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Human Polyclonal EIF2AK4 Primary Antibody for IHC (p), WB - ABIN391197
Lu, László, Miao, Chen, Wu: The role of nitric-oxide synthase in the regulation of UVB light-induced phosphorylation of the alpha subunit of eukaryotic initiation factor 2. in The Journal of biological chemistry 2009
Show all 2 Pubmed References
Human Polyclonal EIF2AK4 Primary Antibody for IP, WB - ABIN151140
Rahmani, Davis, Crabtree, Habibi, Nguyen, Dent, Grant: The kinase inhibitor sorafenib induces cell death through a process involving induction of endoplasmic reticulum stress. in Molecular and cellular biology 2007
Human Polyclonal EIF2AK4 Primary Antibody for IF (p), IHC (p) - ABIN684943
Lehman, Ryeom, Koumenis: Signaling through alternative Integrated Stress Response pathways compensates for GCN2 loss in a mouse model of soft tissue sarcoma. in Scientific reports 2015
Diet-driven interferon-gamma enhances malignant transformation of primary bovine mammary epithelial cells through nutrient sensor GCN2-activated autophagy.
Data show that siRNA-mediated depletion of general control nonderepressible 2 (GCN2) increases small RNA transcripts such as tRNA and 5S rRNA, and induces the p53 (show TP53 Antibodies) pathway activation.
in response to vemurafenib, BRAF (show BRAF Antibodies)-mutated melanoma and colorectal cancer cells rapidly induced the ISR as a cytoprotective mechanism through activation of general control nonderepressible 2 (GCN2), an eIF2alpha (show EIF2A Antibodies) kinase sensing amino acid levels
A novel homozygous EIF2AK4 mutation (c.257+4A>C) was identified in 1 of 9 (11.1%) patients diagnosed with HPAH. The novel EIF2AK4 mutation (c.257+4A>C) was homozygous in two sisters with severe pulmonary hypertension. None of the 72 patients with IPAH had biallelic EIF2AK4 mutations.
This is the first reported case of EIF2AK4 mutation in PVOD in a Chinese patient population. We found the frameshift EIF2AK4 mutation c.1392delT (p.Arg465fs) in this case.
IDO (show IDO1 Antibodies), through GCN2 kinase activation, downregulates the levels of TCRcomplex tchain and cMyc (show MYC Antibodies), resulting in the suppression of Tcell proliferation and a reduction in the levels of LDHA (show LDHA Antibodies) and GLS2 (show GLS2 Antibodies)
EIF2AK4 mutation was associated with pulmonary veno-occlusive disease. PVOD patients who were not significantly exposed to trichloroethylene were more likely to harbour EIF2AK4 mutations.
Data show that sequenced eukaryotic translation initiation factor 2 alpha kinase 4 protein (EIF2AK4) with a homozygous mutation in all five families: c.3344C>T(p.P1115L).
Targeting ALDH18A1 activated the serine/threonine protein kinase GCN2 (general control nonderepressible 2) to inhibit protein synthesis in melanoma.
Upon deprivation of various amino acids, activated GCN2 up-regulates ATF4 (show ATF4 Antibodies) to induce expression of the stress response protein Sestrin2, which is required to sustain repression of mTORC1 by blocking its lysosomal localization
The data of this study suggest an important contribution of the General control non-derepressible 2 (GCN2) in T cell stress response to the resolution of autoimmune neuroinflammation.
GCN2 activation increased phosphorylation of its substrate eIF2alpha (show EIF2A Antibodies) and the induction of the integrated stress response master regulator, ATF4 (show ATF4 Antibodies).
GCN2 predisposes the exocrine pancreas to a maladaptive ER stress response and autophagy during asparaginase treatment.
Inhibition of eIF2alpha phosphorylation via PERK suppression and reversal of de novo protein synthesis deficits can mitigate cognitive deficits in neurodegenerative diseases.
Dietary EAA sensing depends on physiologic need, but not GCN2.
acute amino acid starvation suppressed intestinal inflammation via a mechanism dependent on GCN2; hence, results reveal a mechanism that couples amino acid sensing with control of intestinal inflammation via GCN2
Gcn2 & Atf4 (show ATF4 Antibodies) are involved in L-proline metabolism regulation in embryonic stem cells.
Metabolic stress signals delivered by GCN2 inhibit innate inflammatory responses to apoptotic cells, restricting adaptive immunity and preventing autoimmunity. GCN2 activation by halofunginone halobromide potently reduced autoimmune reactivity.
p58IPK is a general inhibitor of the eIF2alpha kinases in that it also interacts with GCN2. Thus forced overexpression of cytoplasmic p58 delays eIF2alpha phosphorylation, suppresses GCN2 phosphorylation and prolongs protein synthesis
EIF2AK4 belongs to a family of kinases that phosphorylate the alpha subunit of eukaryotic translation initiation factor-2 (EIF2S1\; MIM 603907) to downregulate protein synthesis in response to varied cellular stresses (Berlanga et al., 1999
eukaryotic translation initiation factor 2 alpha kinase 4
, eukaryotic translation initiation factor 2-alpha kinase 4-like
, GCN2 protein
, GCN2 eIF2alpha kinase
, GCN2-like protein
, eukaryotic translation initiation factor 2-alpha kinase 4