Antibodies) is mediated by JunB-independent AP-1 (show FOSB Antibodies) 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 Antibodies), HNF4A (show HNF4A Antibodies) and JUNB are synergistic master regulators of epithelial-to-mesenchymal transition in cancer.
CARMA1 (show CARD11 Antibodies)- and MyD88 (show MYD88 Antibodies)-dependent activation of Jun (show JUN Antibodies)/ATF-type AP-1 (show FOSB Antibodies) complexes is a hallmark of ABC (show ABCB6 Antibodies) diffuse large B-cell lymphomas.
PDK1 (show PDK1 Antibodies) 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 (show CBFB Antibodies) signaling for maintaining sarcomere architecture and function.
JunB is a regulator of tail organization possibly through integration of several morphogen (show SHH Antibodies) signaling pathways.
The present data indicate that bovine dialyzable leukocyte extract can block the AP-1 (show JUN Antibodies) DNA-binding activity and expression of several transcriptions factors in breast cancer cells.
JunB has an essential role in IL-23 (show IL23A Antibodies)-dependent pathogenicity of Th17 cells
Data show that JunB is a nonredundant regulator of transcriptional programs that support Th17 cell identity and restrain alternative Th1 (show HAND1 Antibodies) 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 Antibodies)) in epithelial cells.
JunB and c-Jun (show JUN Antibodies) 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 Antibodies) as a key mediator of JunB suppression of NF-kappaB (show NFKB1 Antibodies)-dependent inflammation
our results suggest a functional cooperation between NFAT1 (show NFAT1 Antibodies) and JunB in mediating IL-31 (show IL31 Antibodies) gene expression in CD4 (show CD4 Antibodies)(+) T cells
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
, JunB proto-oncogene, AP-1 transcription factor subunit b
, jun B proto-oncogene b
, jun B proto-oncogene, like