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Transcription factor involved in regulating gene activity following the primary growth factor response. De plus, nous expédions JUNB Anticorps (273) et JUNB Protéines (10) et beaucoup plus de produits pour cette protéine.
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It has been shown that the AP-1 (Montrer FOSB Kits ELISA) family member JunB and retinoic acid receptor alpha (RARa (Montrer RARA Kits ELISA)) mediate catalase (Montrer CAT Kits ELISA) 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 Kits ELISA)-B and BATF/C-JUN (Montrer JUN Kits ELISA) complexes play important roles in OA cartilage destruction through regulating anabolic and catabolic gene expression in chondrocytes.
VEGF (Montrer VEGFA Kits ELISA)-induced endothelial migration is mediated primarily by induction of JunB whereas the promotion of endothelial proliferation by VEGF (Montrer VEGFA Kits ELISA) is mediated by JunB-independent AP-1 (Montrer FOSB Kits ELISA) 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 Kits ELISA), HNF4A (Montrer HNF4A Kits ELISA) and JUNB are synergistic master regulators of epithelial-to-mesenchymal transition in cancer.
CARMA1- and MyD88 (Montrer MYD88 Kits ELISA)-dependent activation of Jun (Montrer JUN Kits ELISA)/ATF-type AP-1 (Montrer FOSB Kits ELISA) complexes is a hallmark of ABC (Montrer ABCB6 Kits ELISA) diffuse large B-cell lymphomas.
PDK1 (Montrer PDK1 Kits ELISA) 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 (Montrer SHH Kits ELISA) signaling pathways.
The present data indicate that bovine dialyzable leukocyte extract can block the AP-1 (Montrer JUN Kits ELISA) DNA-binding activity and expression of several transcriptions factors in breast cancer cells.
JunB has an essential role in IL-23 (Montrer IL23A Kits ELISA)-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 Kits ELISA) 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 Kits ELISA)) in epithelial cells.
JunB and c-Jun (Montrer JUN Kits ELISA) 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 Kits ELISA) as a key mediator of JunB suppression of NF-kappaB (Montrer NFKB1 Kits ELISA)-dependent inflammation
our results suggest a functional cooperation between NFAT1 (Montrer NFAT1 Kits ELISA) and JunB in mediating IL-31 (Montrer IL31 Kits ELISA) gene expression in CD4 (Montrer CD4 Kits ELISA)(+) 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