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ATF3 encodes a member of the mammalian activation transcription factor/cAMP responsive element-binding (CREB) protein family of transcription factors. Additionally we are shipping ATF3 Antibodies (122) and ATF3 Proteins (9) and many more products for this protein.
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Data show that Atf3 was detected in retinal ganglion cell axons in both the nerve fiber layer and the optic nerve on the injured side.
Data show that ATF3 may be an important mediator of optic nerve regeneration-promoting gene expression in fish, a role which merits further investigation.
ATF3 overexpression increased PFF-A-mediated cleaved PARP (show COL11A2 ELISA Kits).
Ang II (show AGT ELISA Kits)-induced upregulation of ATF3 and SUMO1 (show SUMO1 ELISA Kits) in vitro and in vivo was blocked by Ang II (show AGT ELISA Kits) type I receptor antagonist olmesartan. Moreover, Ang II (show AGT ELISA Kits) induced ATF3 SUMOylation at lysine 42, which is SUMO1 (show SUMO1 ELISA Kits) dependent.
As a result, ATF3 rather protected the p53 (show TP53 ELISA Kits) wild-type cells from UV-induced apoptosis. Our results thus indicate that ATF3 regulates cell fates upon UV irradiation in a p53 (show TP53 ELISA Kits)-dependent manner.
CARMA1 (show CARD11 ELISA Kits)- 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.
Activating transcription factor 3 represses inflammatory responses by binding to the p65 (show GORASP1 ELISA Kits) subunit of NF-kappaB (show NFKB1 ELISA Kits)
TGRL lipolysis products induce stress protein ATF3 via the TGF-beta (show TGFB1 ELISA Kits) receptor pathway, resulting in induction of apoptosis in aortic endothelial cells
ATF3 regulates canonical TGFbeta and Smad signaling and fibroblast (show TGFB1 ELISA Kits)activation in systemic sclerosis.
ATF3 overexpression leads to an increase of collective cell invasion phenotype in Colorectal Cancer.
Data suggest that after the expression of activating transcription factor 3 (ATF3) and microRNA miR (show MLXIP ELISA Kits)-30c-2-3p elicited by lysophosphatidic acid, miR (show MLXIP ELISA Kits)-30c-2-3p negatively regulates the expression of ATF3 through post-transcriptional silencing.
Taken together, these results suggest that ATF3 promotes the progression of human gliomas
Study shows that ATF3 regulates multiple targets in cardiomyocytes and plays critical roles in hypertrophy, apoptosis and autophagy of cardiomyocyte.
ATF3 was up-regulated in brain after reperfusion following transient middle cerebral artery occlusion.
Activating transcription factor 3 represses inflammatory responses by binding to the p65 (show NFkBP65 ELISA Kits) subunit of NF-kappaB (show NFKB1 ELISA Kits)
Knockout of the ATF3 gene reduced the stimulatory effect of TGFbeta (show TGFB1 ELISA Kits) on fibroblasts by interfering with canonical Smad (show SMAD1 ELISA Kits) signalling and protected the mice from experimental fibrosis in two different models.
ATF3 is a key regulator in cardiac hypertrophy through a cross-talk between cardiomyocytes and macrophages.
Data show that activating transcription factor 3 (ATF3) acted as a transcriptional repressor and regulated interferon-beta (IFN-beta (show IFNB1 ELISA Kits)) via direct binding to a regulatory site distal to the Ifnb1 (show IFNB1 ELISA Kits) promoter.
ATF3 binds to carboxyl-terminal modulator protein (show THEM4 ELISA Kits) and suppresses its transcription following brain ischemia.
Involvement of ATF3 in the negative regulation of iNOS (show NOS2 ELISA Kits) expression and NO production in activated macrophages
ATF3 suppresses fibrosis early but not late during infarct-induced heart failure. Although ATF3 deficiency was associated with more fibrosis, this did not occur at the expense of survival, which was higher in the ATF3-null mice.
these results demonstrate that during acute inflammation Atf3 negatively regulates Ptgs2 (show PTGS2 ELISA Kits)
ATF3 appears to affect gonadotropin-stimulated progesterone secretion at a step or steps downstream of PKA signaling and before cholesterol conversion to progesterone.
ATF3 induction by acute hypoxia is mediated by nitric oxide and the JNK (show MAPK8 ELISA Kits) pathway in endothelial cells
Data indicate increasing expression for CREB (show CREB1 ELISA Kits), ATF1 (show AFT1 ELISA Kits), and ATF3 during gastrulation.
This gene encodes a member of the mammalian activation transcription factor/cAMP responsive element-binding (CREB) protein family of transcription factors. This gene is induced by a variety of signals, including many of those encountered by cancer cells, and is involved in the complex process of cellular stress response. Multiple transcript variants encoding different isoforms have been found for this gene. It is possible that alternative splicing of this gene may be physiologically important in the regulation of target genes.
cyclic AMP-dependent transcription factor ATF-3
, activating transcription factor 3
, cAMP-dependent transcription factor ATF-3
, transcription factor LRG-21
, liver regeneration factor 1