PERK Positive Control peptide (STJ504690)
SPECIFICATIONS
General Information
| Short Description | PERK Positive Control is synthetically produced from the sequence and is suitable for use in western blot applications. |
| Applications | WB |
| Note | STRICTLY FOR FURTHER SCIENTIFIC RESEARCH USE ONLY (RUO). MUST NOT TO BE USED IN DIAGNOSTIC OR THERAPEUTIC APPLICATIONS. |
Product Properties
| Dilution Range | WB: 1:500 |
| 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 |
| Storage Instruction | Store at-20°C for long term storage. Avoid freeze-thaw cycles. |
Target Information
| Gene Symbol | EIF2AK3 |
| Gene ID | 9451 |
| Uniprot ID | E2AK3_HUMAN |
Additional Info
| 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 EIF2AK3/PERK trans-autophosphorylation of the C-terminal cytoplasmic kinase domain at multiple residues including Thr-982 on the kinase activation loop. Autophosphorylated at Tyr-619 following endoplasmic reticulum stress, leading to activate its activity. Dephosphorylated at Tyr-619 by PTPN1/PTP1B, leading to inactivate its enzyme activity. Phosphorylation at Thr-802 by AKT (AKT1, AKT2 and/or AKT3) inactivates EIF2AK3/PERK. 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. |
| Peptide Name | Eukaryotic Translation Initiation Factor 2-Alpha Kinase 3Prkr-Like Endoplasmic Reticulum KinasePancreatic Eif2-Alpha KinaseHspekProtein Tyrosine Kinase Eif2ak3 |
| Database Links | Reactome: R-HSA-381042Reactome: R-HSA-9700645Reactome: R-HSA-9725370Reactome: R-HSA-9755511 |
| Cellular Localisation | Endoplasmic Reticulum MembraneSingle-Pass Type I Membrane ProteinLocalizes To The Localizes To Endoplasmic Reticulum MembraneAlso Present At Mitochondria-Endoplasmic Reticulum Contact SitesWhere It Interacts With Atad3a |
| Alternative Peptide Names | Eukaryotic Translation Initiation Factor 2-Alpha Kinase 3 proteinPrkr-Like Endoplasmic Reticulum Kinase proteinPancreatic Eif2-Alpha Kinase proteinHspek proteinProtein Tyrosine Kinase Eif2ak3 proteinEIF2AK3 proteinPEK proteinPERK protein |
Information sourced from Uniprot.org