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Human Polyclonal EIF2AK4 Primary Antibody für 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 für 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
Human Polyclonal EIF2AK4 Primary Antibody für 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
Diet-driven interferon-gamma enhances malignant transformation of primary bovine mammary epithelial cells through nutrient sensor GCN2-activated autophagy.
EIF2AK4 mutations can also contribute to autosomal dominantly inherited pulmonary arterial hypertension.
Heritable pulmonary veno-occlusive disease and/or pulmonary capillary haemangiomatosis due to bi-allelic EIF2AK4 mutations is characterised by a younger age at diagnosis but these patients display similar disease severity compared with mutation non-carriers. Response to therapy approved for pulmonary arterial hypertension in pulmonary veno-occlusive disease and/or pulmonary capillary haemangiomatosis is rare.
Biallelic EIF2AK4 mutations are found in patients classified clinically as having idiopathic and heritable pulmonary arterial hypertension.
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 (zeige TP53 Antikörper) pathway activation.
in response to vemurafenib, BRAF (zeige BRAF Antikörper)-mutated melanoma and colorectal cancer cells rapidly induced the ISR as a cytoprotective mechanism through activation of general control nonderepressible 2 (GCN2), an eIF2alpha (zeige EIF2A Antikörper) 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 (zeige IDO1 Antikörper), through GCN2 kinase activation, downregulates the levels of TCRcomplex tchain and cMyc (zeige MYC Antikörper), resulting in the suppression of Tcell proliferation and a reduction in the levels of LDHA (zeige LDHA Antikörper) and GLS2 (zeige GLS2 Antikörper)
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.
We hypothesize that the essential role of methionine-charged initiator tRNA in forming ternary complex is responsible for the robust ability of methionine deficiency to induce ATF4 (zeige ATF4 Antikörper) and the ISR even in the absence of GCN2 or eIF2alpha (zeige EIF2A Antikörper) kinase activity.
GCN2 is only transiently required for LP-induced FGF21 (zeige FGF21 Antikörper).
GCN2 is required for normal cytotoxic T cell function.
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 (zeige EIF2A Antikörper) and the induction of the integrated stress response master regulator, ATF4 (zeige ATF4 Antikörper).
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.
Targeting ALDH18A1 activated the serine/threonine protein kinase GCN2 (general control nonderepressible 2) to inhibit protein synthesis in melanoma.
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
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