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Transcription factor involved in regulating gene activity following the primary growth factor response. De plus, nous expédions JUNB Kits (12) et JUNB Protéines (10) et beaucoup plus de produits pour cette protéine.
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Human Polyclonal JUNB Primary Antibody pour 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. dans The Journal of biological chemistry 2004
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Human Polyclonal JUNB Primary Antibody pour IHC, WB - ABIN361926
Beausoleil, Jedrychowski, Schwartz, Elias, Villén, Li, Cohn, Cantley, Gygi: Large-scale characterization of HeLa cell nuclear phosphoproteins. dans Proceedings of the National Academy of Sciences of the United States of America 2004
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Cow (Bovine) Polyclonal JUNB Primary Antibody pour 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. dans The Journal of molecular diagnostics : JMD 2004
Human Polyclonal JUNB Primary Antibody pour 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. dans 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 (Montrer FOSB Anticorps) family member JunB and retinoic acid receptor alpha (RARa (Montrer RARA Anticorps)) mediate catalase (Montrer CAT Anticorps) 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 (Montrer JUN Anticorps)-B and BATF/C-JUN (Montrer JUN Anticorps) complexes play important roles in OA cartilage destruction through regulating anabolic and catabolic gene expression in chondrocytes.
VEGF (Montrer VEGFA Anticorps)-induced endothelial migration is mediated primarily by induction of JunB whereas the promotion of endothelial proliferation by VEGF (Montrer VEGFA Anticorps) is mediated by JunB-independent AP-1 (Montrer FOSB Anticorps) 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 (Montrer ETS2 Anticorps), HNF4A (Montrer HNF4A Anticorps) and JUNB are synergistic master regulators of epithelial-to-mesenchymal transition in cancer.
CARMA1 (Montrer CARD11 Anticorps)- and MyD88 (Montrer MYD88 Anticorps)-dependent activation of Jun (Montrer JUN Anticorps)/ATF-type AP-1 (Montrer FOSB Anticorps) complexes is a hallmark of ABC (Montrer ABCB6 Anticorps) diffuse large B-cell lymphomas.
PDK1 (Montrer PDK1 Anticorps) 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 (Montrer CBFB Anticorps) signaling for maintaining sarcomere architecture and function.
JunB is a regulator of tail organization possibly through integration of several morphogen (Montrer SHH Anticorps) signaling pathways.
The present data indicate that bovine dialyzable leukocyte extract can block the AP-1 (Montrer JUN Anticorps) DNA-binding activity and expression of several transcriptions factors in breast cancer cells.
JunB has an essential role in IL-23 (Montrer IL23A Anticorps)-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 (Montrer HAND1 Anticorps) 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 (Montrer CDKN1A Anticorps)) in epithelial cells.
JunB and c-Jun (Montrer JUN Anticorps) 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 (Montrer SQSTM1 Anticorps) as a key mediator of JunB suppression of NF-kappaB (Montrer NFKB1 Anticorps)-dependent inflammation
our results suggest a functional cooperation between NFAT1 (Montrer NFAT1 Anticorps) and JunB in mediating IL-31 (Montrer IL31 Anticorps) gene expression in CD4 (Montrer CD4 Anticorps)(+) 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