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Mouse Anti-EIF2AK4 (AA 22-139) Recombinant Antibody (CBFYE-0649) (CBMAB-E1061-FY)

This product is mouse antibody that recognizes EIF2AK4. The antibody CBFYE-0649 can be used for immunoassay techniques such as: WB.
See all EIF2AK4 antibodies

Summary

Host Animal
Mouse
Specificity
Human
Clone
CBFYE-0649
Antibody Isotype
IgG2b
Application
WB

Basic Information

Immunogen
Recombinant corresponding to AA 22-139 from human GCN2 expressed in E.coli
Specificity
Human
Antibody Isotype
IgG2b
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Lyophilized
Concentration
0.5 mg/mL
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.
Epitope
AA 22-139

Target

Full Name
EUKARYOTIC TRANSLATION INITIATION FACTOR 2 ALPHA KINASE 4
Introduction
This gene encodes a member of a family of kinases that phosphorylate the alpha subunit of eukaryotic translation initiation factor-2 (EIF2), resulting in the downregulaton of protein synthesis. The encoded protein responds to amino acid deprivation by binding uncharged transfer RNAs. It may also be activated by glucose deprivation and viral infection. Mutations in this gene have been found in individuals suffering from autosomal recessive pulmonary venoocclusive-disease-2.
Entrez Gene ID
440275
UniProt ID
Q9P2K8
Alternative Names
Eukaryotic Translation Initiation Factor 2 Alpha Kinase 4; GCN2-Like Protein; GCN2; Eukaryotic Translation Initiation Factor 2-Alpha Kinase 4; General Control Nonderepressible 2; EIF-2-Alpha Kinase GCN2
Research Area
Metabolic-stress sensing protein kinase that phosphorylates the alpha subunit of eukaryotic translation initiation factor 2 (EIF2S1/eIF-2-alpha) in response to low amino acid availability (PubMed:25329545).

Plays a role as an activator of the integrated stress response (ISR) required for adaptation to amino acid starvation (By similarity).

EIF2S1/eIF-2-alpha phosphorylation in response to stress converts EIF2S1/eIF-2-alpha in a global protein synthesis inhibitor, leading to a global attenuation of cap-dependent translation, and thus to a reduced overall utilization of amino acids, while concomitantly initiating the preferential translation of ISR-specific mRNAs, such as the transcriptional activator ATF4, and hence allowing ATF4-mediated reprogramming of amino acid biosynthetic gene expression to alleviate nutrient depletion (By similarity).

Binds uncharged tRNAs (By similarity).

Involved in cell cycle arrest by promoting cyclin D1 mRNA translation repression after the unfolded protein response pathway (UPR) activation or cell cycle inhibitor CDKN1A/p21 mRNA translation activation in response to amino acid deprivation (PubMed:26102367).

Plays a role in the consolidation of synaptic plasticity, learning as well as formation of long-term memory (By similarity).

Plays a role in neurite outgrowth inhibition (By similarity).

Plays a proapoptotic role in response to glucose deprivation (By similarity).

Promotes global cellular protein synthesis repression in response to UV irradiation independently of the stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK) and p38 MAPK signaling pathways (By similarity).

Plays a role in the antiviral response against alphavirus infection; impairs early viral mRNA translation of the incoming genomic virus RNA, thus preventing alphavirus replication (By similarity).

