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Human Monoclonal ATF4 Primary Antibody für IF, ELISA - ABIN559979
Meister, Frey, Lang, Gaipl, Schett, Schlötzer-Schrehardt, Voll: Calcium channel blocker verapamil enhances endoplasmic reticulum stress and cell death induced by proteasome inhibition in myeloma cells. in Neoplasia (New York, N.Y.) 2010
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Mouse (Murine) Polyclonal ATF4 Primary Antibody für IHC, WB - ABIN2779918
Smith, Schmechel, Raghavan, Abelson, Reilly, Katze, Kaufman, Bohjanen, Schiff: Reovirus induces and benefits from an integrated cellular stress response. in Journal of virology 2006
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Human Polyclonal ATF4 Primary Antibody für IF (p), IHC (p) - ABIN687862
Jiang, Ren, Jiang, Wang, Zhang, Yin, Wang, Qi, Wang, Feng: Guanabenz delays the onset of disease symptoms, extends lifespan, improves motor performance and attenuates motor neuron loss in the SOD1 G93A mouse model of amyotrophic lateral sclerosis. in Neuroscience 2014
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Human Polyclonal ATF4 Primary Antibody für ELISA, WB - ABIN257681
Tsujimoto, Nyunoya, Morita, Sato, Shimotohno: Isolation of cDNAs for DNA-binding proteins which specifically bind to a tax-responsive enhancer element in the long terminal repeat of human T-cell leukemia virus type I. in Journal of virology 1991
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Human Polyclonal ATF4 Primary Antibody für IF (p), IHC (p) - ABIN756172
Jiang, Yun, Shi, Niu, Gao, Xie, Yu: Downregulation of miR-384-5p attenuates rotenone-induced neurotoxicity in dopaminergic SH-SY5Y cells through inhibiting endoplasmic reticulum stress. in American journal of physiology. Cell physiology 2016
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Cow (Bovine) Polyclonal ATF4 Primary Antibody für WB - ABIN2780377
Kalinec, Thein, Parsa, Yorgason, Luxford, Urrutia, Kalinec: Acetaminophen and NAPQI are toxic to auditory cells via oxidative and endoplasmic reticulum stress-dependent pathways. in Hearing research 2014
Human Polyclonal ATF4 Primary Antibody für IHC - ABIN965616
Yang, Matsuda, Bialek, Jacquot, Masuoka, Schinke, Li, Brancorsini, Sassone-Corsi, Townes, Hanauer, Karsenty: ATF4 is a substrate of RSK2 and an essential regulator of osteoblast biology; implication for Coffin-Lowry Syndrome. in Cell 2004
Human Polyclonal ATF4 Primary Antibody für ICC, IF - ABIN4282025
Oh, Pan, Yalcin, Zhang, Guilarte, Hotamisligil, Christiani, Lu: Functional RNA interference (RNAi) screen identifies system A neutral amino acid transporter 2 (SNAT2) as a mediator of arsenic-induced endoplasmic reticulum stress. in The Journal of biological chemistry 2012
results suggest a conditional regulation of KRT16 gene by ATF4 that may be inhibited in normal cells, but engaged during cancer progression. Potential roles of KRT16, FAM129A and HKDC1 genes upregulation in adaptive stress responses and pathologies are discussed
Results provide evidence that the availability of glucose controls ATF4-mediated MITF (zeige MITF Antikörper) suppression to drive melanoma cell proliferation.
Decreased ATF4 expression as a mechanism of acquired resistance to long-term amino acid limitation in cancer cells
These results suggest that p21 (zeige CDKN1A Antikörper) induction plays a vital role in the cellular response to ER stress and indicate that p21 (zeige CDKN1A Antikörper) is a prosurvival effector of ATF4.
GRP78 (zeige HSPA5 Antikörper) inhibition enhances ATF4-induced cell death by the deubiquitination and stabilization of CHOP (zeige DDIT3 Antikörper) in human osteosarcoma cells.
Expression of either dominant-negative or constitutively active mutants of Nrf2 (zeige GABPA Antikörper), ATF4, or c-Jun (zeige JUN Antikörper) confirmed that distinct transcription units are regulated by these transcription factors.
ATF4 contributes to tumor growth of endometrial cancer (EC) by promoting CCL2 (zeige CCL2 Antikörper) and subsequent recruitment of macrophage, and ATF4/CCL2 (zeige CCL2 Antikörper) axis might be a potential therapeutic target for EC.
ATF4 expression fosters the malignancy of primary brain tumors and increases proliferation and tumor angiogenesis; experiments revealed that ATF4-dependent tumor promoting effects are mediated by transcriptional targeting the glutamate (zeige GRIN1 Antikörper) antiporter xCT (zeige SLC7A11 Antikörper)
The PERK (zeige EIF2AK3 Antikörper)-eIF2alpha (zeige EIF2A Antikörper)-ATF4-CHOP (zeige DDIT3 Antikörper) signaling pathway has a critical role in tumor progression during endoplasmic reticulum stress. (Review)
ATF4 pathway is activated in vivo upon mitochondrial stress.
