- CITATIONS: 1
|Calculated MW||186911 Da|
|Other Names||Eukaryotic translation initiation factor 2-alpha kinase 4, GCN2-like protein, EIF2AK4, GCN2, KIAA1338|
|Target/Specificity||A phospho specific peptide corresponding to residues surrounding threonine 667 of human GCN2 was used as an immunogen. This antibody detects GCN2 phosphorylyated at threonine 667.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||GCN2 Antibody Phospho (pT667) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Can phosphorylate the alpha subunit of EIF2 and may mediate translational control.|
|Tissue Location||Widely expressed. Expressed in the lung in smooth muscle cells of the pulmonary vessel wall, interstitial tissue and macrophages.|
Provided below are standard protocols that you may find useful for product applications.
In eukaryotic cells, protein synthesis is regulated in response to various environmental stresses by phosphorylating the alpha subunit of the eukaryotic initiation factor 2 (eIF2alpha). Four different eIF2alpha kinases have been identified in mammalian cells, the heme-regulated inhibitor (HRI), the interferon-inducible RNA-dependent kinase (PKR) and the endoplasmic reticulum-resident kinase (PERK) and GCN2, which was previously characterized from Saccharomyces cerevisiae, Drosophila melanogaster and Neurospora crassa. GCN2 is the unique eIF2alpha kinase present in all eukaryotes from yeast to mammals (1). GCN2, a sensor of amino acid deficiency, plays a key role in yeast and mammals in modulating amino acid metabolism as part of adaptation to nutrient deprivation. The role of GCN2 in adaptation to long-term amino acid deprivation in mammals, however, is poorly understood. GCN2-deficient mice developed liver steatosis and exhibited reduced lipid mobilization. Liver steatosis in Gcn2(-/-) mice was found to be caused by unrepressed expression of lipogenic genes, including Srebp-1c and Fa (2). Results demonstrate that PERK and GCN2 function to cooperatively regulate eIF2alpha phosphorylation and cyclin D1 translation after unfolded protein response pathway activation (3).
1. Berlanga JJ, et al. Eur J Biochem 265(2):754-62
2. Guo F, et al. Cell Metab 5(2):103-14, 2007
3. Hamanaka RB, et al. Mol Bio Cell 16(12):5493-501, 2005
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