ATF4 Antibody (YA605),MedChemexpress,HY-P80486

ATF4 is a transcription factor that binds the cAMP response element (CRE) (consensus: 5'-GTGACGT[AC][AG]-3') and functions as a regulator of metabolic and redox processes under normal cellular conditions, as well as a master transcription factor during the integrated stress response (ISR). It binds to asymmetric CREs as a heterodimer and to palindromic CREs as a homodimer (By similarity). As a core effector of ISR, ATF4 is essential for adaptation to various stresses, including endoplasmic reticulum (ER) stress, amino acid starvation, mitochondrial stress, and oxidative stress. During ISR, ATF4 translation is induced via an alternative ribosome translation re-initiation mechanism in response to EIF2S1/eIF-2-alpha phosphorylation, and stress-induced ATF4 acts as a master regulator of stress-responsive genes to promote cell recovery. It also activates the transcription of genes linked to amino acid sufficiency and oxidative stress resistance (By similarity). In ER stress, ATF4 may cooperate with other factors to activate NLRP1 transcription and induces asparagine synthetase (ASNS) expression in response to amino acid deprivation or ER stress. However, when associated with DDIT3/CHOP, ATF4-mediated ASNS transcription is inhibited under amino acid deprivation. ATF4, together with DDIT3/CHOP, promotes programmed cell death by regulating genes involved in cellular amino acid metabolism, mRNA translation, and the terminal unfolded protein response (terminal UPR) (By similarity). Additionally, ATF4 activates COX7A2L/SCAF1 expression downstream of the EIF2AK3/PERK-mediated UPR, enhancing respiratory chain supercomplex formation and mitochondrial oxidative phosphorylation. Under non-stress conditions, ATF4 is involved in embryonic lens formation, fetal liver hematopoiesis, bone development, and synaptic plasticity (By similarity). In osteoblasts, ATF4 phosphorylation by RPS6KA3/RSK2 enhances its transactivation activity and promotes osteoblast-specific gene expression. ATF4 also cooperates with FOXO1 to regulate glucose homeostasis by suppressing β-cell production and insulin secretion (By similarity). Furthermore, ATF4 activates SIRT4 transcription and regulates circadian expression of PER2 and SLC6A4 by periodically binding to CREs in their promoters (By similarity). While primarily functioning as a transcriptional activator in stress adaptation, ATF4 can also act as a repressor, inhibiting long-term memory formation. In neurons, DISC1 interaction disrupts ATF4 dimerization and DNA-binding, suppressing its transcriptional activity (Microbial infection) ATF4 binds to a Tax-responsive enhancer element in the HTLV-I long terminal repeat.