ATF4 Proteins

ATF4 (Activating Transcription Factor 4) is a Protein Coding gene. Diseases associated with ATF4 include T-Cell Leukemia and Coffin-Lowry Syndrome. Among its related pathways are NGF Pathway and Sertoli-Sertoli Cell Junction Dynamics. Gene Ontology (GO) annotations related to this gene include DNA-binding transcription factor activity and protein heterodimerization activity. An important paralog of this gene is ATF5.

The following recombinant ATF4 proteins are manufactured in house under a complete QC system by CUSABIO. They are expressed by Yeast, E.coli, Baculovirus, Mammalian cell, In Vivo Biotinylation in E.coli. Highlights of these recombinant ATF4 proteins as follow:
High purity, Low endotoxin, Multiple Tags, Animal-free, Wide applications (Cell assay, Protein-protein interaction, Drug-related studies, Enzymatic activity in vitro, Protein structure analysis, etc.)
In addition, various options on sizes, excellent technical support, and recombinant ATF4 proteins custom service will be also offered.

ATF4 Proteins Catalog

ATF4 Proteins for Mus musculus (Mouse)

ATF4 Proteins for Homo sapiens (Human)

ATF4 Proteins for Bos taurus (Bovine)

ATF4 Proteins for Danio rerio (Zebrafish) (Brachydanio rerio)

ATF4 Proteins for Rattus norvegicus (Rat)

ATF4 Background

The ATF4 gene codes for activating transcription factor 4 (ATF4) that belongs to the ATF subfamily of the basic leucine zipper (bZIP) transcription factor superfamily [1]. ATF4 is induced and expressed by stress signals such as anoxic insult, endoplasmic reticulum (ER) stress, oxidative stress, nutrition deprivation, and other cellular stresses. Upon binding to C/EBP-ATF Response Element (CARE) sequences of a subset of specific target genes, ATF4 induces increased transcription of these genes [2][3][4]. The expression of these adaptive genes allows cells to endure periods of stress. Whereas, under prolonged stress conditions, ATF4 promotes the induction of apoptosis. ATF4 expression is regulated transcriptionally and translationally via the PERK pathway of eIF2alpha phosphorylation, and then posttranslationally by phosphorylation. The eventual result is ATF4 degradation by proteasomal. ATF4 also mediates the induction of the Integrated Stress Response (ISR) and is involved in amino acid metabolism, differentiation, metastasis, angiogenesis [5], and drug resistanc [6]. Transgenic studies have demonstrated ATF4 to be involved in hematopoiesis, lens & skeletal development, fertility, proliferation, differentiation, and long-term memory. ATF4 expression is upregulated in cancer. ATF4 reduces tumor burden by controlling the expression of target genes implicated in the induction of apoptosis. Since ATF4 is induced by tumor microenvironmental factors and regulates processes relevant to cancer progression, it might serve as a potential therapeutic target in cancer. Jie Luo et al. demonstrated that ATF4 plays a crucial role in blocking the progression and resistance response in RET/GRP78-positive human osteosarcoma [7]. Evidence shows ATF4 activation is responsible for proteasome inhibitor bortezomib (BTZ)-induced osteosarcoma (OS) cell death [7].

[1] Ameri K, Harris AL. Activating transcription factor 4 [J]. Int. J. Biochem. Cell Biol. 2008;40:14-21.
[2] Siu F, Bain PJ, et al. ATF4 is a mediator of the nutrient-sensing response pathway that activates the human asparagine synthetase gene [J]. J. Biol. Chem., 2002, vol. 277 (pg. 24120-24127).
[3] Averous J, Bruhat A, et al. Induction of CHOP expression by amino acid limitation requires both ATF4 expression and ATF2 phosphorylation [J]. J. Biol. Chem., 2004, vol. 279 (pg. 5288-5297).
[4] Bruhat A, Cherasse Y, et al. Amino acids as regulators of gene expression in mammals: molecular mechanisms [J]. Biofactors, 2009, vol. 35 (pg. 249-257).
[5] Harding HP, Zhang Y, et al. An integrated stress response regulates amino acid metabolism and resistance to oxidative stress [J]. Mol. Cell, 2003, vol. 11 (pg. 619-633).
[6] Rzymski T, Milani M, et al. Role of ATF4 in regulation of autophagy and resistance to drugs and hypoxia [J]. Cell Cycle, 2009, vol. 8 (pg. 3838-3847).
[7] Jie Luo, Yuanzheng Xia, et al. ATF4 Destabilizes RET Through Nonclassical GRP78 Inhibition to Enhance Chemosensitivity to Bortezomib in Human Osteosarcoma. [J] Theranostics, 2019 Aug, 9 (21), 6334-6353.


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