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Activating transcription factor 3

ATF3, Activating Transcription Factor 3
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. [provided by RefSeq, Apr 2011] (from NCBI)
Top mentioned proteins: GDNF, AP-1, CAN, V1a, HAD
Papers using ATF3 antibodies
Selective targeting of radiation-resistant tumor-initiating cells.
Oshima Robert, In PLoS ONE, 2009
... The derivation of the BK5.ATF3 transgenic mice has been described ...
GDNF and BDNF alter the expression of neuronal NOS, c-Jun, and p75 and prevent motoneuron death following spinal root avulsion in adult rats
Ochsmann Thomas et al., In Frontiers in Neurology, 2002
... buffer for 10 min and incubated overnight in a humid chamber at 4°C with either rabbit polyclonal anti-ATF3 sc-188, 1:100 (Santa Cruz Biotechnology, Inc ...
Papers on ATF3
Upregulation of CCL2 via ATF3/c-Jun interaction mediated the Bortezomib-induced peripheral neuropathy.
Xin et al., Guangzhou, China. In Brain Behav Immun, 07 Dec 2015
In addition, the present results showed that an upregulated expression of ATF3 was co-expressed with c-Jun in the DRG neurons, and the enhanced interaction between c-Jun and ATF3 was observed in DRG in the rats treated with BTZ.
Activating transcription factor 3 ‑ an endogenous inhibitor of myocardial ischemia-reperfusion injury (Review).
Yang et al., Yichang, China. In Mol Med Report, 06 Dec 2015
Studies have demonstrated that activating transcription factor (ATF)/cyclic adenosine monophosphate response element binding family member ATF3 had a negative regulatory role in IRI, particularly in the kidney, cerebrum and liver.
Loss of ATF3 promotes hormone-induced prostate carcinogenesis and the emergence of CK5(+)CK8(+) epithelial cells.
Yan et al., Augusta, United States. In Oncogene, 02 Dec 2015
Here, we report that activating transcription factor 3 (ATF3)-a broad stress sensor-suppressed hormone-induced prostate carcinogenesis in mice.
Further insight into molecular mechanism underlying thoracic spinal cord injury using bioinformatics methods.
Cao et al., Jinan, China. In Mol Med Report, 14 Nov 2015
Furthermore, ATF3, JUN and EGR1 were identified as TFs associated with SCI.
Toll-like receptors: Activation, signalling and transcriptional modulation.
De Nardo, Australia. In Cytokine, Aug 2015
Finally, I will discuss the importance of mechanisms that regulate TLRs with a focus on the role of activating transcription factor 3 (ATF3) in modulating transcriptional responses downstream of TLRs.
Iterative sub-network component analysis enables reconstruction of large scale genetic networks.
Bar et al., Trondheim, Norway. In Bmc Bioinformatics, Dec 2014
Importantly, FOXA1, ATF2, ATF3 and many other known key regulators in breast cancer could not be incorporated by any NCA algorithm because of the necessary conditions.
Increased gene copy number of VAMP7 disrupts human male urogenital development through altered estrogen action.
Lamb et al., Houston, United States. In Nat Med, Jul 2014
Elevated levels of VAMP7 markedly intensified ESR1-potentiated transcriptional activity by increasing ESR1 protein cellular content upon ligand stimulation and upregulated the expression of estrogen-responsive genes including ATF3, CYR61 and CTGF, all of which have been implicated in human hypospadias.
Nonsteroidal anti-inflammatory drug activated gene-1 (NAG-1) modulators from natural products as anti-cancer agents.
Khan et al., United States. In Life Sci, May 2014
Several transcription factors including EGR-1, p53, ATF-3, Sp1 and PPARγ were involved in natural products-induced NAG-1 transcriptional signaling pathway.
High-density lipoproteins put out the fire.
Fisher et al., New York City, United States. In Cell Metab, Mar 2014
(2013), now report that high-density lipoproteins (HDL) can reprogram macrophages to be less inflammatory through an ATF3-dependent pathway, providing another mechanistic basis for the atheroprotective properties of HDL.
High-density lipoprotein mediates anti-inflammatory reprogramming of macrophages via the transcriptional regulator ATF3.
