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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).
HIV/SIV exploits the early host antiviral response through GCN2 (show EIF2AK4 ELISA Kits)-ATF4 signaling by utilizing ATF4 for activating the viral LTR transcription to establish initial viral replication
These results suggest that p21 (show CDKN1A ELISA Kits) induction plays a vital role in the cellular response to ER stress and indicate that p21 (show CDKN1A ELISA Kits) is a prosurvival effector of ATF4.
GRP78 (show HSPA5 ELISA Kits) inhibition enhances ATF4-induced cell death by the deubiquitination and stabilization of CHOP (show DDIT3 ELISA Kits) in human osteosarcoma cells.
Expression of either dominant-negative or constitutively active mutants of Nrf2 (show GABPA ELISA Kits), ATF4, or c-Jun (show JUN ELISA Kits) confirmed that distinct transcription units are regulated by these transcription factors.
ATF4 contributes to tumor growth of endometrial cancer (EC) by promoting CCL2 (show CCL2 ELISA Kits) and subsequent recruitment of macrophage, and ATF4/CCL2 (show CCL2 ELISA Kits) 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 (show GRIN1 ELISA Kits) antiporter xCT (show SLC7A11 ELISA Kits)
The PERK (show EIF2AK3 ELISA Kits)-eIF2alpha (show EIF2A ELISA Kits)-ATF4-CHOP (show DDIT3 ELISA Kits) signaling pathway has a critical role in tumor progression during endoplasmic reticulum stress. (Review)
ATF4 pathway is activated in vivo upon mitochondrial stress.
a shortage of tryptophan caused by expression of indoleamine 2,3-dioxygenase (IDO (show IDO1 ELISA Kits)) and tryptophan 2,3-dioxygenase (TDO (show TDO2 ELISA Kits)) resulted in ATF4-dependent upregulation of several amino acid transporters.
SLC30A10 has a protective role in 1-methyl-4-phenylpyridinium-induced toxicity via PERK (show EIF2AK3 ELISA Kits)-ATF4 pathway.
There was decreased or loss of ATF4 in 52% of medullary thyroid cancer (MTC) (show RET ELISA Kits)tumors (n = 39) compared with normal thyroid follicle cells. A negative correlation was observed between RET and ATF4 protein levels in MTC tumors.
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 (show EIF2AK4 ELISA Kits) or eIF2alpha (show EIF2A ELISA Kits) kinase activity.
BTG1 (show BTG1 ELISA Kits) has a role in regulating hepatic lipid metabolism and in preventing ATF4 and SCD1 (show SCD ELISA Kits) from inducing liver steatosis
Transcriptional profiling reveals that mouse neuroblastoma (show ARHGEF16 ELISA Kits) 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 (show HSPA5 ELISA Kits)/D-DT is an early response cytokine in the I/R injury repair of the proximal tubule, enhancing regeneration through SLPI (show SLPI ELISA Kits)- 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 (show CYP7A1 ELISA Kits)), esterification of cholesterol (SOAT2 (show SOAT2 ELISA Kits)), and transport from the hepatocyte (ABCA1 (show ABCA1 ELISA Kits)); when ATF4 loss is coupled with ER stress, results in increase in free cholesterol within hepatocyte
Data, including data from studies using cells from knockout mice, suggest that gasotransmitter H(2)S up-regulates eIF2a (show EIF2A ELISA Kits) phosphorylation by inhibiting PPP1CA (show PPP1CA ELISA Kits) via persulfidation, which in turn leads to transient suppression of global translation and activation of Atf4 expression. (eIF2a (show EIF2A ELISA Kits) = eukaryotic initiation factor-2alpha (show EIF2S1 ELISA Kits); PPP1CA (show PPP1CA ELISA Kits) = protein phosphatase 1 catalytic subunit alpha; Atf4 = activating transcription factor 4)
Results identify the beneficial role of hypothalamic ATF4/ATG5 axis in the regulation of energy expenditure, obesity, and obesity-related metabolic disorders.
SLC30A10 (show SLC30A10 ELISA Kits) has a protective role in 1-methyl-4-phenylpyridinium-induced toxicity via PERK (show EIF2AK3 ELISA Kits)-ATF4 pathway.
ER stress-induced increase in ATF4 and CHOP (show DDIT3 ELISA Kits) expression is initiated by an increase in Atf4 and Chop (show DDIT3 ELISA Kits) mRNA, which is also dependent upon eIF2alpha (show EIF2A ELISA Kits) phosphorylation.
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 (show ATF2 ELISA Kits) and CREB3 (show CREB3 ELISA Kits) mRNA were ubiquitously detected in all examined tissues.
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.
cyclic AMP-dependent transcription factor ATF-4
, activating transcription factor 4 (tax-responsive enhancer element B67)
, cAMP-dependent transcription factor ATF-4
, activating transcription factor 4C
, activating transcription factor 4
, DNA-binding protein TAXREB67
, cAMP response element-binding protein 2
, cAMP-responsive element-binding protein 2
, cyclic AMP-responsive element-binding protein 2
, tax-responsive enhancer element B67
, tax-responsive enhancer element-binding protein 67
, c/EBP-related ATF
, tax-responsive enhancer element-binding protein 67 homolog
, taxREB67 homolog
, activating transcription factor ATF-4