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Validated All-in-One™ qPCR Primer for ATF4(NM_001675.2) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
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 chromsome at q28 in a region containing a large inverted duplication. [provided by RefSeq].
Gene References into function
- mediator of the nutrient-sensing response pathway that activates the asparagine synthetase gene
- interaction between RPB3 and ATF4
- ATF4 and ATF2 have roles in regulating CHOP expression
- Expression of ATF4 was found to correlate with cisplatin sensitivity in human cancer cell lines.
- ATF4 has a role in regulating VEGF expression
- Data demonstrate the essential role of activating transcription factor 4 (ATF4) in the response to hypoxic stress, and reveal that GADD34, a target of ATF4 activation, negatively regulates the eIF2alpha-mediated inhibition of translation.
- ATF3-FL and C/EBPbeta act as transcriptional suppressors for the ASNS gene to counterbalance the transcription rate activated by ATF4 following amino acid deprivation
- Results suggest that mitosin is a negative regulator of ATF4 in interphase through direct interaction.
- both p300 and CBP increase ATF4 transcriptional activity
- activation by nephrocystin-6 in Joubert syndrome
- Endoplasmic reticulum stress induction of IGFBP-1 involves ATF4
- Contribution of common variations of ATF4 and ATF5 to the pathophysiology of bipolar disorder may be minimal if any.
- ATF4 may regulate myeloid gene expression differentially by potentiating C/EBPepsilon but inhibiting C/EBPalpha-mediated transcriptional activation.
- TRB3 and ATF4 belong to the same protein complex bound to the sequence involved in the ATF4-dependent regulation of gene expression by amino acid limitation.
- PHD-dependent oxygen-sensing recruits both the hypoxia-inducible factor (HIF) and ATF-4 systems.
- The results indicate that TRB3 protects cells against the growth inhibitory and cytotoxic effect of ATF4.
- overexpression of either CREB or ATF4 enhanced the activation of the HEC1 promoter and overexpression of both of them had an additive effect on the activation of the HEC1 transcription.
- The ATF4-mediated up-regulation of Ape1 and other genes plays a key role against arsenite-mediated toxicity and mutagenesis.
- 23P-ATF4 peptide fits the binding pocket of protein beta-TrCP very well, considering that the DpSGIXXpSXE motif adopts an S-turning conformation contrary to the extended DpSGXXpS motif in the other known beta-TrCP ligands.
- ATF4 gene may be involved in susceptibility to schizophrenia with sex-dependent effect.
- TFIIA gamma together with ATF4 and Runx2 stimulates osteocalcin promoter activity and endogenous mRNA expression.
- ATF4 contributes to basal ATF5 transcription, and eIF2 kinases direct the translational expression of multiple transcription regulators by a mechanism involving delayed translation reinitiation
- Multiple pathways are involved in the anoxia response of SKIP3 including HuR-regulated RNA stability, NF-kappaB and ATF4
- characterize unfolded protein response ATF4 branch as an important mechanism mediating up-regulation of VEGF by OxPLs
- Compared with COPD and donor lungs, protein levels of ER stress mediators, such as ATF-6 and ATF-4 and the apoptosis-inductor CHOP as well as XBP-1, were significantly elevated in lung homogenates and AECIIs of IPF lungs
- Despite increased ATF4 binding at the C/EBP-ATF composite site following activation of the unfolded protein response, system A transporter 2 (SNAT2) transcription activity is repressed
- CHOP is a member of the transcription factor network that controls the stress-induced regulation of specific C/EBP-ATF4-containing genes, such as ASNS
- ATF4 and phospho-eIF2alpha levels are tightly correlated and up-regulated in Alzheimer disease
- The results suggest that REDD1 expression is upregulated during ER stress through a mechanism involving activation of PERK, phosphorylation of eIF2alpha, and increased ATF4 expression.