Latz et al., Bonn, Germany. In Nat Immunol, Feb 2014
Here we identify the transcriptional regulator ATF3, as an HDL-inducible target gene in macrophages that downregulates the expression of Toll-like receptor (TLR)-induced proinflammatory cytokines.
Regulatory SNPs and transcriptional factor binding sites in ADRBK1, AKT3, ATF3, DIO2, TBXA2R and VEGFA.
Buroker, Seattle, United States. In Transcription, 2013
Abstract Regulatory single nucleotide polymorphisms (rSNPs) which change the transcriptional factor binding sites (TFBS) for transcriptional factors (TFs) to bind DNA were reviewed for the ADRBK1 (GRK2), AKT3, ATF3, DIO2, TBXA2R and VEGFA genes.
A review of adaptive mechanisms in cell responses towards oxidative stress caused by dental resin monomers.
Schweikl et al., Regensburg, Germany. In Biomaterials, 2013
We will also consider the influence of monomer-induced oxidative stress on central signal transduction pathways including mitogen-activated protein kinases (MAPK) ERK1/2, p38, and JNK as well as the stress-activated transcription factors downstream Elk-1, ATF-2, ATF-3, and cJun.
In vivo RNAi screen for BMI1 targets identifies TGF-β/BMP-ER stress pathways as key regulators of neural- and malignant glioma-stem cell homeostasis.
van Lohuizen et al., Amsterdam, Netherlands. In Cancer Cell, 2013
We discovered that Bmi1 is important in the cellular response to the transforming growth factor-β/bone morphogenetic protein (TGF-β/BMP) and endoplasmic reticulum (ER) stress pathways, in part converging on the Atf3 transcriptional repressor.
The transcription factor Jdp2 controls bone homeostasis and antibacterial immunity by regulating osteoclast and neutrophil differentiation.
Akira et al., Ōsaka, Japan. In Immunity, 2013
We also found that ATF3 was an inhibitor of neutrophil differentiation and that Jdp2 directly suppresses its expression via inhibition of histone acetylation.
The stress response mediator ATF3 represses androgen signaling by binding the androgen receptor.
Yan et al., Albany, United States. In Mol Cell Biol, 2012
ATF3 is a novel repressor of androgen signaling that can inhibit AR functions, allowing prostate cells to restore homeostasis
Enhancement of cisplatin cytotoxicity by disulfiram involves activating transcription factor 3.
Dimitroulakos et al., Ottawa, Canada. In Anticancer Res, 2012
ATF3 protein expression was up-regulated after cytotoxic doses of cisplatin treatment and it directly bound to the CHOP gene promoter, increasing this pro-apoptotic protein's expression.
ATF3 inhibits adipocyte differentiation of 3T3-L1 cells.
Jung et al., Yangsan, South Korea. In Biochem Biophys Res Commun, 2012
these results demonstrate that ATF3 represses the C/EBPalpha gene, resulting in inhibition of adipocyte differentiation, and thus plays a role in hypoxia-mediated inhibition of adipocyte differentiation.
The response of the prostate to circulating cholesterol: activating transcription factor 3 (ATF3) as a prominent node in a cholesterol-sensing network.
Freeman et al., Los Angeles, United States. In Plos One, 2011
the role of cholesterol in prostate health, and provide a novel role for ATF3, and associated proteins within a large signaling network, as a cholesterol-sensing mechanism.
Screening for adiponectin secretion regulators.
Nagata et al., Ōsaka, Japan. In Vitam Horm, 2011
On the other hand, transcription factors such as peroxisome proliferator-activated receptor-γ (PPARγ), CCAAT-enhancer-binding protein α, and forkhead box O1 (FoxO1) upregulate adiponectin expression, although the activating transcription factor 3 and cAMP response element-binding protein downregulate it.
Comparative study of the expression of ATF-3 and ATF-4 genes in vessels involved into atherosclerosis process and in psoriatic skin.
Bruskin et al., Moscow, Russia. In Bull Exp Biol Med, 2011
Opposite changes in the expression of ATF-3 and ATF-4 genes in atherosclerotic and psoriatic samples were revealed and a hypothesis was put forward that this parameter could be a criterion of pathological process in both diseases.
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