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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
ATF3 Is a Key Regulator of Macrophage IFN Responses.
De Nardo et al., Bonn, Germany. In J Immunol, 28 Oct 2015
Activating transcription factor 3 (ATF3) is an important transcriptional modulator that limits the inflammatory response by controlling the expression of a number of cytokines and chemokines.
Over-expression of ATF3 or the combination of ATF3, c-Jun, STAT3 and Smad1 promotes regeneration of the central axon branch of sensory neurons but without synergistic effects.
Mason et al., Amsterdam, Netherlands. In Hum Mol Genet, 18 Oct 2015
Among known RAG TFs, ATF3, Smad1, STAT3 and c-Jun have all been linked to successful axonal regeneration, and have known functional and physical interactions.
Special issue in the European Journal of Neuroscience Nerve regeneration in chitosan conduits and in autologous nerve grafts in healthy and in type 2 diabetic Goto-Kakizaki rats.
Dahlin et al., Malmö, Sweden. In Eur J Neurosci, 10 Oct 2015
There was a higher percentage of activating transcription factor 3 (ATF-3) immunostained cells in nerve segments from healthy rats compared to diabetic rats after autologous nerve graft reconstruction.
Toll-like receptors: Activation, signalling and transcriptional modulation.
De Nardo, Australia. In Cytokine, 31 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.
Lysophosphatidic Acid Mediates Activating Transcription Factor 3 Expression Which Is a Target for Post-Transcriptional Silencing by miR-30c-2-3p.
Murph et al., Athens, United States. In Plos One, Dec 2014
The goal here is to confirm that ATF3 mRNA is a target of miR-30c-2-3p silencing, thereby further establishing the functional role of miR-30c-2-3p.
Activating transcription factor 3 represses inflammatory responses by binding to the p65 subunit of NF-κB.
Choi et al., Suwŏn, South Korea. In Sci Rep, Dec 2014
UNASSIGNED: Activating transcription factor 3 (ATF3) is induced by inflammatory responses, cell death, cytokines, and oxidative stress 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.
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.
Aetiology of hypospadias: a systematic review of genes and environment.
Roeleveld et al., Nijmegen, Netherlands. In Hum Reprod Update, 2012
Studies screening groups of patients with hypospadias for single gene defects found mutations in WT1, SF1, BMP4, BMP7, HOXA4, HOXB6, FGF8, FGFR2, AR, HSD3B2, SRD5A2, ATF3, MAMLD1, MID1 and BNC2.
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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