atf4 Antibody

Transcription factor that binds the cAMP response element (CRE) (consensus: 5'-GTGACGT[AC][AG]-3') and displays two biological functions, as regulator of metabolic and redox processes under normal cellular conditions, and as master transcription factor during integrated stress response (ISR). Binds to asymmetric CRE's as a heterodimer and to palindromic CRE's as a homodimer. Core effector of the ISR, which is required for adaptation to various stress such as endoplasmic reticulum (ER) stress, amino acid starvation, mitochondrial stress or 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 transcription factor of stress-responsive genes in order to promote cell recovery. Promotes the transcription of genes linked to amino acid sufficiency and resistance to oxidative stress to protect cells against metabolic consequences of ER oxidation. In the absence of stress, atf4 translation is at low levels and it is required for normal metabolic processes such as embryonic lens formation, fetal liver hematopoiesis, bone development and synaptic plasticity. Acts as a regulator of osteoblast differentiation by promoting expression of osteoblast-specific genes. Regulates the circadian expression of the core clock components. Mainly acts as a transcriptional activator in cellular stress adaptation, but it can also act as a transcriptional repressor.