(Microbial infection) Plays a role in modulating the adaptive immune response to yellow fever virus infection; promotes dendritic cells to initiate autophagy and antigene presentation to both CD4+ and CD8+ T-cells under amino acid starvation (PubMed:24310610).
Biological Process
Adaptive immune response Source: UniProtKB-KW
Cell cycle Source: UniProtKB-KW
Cellular response to amino acid starvation Source: UniProtKB
Cellular response to cold Source: UniProtKB
Cellular response to leucine starvation Source: UniProtKB
Cellular response to UV Source: UniProtKB
Defense response to virus Source: UniProtKB-KW
DNA damage checkpoint signaling Source: InterPro
EiF2alpha phosphorylation in response to endoplasmic reticulum stress Source: UniProtKB
GCN2-mediated signaling Source: UniProtKB
Induction by virus of host autophagy Source: UniProtKB
Learning Source: UniProtKB
Long-term memory Source: UniProtKB
Negative regulation by host of viral genome replication Source: UniProtKB
Negative regulation of CREB transcription factor activity Source: UniProtKB
Negative regulation of neuron differentiation Source: UniProtKB
Negative regulation of translational initiation Source: UniProtKB
Negative regulation of translational initiation in response to stress Source: UniProtKB
Neuron projection extension Source: UniProtKB
Positive regulation of adaptive immune response Source: UniProtKB
Positive regulation of defense response to virus by host Source: UniProtKB
Positive regulation of long-term synaptic potentiation Source: UniProtKB
Positive regulation of protein phosphorylation Source: Ensembl
Positive regulation of translational initiation in response to starvation Source: UniProtKB
Protein autophosphorylation Source: UniProtKB
Protein phosphorylation Source: UniProtKB
Regulation of feeding behavior Source: UniProtKB
Regulation of translational initiation Source: UniProtKB
Regulation of translational initiation by eIF2 alpha phosphorylation Source: UniProtKB
T cell activation involved in immune response Source: UniProtKB
Viral translation Source: UniProtKB
Cellular Location
Cytoplasm
Involvement in disease
Pulmonary venoocclusive disease 2, autosomal recessive (PVOD2):
A disease characterized by widespread fibrous obstruction and intimal thickening of septal veins and preseptal venules, a low diffusing capacity for carbon monoxide, occult alveolar hemorrhage, and nodular ground-glass opacities, septal lines and lymph node enlargement showed by high-resolution computed tomography of the chest. It is frequently associated with pulmonary capillary dilatation and proliferation, and is a rare and devastating cause of pulmonary hypertension.
PTM
Autophosphorylated; autophosphorylation on Thr-899 is increased upon amino acid starvation and in UV irradiation cells and inhibited in presence of IMPACT.

Lechartier, B., Girerd, B., Eyries, M., Beurnier, A., Humbert, M., & Montani, D. (2022). Screening for pulmonary veno-occlusive disease in heterozygous EIF2AK4 variant carriers. European Respiratory Journal, 60(2).

Li, Y., Gu, Y., Hong, C., Deng, Y., Chen, Z., & Jiang, J. (2020). Pulmonary capillary hemangiomatosis in Chinese patients without EIF2AK4 mutations. Pathology-Research and Practice, 216(9), 153100.

Alasiri, G., Jiramongkol, Y., Trakansuebkul, S., Ke, H. L., Mahmud, Z., Intuyod, K., & Lam, E. W. F. (2020). Reciprocal regulation between GCN2 (eIF2AK4) and PERK (eIF2AK3) through the JNK-FOXO3 axis to modulate cancer drug resistance and clonal survival. Molecular and Cellular Endocrinology, 515, 110932.

Hu, G., Yu, Y., Tang, Y. J., Wu, C., Long, F., & Karner, C. M. (2020). The amino acid sensor Eif2ak4/GCN2 is required for proliferation of osteoblast progenitors in mice. Journal of Bone and Mineral Research, 35(10), 2004-2014.

Zeng, X., Chen, F., Rathinasabapathy, A., Li, T., Adnan Ali Mohammed Mohammed, A., & Yu, Z. (2020). Rapid disease progress in a PVOD patient carrying a novel EIF2AK4 mutation: a case report. BMC pulmonary medicine, 20(1), 1-5.

Wang, K., Cao, Y., Rong, Y., Ning, Q., Jia, P., Huang, Y., ... & Lei, C. (2019). A novel SNP in EIF2AK4 gene is associated with thermal tolerance traits in Chinese cattle. Animals, 9(6), 375.

Abou Hassan, O. K., Haidar, W., Arabi, M., Skouri, H., Bitar, F., Nemer, G., & Akl, I. B. (2019). Novel EIF2AK4 mutations in histologically proven pulmonary capillary hemangiomatosis and hereditary pulmonary arterial hypertension. BMC medical genetics, 20(1), 1-8.

Montani, D., Dorfmüller, P., Girerd, B., Le Pavec, J., Fadel, E., Simonneau, G., ... & Humbert, M. (2018). Natural history over 8 years of pulmonary vascular disease in a patient carrying biallelic EIF2AK4 mutations. American Journal of Respiratory and Critical Care Medicine, 198(4), 537-541.

Liang, L., Su, H., Ma, X., & Zhang, R. (2018). Good response to PAH-targeted drugs in a PVOD patient carrying Biallelic EIF2AK4 mutation. Respiratory research, 19(1), 1-3.

Hernandez-Gonzalez, I., Navas, P., & Escribano-Subias, P. (2018). Letter by Hernandez-Gonzalez et al Regarding Article,“Phenotypic Characterization of EIF2AK4 Mutation Carriers in a Large Cohort of Patients Diagnosed Clinically With Pulmonary Arterial Hypertension”. Circulation, 137(22), 2411-2412.

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For research use only. Not intended for any clinical use.

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