ATF4

Gene Information
 
Gene Symbol
ATF4
 
Aliases
CREB-2, CREB2, TAXREB67, TXREB
 
Entrez Gene ID
468
 
Gene Name
Activating transcription factor 4
 
Chromosomal Location
22q13.1
 
HGNC ID
 
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 chromosome at q28 in a region containing a large inverted duplication. [provided by RefSeq, Sep 2011]
  e!Ensembl
Gene
Transcript  
Protein

Gene Ontology (GO)

GO ID Ontology Function Evidence Reference
GO:0006357 Biological process Regulation of transcription by RNA polymerase II IBA 21873635
GO:0006520 Biological process Cellular amino acid metabolic process TAS 12689582
GO:0010575 Biological process Positive regulation of vascular endothelial growth factor production IMP 22915762
GO:0010628 Biological process Positive regulation of gene expression IMP 24136195, 24939851
GO:0034976 Biological process Response to endoplasmic reticulum stress IDA 19061639
Protein Information
 
Protein Name
Cyclic AMP-dependent transcription factor ATF-4, DNA-binding protein TAXREB67, cAMP response element-binding protein 2, cAMP-dependent transcription factor ATF-4, 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
 
Function
 
UniProt
 
PDB
 
Pfam
Pfam Accession Pfam ID
PF00170 bZIP_1
Pathways
 
KEGG
 
Reactome
 

MAPK signaling pathway
cGMP-PKG signaling pathway
Mitophagy - animal
Protein processing in endoplasmic reticulum
PI3K-Akt signaling pathway
Apoptosis
Longevity regulating pathway
Adrenergic signaling in cardiomyocytes
TNF signaling pathway
Long-term potentiation
Neurotrophin signaling pathway
Cholinergic synapse
Dopaminergic synapse
Insulin secretion
GnRH signaling pathway
Estrogen signaling pathway
Thyroid hormone synthesis
Glucagon signaling pathway
Aldosterone synthesis and secretion
Relaxin signaling pathway
Cortisol synthesis and secretion
Parathyroid hormone synthesis, secretion and action
Non-alcoholic fatty liver disease (NAFLD)
Cushing syndrome
Cocaine addiction
Amphetamine addiction
Alcoholism
Hepatitis B
Human cytomegalovirus infection
Human T-cell leukemia virus 1 infection
Viral carcinogenesis
Prostate cancer

 

ATF4 activates genes in response to endoplasmic reticulum stress
ATF6 (ATF6-alpha) activates chaperone genes
Response of EIF2AK4 (GCN2) to amino acid deficiency
Response of EIF2AK1 (HRI) to heme deficiency

Interactions
 
STRING MINT IntAct
ENSP00000320866 P27797 P27797
    View interactions
     

Associated Diseases

Disease groupDisease NameReferences
Digestive System Diseases
Fatty Liver
Endocrine System Diseases
PCOS
Neoplasms
Breast Cancer
Psychiatric/Brain disorders
Schizophrenia
Mental Depression
References
 
 
PubMed ID Associated gene/s Associated condition Genetic Mutation Diagnostic Criteria Association with PCOS Ethnicity Conclusion
COX2, PGE2 
PCOS, Hyperprolactinemia,  
 
Rotterdam consensus criteria 
Related 
85 Female participants: 48 were diagnosed with PCOS and received in vitro fertilization-embryo transfer (IVF-ET) & 37 participants in the non-PCOS group were healthy females with regular menstrual cycles (2635 days) and normal ovarian morphology  
ATF4 malfunction in PCOS patients may impact the ovulation process, which could contribute, in part, to the pathogenesis of PCOS. 

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