Applications: |
WB |
Note: |
STRICTLY FOR FURTHER SCIENTIFIC RESEARCH USE ONLY (RUO). MUST NOT TO BE USED IN DIAGNOSTIC OR THERAPEUTIC APPLICATIONS. |
Short Description: |
PERK Positive Control is synthetically produced from the sequence and is suitable for use in western blot applications. |
Formulation: |
Provided as 100 uL ready-to-use, in SDS-PAGE sample buffer (Laemelli's buffer) containing Tris, pH 6.8, 1 % SDS, Glycerol and Bromophenolblue blue as tracking dye. The sample is reduced by adding 2% beta mercaptoethanol. The protein concentration is |
Dilution Range: |
WB: 1:500 |
Storage Instruction: |
Store at-20°C for long term storage. Avoid freeze-thaw cycles. |
Tissue Specificity | Ubiquitous. A high level expression is seen in secretory tissues. |
Post Translational Modifications | Oligomerization of the N-terminal ER luminal domain by ER stress promotes PERK trans-autophosphorylation of the C-terminal cytoplasmic kinase domain at multiple residues including Thr-982 on the kinase activation loop. Autophosphorylated. Phosphorylated at Tyr-619 following endoplasmic reticulum stress, leading to activate its tyrosine-protein kinase activity. Dephosphorylated by PTPN1/TP1B, leading to inactivate its enzyme activity. 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 conditions. Key activator of the integrated stress response (ISR) required for adaptation to various stress, such as unfolded protein response (UPR) and low amino acid availability. 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. 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. |
Peptide Name | Eukaryotic Translation Initiation Factor 2-Alpha Kinase 3Prkr-Like Endoplasmic Reticulum KinasePancreatic Eif2-Alpha KinaseHspek |
Database Links | Reactome: R-HSA-381042Reactome: R-HSA-9700645Reactome: R-HSA-9725370 |
Cellular Localisation | Endoplasmic Reticulum MembraneSingle-Pass Type I Membrane Protein |
Alternative Peptide Names | Eukaryotic Translation Initiation Factor 2-Alpha Kinase 3 proteinPrkr-Like Endoplasmic Reticulum Kinase proteinPancreatic Eif2-Alpha Kinase proteinHspek proteinEIF2AK3 proteinPEK proteinPERK protein |
Information sourced from Uniprot.org
12 months for antibodies. 6 months for ELISA Kits. Please see website T&Cs for further guidance