No Products on your Comparison List.
Your basket is empty.
Find out more
Show all synonyms
Select your origin of interest
Human ATF4 Protein expressed in Wheat germ - ABIN1345933
Zhang, Khachigian et al.: Injury-induced platelet-derived growth factor receptor-alpha expression mediated by interleukin-1beta (IL-1beta) release and cooperative transactivation by NF-kappaB and ATF-4: IL-1beta facilitates ... in The Journal of biological chemistry 2009
The data also support a potential role for the PERK/eIF2a/ATF4 axis in modulating cell viability in irradiated glioblastoma multiforme (GBM). The dual function of PERK as a mediator of survival and death may be exploited to enhance the efficacy of radiation therapy
The miR-193a-3p regulates osteoblast differentiation by modulating LGR4/ATF4 signaling and suggests that the miR-193a-3p/LGR4/ATF4 regulation axis may play an important role in regulating bone remodeling.
Our findings indicate that the synergism of T cells and sorafenib is mediated via reduced ATF4 expression, causing activation of the IRF7-IL-15 axis in leukemia cells and thereby leading to metabolic reprogramming of leukemia-reactive T cells in humans
High ATF4 expression is associated with acute myeloid leukemia.
Overexpression of miR-1283 inhibited cell proliferation and invasion of glioma cells by directly downregulating ATF4 expression.
ATF4 is expressed in human atrial cardiomyocytes and is induced in response to different types of cell stress. High rate electrical field stimulation seems to result in ATF4 induction, and forced expression of ATF4 reduces cardiomyocyte viability.
The present study shows that ALP mRNA and activity were significantly increased by ER stress treatment of human primary VSMCs in vitro and that this was ATF4-dependent.
phosphorylated PERK and ATF4 would be upregulated in Orexin neurons in Sudden Infant Death Syndrome (SIDS) compared to non-SIDS.
Our data suggests a novel interaction between Nrf2 and ATF4 under oxidative and endoplasmic reticulum stress, thus drives specific enzymatic and non-enzymatic reactions of antioxidant mechanisms maintaining redox homeostasis.
PSAT1, which is overexpressed in ER-negative breast cancers, is activated by ATF4 and promotes cell cycle progression via regulation of the GSK3beta/beta-catenin/cyclin D1 pathway.
POSTN may function as a protective factor for osteoblasts during this process by inhibiting the eIF2alphaATF4 pathway.
p62 directly targets nuclear transcription factors to control metabolic reprogramming in the microenvironment and repress tumorigenesis, and identifies ATF4 as a synthetic vulnerability in p62-deficient tumor stroma.
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 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 induction plays a vital role in the cellular response to ER stress and indicate that p21 is a prosurvival effector of ATF4.
GRP78 inhibition enhances ATF4-induced cell death by the deubiquitination and stabilization of CHOP in human osteosarcoma cells.
Expression of either dominant-negative or constitutively active mutants of Nrf2, ATF4, or c-Jun confirmed that distinct transcription units are regulated by these transcription factors.
ATF4 contributes to tumor growth of endometrial cancer (EC) by promoting CCL2 and subsequent recruitment of macrophage, and ATF4/CCL2 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 antiporter xCT
HIV/SIV exploits the early host antiviral response through GCN2-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 and CREB3 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).
In mice, ATF4 deficiency reduces glutamine uptake by intestinal epithelial cells and expression of antimicrobial peptides by decreasing transcription of Slc1a5.
MEG3 promoted hepatic insulin resistance by serving as a competitive endogenous RNA of miR214 to facilitate ATF4 expression.
CO-stimulated PERK activation and enhanced the levels of FGF21 via the eIF2alpha-ATF4 signaling pathway. The induction of FGF21 by CO attenuated endoreticulum stress- or diet-induced, obesity-dependent hepatic steatosis.
Data suggest that endoplasmic reticulum stress-induced CHOP/Ddit3 inhibits expression of Bip/Grp78 and Atf4; ATF4, in turn, plays critical role in CHOP-mediated regulation of B-cell receptor-controlled murine gammaherpesvirus-68 lytic replication. (CHOP/Ddit3 = DNA-damage inducible transcript-3; Bip/Grp78 = chaperone BiP 78 kDa; Atf4 = activating transcription factor-4)
The results suggest that ATF4 may serve a protective role in the mouse liver.
Golgi stress response elicited by monensin stimulates CSE by acting via ATF4 with characteristics distinguishable from the endoplasmic reticulum stress response
established Neuro2a cells with edited GADD34 and ATF4/GADD34 genes and found that ATF4 acts as a proapoptotic factor, but GADD34 depletion did not attenuate the expression of cleaved caspase-3 induced by tunicamycin treatment.
Atg7 ablation mainly induced the PERK-ATF4-CHOP axis of the endoplasmic reticulum (ER) stress response in growth plate chondrocytes.
under nutrient-limiting conditions that stimulate ATF4 activity, TRIB3 is implicated in the regulation of metabolic adaptation by restraining the transcription of Fgf21.
these findings reveal a new crucial combined effect of the silencing of PERK and ATF4 in modulating ER stressmediated apoptosis during chondrocyte differentiation and proliferation.
Sirt1 reduced endoplasmic reticulum stress and apoptosis of brown adipocytes in vivo/in vitro by inhibiting Smad3/ATF4 signaling pathway.
These findings indicate that the aggregation of S-opsin 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 or eIF2alpha kinase activity.
BTG1 has a role in regulating hepatic lipid metabolism and in preventing ATF4 and SCD1 from inducing liver steatosis
Transcriptional profiling reveals that mouse neuroblastoma 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/D-DT is an early response cytokine in the I/R injury repair of the proximal tubule, enhancing regeneration through SLPI- 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), esterification of cholesterol (SOAT2), and transport from the hepatocyte (ABCA1); when ATF4 loss is coupled with ER stress, results in increase in free cholesterol within hepatocyte
ATF4 pathway is activated in vivo upon mitochondrial stress.
Data, including data from studies using cells from knockout mice, suggest that gasotransmitter H(2)S up-regulates eIF2a phosphorylation by inhibiting PPP1CA via persulfidation, which in turn leads to transient suppression of global translation and activation of Atf4 expression. (eIF2a = eukaryotic initiation factor-2alpha; PPP1CA = protein phosphatase 1 catalytic subunit alpha; Atf4 = activating transcription factor 4)
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