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Human Polyclonal ATF3 Primary Antibody für IF (p), IHC (p) - ABIN669561
Hu, Li, Li: MARVELD1 Inhibits Nonsense-Mediated RNA Decay by Repressing Serine Phosphorylation of UPF1. in PLoS ONE 2013
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Human Polyclonal ATF3 Primary Antibody für ICC, IF - ABIN4282009
Wu, Nguyen, Dziunycz, Chang, Brooks, Lefort, Hofbauer, Dotto: Opposing roles for calcineurin and ATF3 in squamous skin cancer. in Nature 2010
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Human Monoclonal ATF3 Primary Antibody für RNAi, ELISA - ABIN559974
Chen, Huang, Chu, Chen, Chou, Wang, Kulp, Teng, Wang, Chen: Energy restriction-mimetic agents induce apoptosis in prostate cancer cells in part through epigenetic activation of KLF6 tumor suppressor gene expression. in The Journal of biological chemistry 2011
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Human Polyclonal ATF3 Primary Antibody für IHC (p), IHC - ABIN315461
Maciag, Nandurdikar, Hong, Chakrapani, Diwan, Morris, Shami, Shiao, Anderson, Keefer, Saavedra: Activation of the c-Jun N-terminal kinase/activating transcription factor 3 (ATF3) pathway characterizes effective arylated diazeniumdiolate-based nitric oxide-releasing anticancer prodrugs. in Journal of medicinal chemistry 2011
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Human Monoclonal ATF3 Primary Antibody für ELISA, WB - ABIN559976
Hsueh, Kuo, Chen: Transcriptional regulators of the ?Np63: their role in limbal epithelial cell proliferation. in Journal of cellular physiology 2012
Human Polyclonal ATF3 Primary Antibody für FACS, WB - ABIN1536715
Mo, Dai, Kang, Cui, He et al.: Ectopic expression of human MutS homologue 2 on renal carcinoma cells is induced by oxidative stress with interleukin-18 promotion via p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal ... in The Journal of biological chemistry 2012
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.
Study identified ATF3 as a tumor suppressor for inhibiting cell proliferation and metastasis in hepatocellular carcinoma (HCC) through targeting and regulating CYR61. Clinically, ATF3 was down-regulated in HCC tissues, and its expression significantly associated with intrahepatic metastases and overall survival.
under pathological conditions such as those during breast cancer, a sustained and prolonged expression of ATF3 has been observed. In this review, the structure and function of ATF3, its posttranslational modifications (PTM), and its interacting proteins are discussed with a special emphasis on breast cancer metastasis.
Therefore, though ATF3 is activated downstream of the Wnt/beta-catenin pathway, it acts as a negative regulator of the migration and invasion of HCT116 human colon cancer cells exhibiting aberrant Wnt/beta-catenin activity. ATF3 is a candidate biomarker and target for human colorectal cancer treatment and prevention.
Luciferase reporter assay identified a direct interaction of 3' UTRs of ATF3 and Runx2 with miR-590-3p in these cells. Overexpression of miR-590-3p also decreased proliferation and increased apoptosis of breast cancer cells.
ATF3 mediates the inhibitory action of TNF-alpha on osteoblast differentiation and that the TNF-alpha-activated JNK pathway is responsible for the induction of Atf3 expression.
these data indicated that ATF3 might promote intestinal epithelial cell apoptosis in Crohn's disease via up-regulating the stability and transcription activity of p53
electrophilic properties of itaconate and derivatives regulate the IkappaBzeta-ATF3 inflammatory axis; results demonstrate that targeting the DI-IkappaBzeta regulatory axis could be an important new strategy for the treatment of IL-17-IkappaBzeta-mediated autoimmune diseases
High ATF3 expression is associated with breast cancer.
ATF3 and EGR1 are involved in the beginning of inflammatory processes. Whether these two transcription factors act as tumour suppressors or promoters is context dependent and warrants analysis in further studies
ATF3 and PRAP1 play important roles in cisplatin-induced DNA damage repair process.
Data show that amino acid limitation (amino acid response, AAR) activation of activating transcription factor 3 (ATF3) transcription is transient relative to activation by the unfolded protein response (UPR).