HIV/SIV exploits the early host antiviral response through GCN2 (zeige EIF2AK4 Antikörper)-ATF4 signaling by utilizing ATF4 for activating the viral LTR transcription to establish initial viral replication
expression levels of porcine ATF4 gene were up-regulated 60 days and 120 days after birth in both breeds and the expression level in Meishan pigs was obviously higher than that in Large White pigs
Tissue transcription analysis revealed that both porcine CREB2 (zeige ATF2 Antikörper) and CREB3 (zeige CREB3 Antikörper) mRNA were ubiquitously detected in all examined tissues.
Over-expression of atf4 in embryos interferes with neurogenesis and eye formation.
Unlike other CREB2 (ATF4) proteins, the ATF4 isolated from the gonads of Xenopus embryos contains a consensus phosphorylation site for protein kinase A (PKA).
Atg7 (zeige ATG7 Antikörper) ablation mainly induced the PERK (zeige EIF2AK3 Antikörper)-ATF4-CHOP (zeige DDIT3 Antikörper) axis of the endoplasmic reticulum (ER) stress response in growth plate chondrocytes.
under nutrient-limiting conditions that stimulate ATF4 activity, TRIB3 (zeige TRIB3 Antikörper) is implicated in the regulation of metabolic adaptation by restraining the transcription of Fgf21 (zeige FGF21 Antikörper).
these findings reveal a new crucial combined effect of the silencing of PERK (zeige EIF2AK3 Antikörper) and ATF4 in modulating ER stressmediated apoptosis during chondrocyte differentiation and proliferation.
Sirt1 (zeige SIRT1 Antikörper) reduced endoplasmic reticulum stress and apoptosis of brown adipocytes in vivo/in vitro by inhibiting Smad3 (zeige SMAD3 Antikörper)/ATF4 signaling pathway.
These findings indicate that the aggregation of S-opsin (zeige OPN1SW Antikörper) induced by exposure to blue -emitting diode light causes endoplasmic reticulum stress, and ATF4 activation in particular.
We hypothesize that the essential role of methionine-charged initiator tRNA in forming ternary complex is responsible for the robust ability of methionine deficiency to induce ATF4 and the ISR even in the absence of GCN2 (zeige EIF2AK4 Antikörper) or eIF2alpha (zeige EIF2A Antikörper) kinase activity.
BTG1 (zeige BTG1 Antikörper) has a role in regulating hepatic lipid metabolism and in preventing ATF4 and SCD1 (zeige SCD Antikörper) from inducing liver steatosis
Transcriptional profiling reveals that mouse neuroblastoma (zeige ARHGEF16 Antikörper) sphere-forming cells acquire a metabolic program characterized by transcriptional activation of the cholesterol and serine-glycine synthesis pathways, primarily as a result of increased expression of sterol regulatory element binding factors and Atf4, respectively
MIF-2 (zeige HSPA5 Antikörper)/D-DT is an early response cytokine in the I/R injury repair of the proximal tubule, enhancing regeneration through SLPI (zeige SLPI Antikörper)- and ATF4-dependent mechanisms.
ATF4 has a role in gene expression during basal conditions, with 385 genes altered by the loss of ATF4 in the absence of apparent stress. Deletion of ATF4 alters genes that are required for the conversion of cholesterol to bile acid (CYP7A1 (zeige CYP7A1 Antikörper)), esterification of cholesterol (SOAT2 (zeige SOAT2 Antikörper)), and transport from the hepatocyte (ABCA1 (zeige ABCA1 Antikörper)); when ATF4 loss is coupled with ER stress, results in increase in free cholesterol within hepatocyte
This gene encodes a transcription factor that was originally identified as a widely expressed mammalian DNA binding protein that could bind a tax-responsive enhancer element in the LTR of HTLV-1. The encoded protein was also isolated and characterized as the cAMP-response element binding protein 2 (CREB-2). The protein encoded by this gene belongs to a family of DNA-binding proteins that includes the AP-1 family of transcription factors, cAMP-response element binding proteins (CREBs) and CREB-like proteins. These transcription factors share a leucine zipper region that is involved in protein-protein interactions, located C-terminal to a stretch of basic amino acids that functions as a DNA binding domain. Two alternative transcripts encoding the same protein have been described. Two pseudogenes are located on the X chromosome at q28 in a region containing a large inverted duplication.
DNA-binding protein TAXREB67
, cAMP response element-binding protein 2
, cAMP-dependent transcription factor ATF-4
, cAMP-responsive element-binding protein 2
, cyclic AMP-dependent transcription factor ATF-4
, cyclic AMP-responsive element-binding protein 2
, tax-responsive enhancer element B67
, tax-responsive enhancer element-binding protein 67
, activating transcription factor 4 (tax-responsive enhancer element B67)
, activating transcription factor ATF-4
, activating transcription factor 4
, c/EBP-related ATF
, tax-responsive enhancer element-binding protein 67 homolog
, taxREB67 homolog
, Activating Transcription Factor 4 -I
, Activating Transcription Factor 4 -II
, activating transcription factor 4 S homeolog