Mouse EIF2aK3 (Eukaryotic Translation Initiation Factor 2 Alpha Kinase 3) Sandwich ELISA Kit (STJE0008607)

SPECIFICATIONS
STJE0008607
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General Information

Short DescriptionThis EIF2aK3 Sandwich ELISA Kit is an in-vitro enzyme-linked immunosorbent assay for the measurement of samples in mouse tissue homogenates or other biological fluids..
ApplicationsELISA
ReactivityMouse
Sensitivity0.108ng/mL
Detection Limit0.312-20ng/mL
NoteSTRICTLY FOR FURTHER SCIENTIFIC RESEARCH USE ONLY (RUO). MUST NOT TO BE USED IN DIAGNOSTIC OR THERAPEUTIC APPLICATIONS.

Product Properties

Storage InstructionStore the unopened kit in the fridge at 2-8°C for up to 6 months. Once opened store individual kit contents according to components table provided with the kit.
Assay Time4.5 hrs

Target Information

Gene SymbolEif2ak3
Gene ID13666
Uniprot IDE2AK3_MOUSE
Sample Typetissue homogenates or other biological fluids.

Additional Info

Tissue Specificity Ubiquitous. Highly expressed in mouse pancreas, an organ active in protein secretion (at protein level).
Post Translational Modifications Oligomerization of the N-terminal ER luminal domain by ER stress promotes EIF2AK3/PERK trans-autophosphorylation of the C-terminal cytoplasmic kinase domain at multiple residues including Thr-980 on the kinase activation loop. Autophosphorylated at Tyr-615 following endoplasmic reticulum stress, leading to activate its activity. Dephosphorylated at Tyr-615 by PTPN1/TP1B, leading to inactivate its enzyme activity. Phosphorylation at Thr-799 by AKT (AKT1, AKT2 and/or AKT3) inactivates EIF2AK3/PERK. N-glycosylated. ADP-ribosylated by PARP16 upon ER stress, which increases kinase activity.
Function Metabolic-stress sensing protein kinase that phosphorylates the alpha subunit of eukaryotic translation initiation factor 2 (EIF2S1/eIF-2-alpha) in response to various stress, such as unfolded protein response (UPR). Key effector of the integrated stress response (ISR) to unfolded proteins: EIF2AK3/PERK specifically recognizes and binds misfolded proteins, leading to its activation and EIF2S1/eIF-2-alpha phosphorylation. 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, while concomitantly initiating the preferential translation of ISR-specific mRNAs, such as the transcriptional activators ATF4 and QRICH1, and hence allowing ATF4- and QRICH1-mediated reprogramming. The EIF2AK3/PERK-mediated unfolded protein response increases mitochondrial oxidative phosphorylation by promoting ATF4-mediated expression of COX7A2L/SCAF1, thereby increasing formation of respiratory chain supercomplexes. In contrast to most subcellular compartments, mitochondria are protected from the EIF2AK3/PERK-mediated unfolded protein response due to EIF2AK3/PERK inhibition by ATAD3A at mitochondria-endoplasmic reticulum contact sites. In addition to EIF2S1/eIF-2-alpha, also phosphorylates NFE2L2/NRF2 in response to stress, promoting release of NFE2L2/NRF2 from the BCR(KEAP1) complex, leading to nuclear accumulation and activation of NFE2L2/NRF2. Serves as a critical effector of unfolded protein response (UPR)-induced G1 growth arrest due to the loss of cyclin-D1 (CCND1). Involved in control of mitochondrial morphology and function.
Protein Name Eukaryotic Translation Initiation Factor 2-Alpha Kinase 3
Prkr-Like Endoplasmic Reticulum Kinase
Pancreatic Eif2-Alpha Kinase
Protein Tyrosine Kinase Eif2ak3
Database Links Reactome: R-MMU-381042
Cellular Localisation Endoplasmic Reticulum Membrane
Single-Pass Type I Membrane Protein
Localizes To The Localizes To Endoplasmic Reticulum Membrane
Also Present At Mitochondria-Endoplasmic Reticulum Contact Sites
Where It Interacts With Atad3a
Alternative ELISA Names Eukaryotic Translation Initiation Factor 2-Alpha Kinase 3 ELISA kit
Prkr-Like Endoplasmic Reticulum Kinase ELISA kit
Pancreatic Eif2-Alpha Kinase ELISA kit
Protein Tyrosine Kinase Eif2ak3 ELISA kit
Eif2ak3 ELISA kit
Pek ELISA kit
Perk ELISA kit
output

Information sourced from Uniprot.org

Citations

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