In patients with NAFLD and/or T2D, a significant positive correlation was observed between hepatic ATF3 expression and surrogate markers of T2D, mitochondrial dysfunction, and macrophage infiltration.
our results suggest that ATF3 promotes the invasion and proliferation of CRC cells, at least in part, via the regulation of CEACAM1-mediated EMT.
ATF3 is involved in promoting particulate matter-induced pulmonary inflammation.
Negative pressure wound therapy exerts an anti-inflammatory effect, possibly through the suppression of proinflammatory enzymes and cytokines resulting from Ik B-alpha inhibition and ATF-3 activation, which may prevent the activation of the NF-kappaB pathway in human diabetic foot wounds.
ATF3 plays a significant role in regulating human endometrial receptivity and embryo attachment in vitro via up-regulation of leukemia inhibitory factor.
Upregulation of ATF3 in lung cancer promotes cell proliferation, migration, and invasion, and may represent a novel therapeutic target for lung cancer
ATF3 is a negative regulator of inflammation in human fetal membranes; in primary amnion cells, ATF3 expression is induced by IL-1beta and fsl-1, and ATF3 silencing further exacerbates the inflammatory response when stimulated with these factors. Subsequently, ATF3 expression is decreased in fetal membranes after term labour and with preterm chorioamnionitis, conditions closely associated with inflammation and infection.
Altering TR4-ATF3 signaling increases the efficacy of cisplatin to suppress hepatocellular carcinoma growth/progression.
ATF3 may be a potential early diagnostic biomarker for silicosis and ATF3 acts as a repressor in inflammatory responses induced by silica
Study reports that Atf3-deficient mice developed spontaneous tumors, and died significantly earlier than wild-type mice.
ATF3 in the host cells regulated a chemotherapeutic agent to immune modulation and cancer metastasis.
this study reveals a novel mechanism of naringenin through AMPK-ATF3-dependent negative regulation of the LPS/TLR4 signalling pathway, which thereby confers protection against murine endotoxaemia.
Conditional deletion of ATF3 in osteoclast precursors protects RANKL-induced osteoclast activation and bone loss.
Data (including data from studies using mutant, transgenic, and knockout mice) suggest that gene targets of leptin/leptin-receptor (Lep/Lepr) signaling in hypothalamic neurons regulate energy metabolism; Lep/Lepr signaling appears to up-regulate expression of Atf3 (activating transcription factor-3) in hypothalamic neurons.
ATF3 promotes macrophage migration and reverses M1polarized macrophages to the M2 phenotype by upregulation of TNC via the Wnt/betacatenin signaling pathway.
Microglia make contact through unknown neuronal signals regulated by ATF3 in hypoglossal nucleus.
ATF3 inhibit the expression and release of TNF-alpha, IL-1beta, IL-6, and IL-18 induced by Mycoplasma pneumonia in vitro and in vivo, which is associated with its negative regulation of Egr-1/Fyn signaling pathway.
The different anti-inflammatory mechanisms of the ApoA-I cysteine mutants might be associated with the regulation of ATF3 level.
ATF3 is a new co-factor of c-Fos and NFATc1 to activate osteoclast differentiation and activity.
This study shows, for the first time, that alpha-lactalbumin isolated in a rare 28kDa dimeric form induces cell death, while 14kDa monomeric alpha-lactalbumin is inactive.
Results show a pro-regenerative ATF3 function during PNS nerve regeneration involving transcriptional activation of a neuropeptide-encoding regeneration-associated gene cluster.
Results reveal a critical role for ATF3 as a key regulator of the acinar cell transcriptional response during injury and may provide a link between chronic pancreatitis and PDAC.
The lung injury score and mortality were higher in ATF3 knock-out mice treated with Pseudomonas aeruginosa. Moreover, ATF3 was demonstrated to bind to lipopolysaccharide binding protein. These findings suggest ATF3 protects mice against acute lung injury induced by Pseudomonas aeruginosa partly due to the binding to lipopolysaccharide binding protein.
ATF3-KO mice escape from PE-dependent maladaptive cardiac remodeling by suppressing the IFNgamma-CXCL10-CXCR3 axis at multiple levels.
ATF3 has a protective role in dampening the high fat-induced cardiac remodeling processes.
ATF3 protects against LPS-induced acute lung injury by inhibiting TL1A expression.
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 pathway in endothelial cells
Data indicate increasing expression for CREB, ATF1, 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