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Hic-5 regulates GR binding site selection by a novel mechanism, exploiting gene-specific requirements for chromatin remodeling enzymes to selectively influence DNA occupancy and gene regulation by a transcription factor.
As aging increased, more ARA55 were expressed in PZ stromal cells, leading to more sensitive androgen/androgen receptor (AR (zeige AR Proteine)) signal pathway, then constituting a more feasible environment to cancer cells.
Hic-5 appears to enhance complex formation between MT1-MMP (zeige MMP14 Proteine) and FAK (zeige PTK2 Proteine) in activated endothelial cells, which likely coordinates matrix proteolysis and cell motility.
Hic-5 plays a central role in the positive feedback ROS (zeige ROS1 Proteine)-JNK (zeige MAPK8 Proteine) signaling cascade that regulates hepatocellular carcinoma progression.
Hic-5 influences the genomic occupancy of multiple steroid receptors and thereby blocks some aspects of hormonal regulation.
Endothelial Hic-5 plays an important role in the formation of microvilli-like structures and in the interaction between ECs and monocytes, leading to monocyte recruitment and subsequent development of atherosclerosis.
Studies in vitro and in vivo using TGF-beta1 (zeige TGFB1 Proteine) and TGFB1I1 shRNA demonstrated that TGFB1I1 is required for TGF-beta (zeige TGFB1 Proteine) stimulated EMT (zeige ITK Proteine) that contributes to malignant progression of astrocytomas.
Hic-5 siRNA also suppressed TGF-beta2 (zeige TGFB2 Proteine)-induced fibrogenic activity and dexamethasone-induced myocilin (zeige MYOC Proteine) expression in HTM cells.
Hic5 coordinates AR signaling with adhesion and extracellular matrix contacts to regulate cell behavior in the tumor microenvironment.
Hic-5 suppresses senescence and profibrotic activities of myofibroblasts by down-regulating Nox4 (zeige NOX4 Proteine) expression.
paxillin (zeige PXN Proteine) and Hic-5 have both redundant and distinctive functions in invadosome formation.
Hic-5 deficiency attenuates the activation of hepatic stellate cells and liver fibrosis though reducing the TGF-beta (zeige TGFB1 Proteine)/Smad2 (zeige SMAD2 Proteine) signaling by upregulation of Smad7 (zeige SMAD7 Proteine)
Hic-5 regulates mesangial cell proliferation in proliferative glomerulonephritis in mice.
Hic-5 is a transcription coregulator that acts before and/or after glucocorticoid receptor (zeige NR3C1 Proteine) genome occupancy in a gene-selective manner.
Hic-5 is expressed in B16-F1 murine melanoma cells.
identified Hic-5 as a novel and specific regulatory factor for thrombin (zeige F2 Proteine)-induced alphaIIbbeta3 activation and subsequent platelet aggregation in mice.
the HIC-5- and KLF4 (zeige KLF4 Proteine)-dependent mechanism transactivates p21(Cip1 (zeige CDKN1A Proteine)) in response to anchorage loss
These data identify discrete roles for paxillin (zeige PXN Proteine) and Hic-5 in Rac1 and RhoA (zeige RHOA Proteine)-dependent cell adhesion formation and maturation; processes essential for productive cell migration.
Transforming growth factor-beta1-induced transcript 1 protein, a novel marker for smooth muscle contractile phenotype, is regulated by serum response factor/myocardin protein.
This gene encodes a coactivator of the androgen receptor, a transcription factor which is activated by androgen and has a key role in male sexual differentiation. The encoded protein is thought to regulate androgen receptor activity and may have a role to play in the treatment of prostate cancer. Multiple transcript variants encoding different isoforms have been found for this gene.
transforming growth factor beta 1 induced transcript 1
, androgen receptor coactivator ARA55
, transforming growth factor beta-1-induced transcript 1 protein-like
, androgen receptor coactivator 55 kDa protein
, androgen receptor-associated protein of 55 kDa
, hydrogen peroxide-inducible clone 5 protein
, transforming growth factor beta-1-induced transcript 1 protein
, TGF beta-stimulated clone 5
, androgen receptor activator of 55 kDa