biological source
rabbit
conjugate
unconjugated
antibody form
IgG fraction of antiserum
antibody product type
primary antibodies
clone
polyclonal
form
buffered aqueous solution
species reactivity
mouse, rat
technique(s)
western blot: 1:500-1:1,000 using whole cell lysates of HEK-293T expressing PERK
UniProt accession no.
shipped in
dry ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
mouse ... Eif2ak3(13666)
rat ... Eif2ak3(29702)
General description
PERK (also known as eIF2AK3, PEK and WRS) is a transmembrane kinase that is highly expressed in thepancreas. It resides in the ER and couples stress signals initiated by protein malfolding in the ER lumen to eIF2α phosphorylation and reduces protei
Protein kinase RNA-like endoplasmic reticulum kinase (PERK) is one of the three mammalian UPR (unfolded protein response) transducers; the other two being activating transcription factor 6 (ATF6), and inositol-requiring enzyme 1 (IRE1). It is a highly conserved eIF2a (eukaryotic initiation factor 2 α) kinase.
Immunogen
synthetic peptide corresponding to amino acids 124-139 of mouse PERK, conjugated to KLH. This sequence is identical in rat and mouse.
Application
Anti-PERK (N-terminal) antibody produced in rabbit may be used in immunoblotting.
Biochem/physiol Actions
Anti-PERK (N-terminal) specifically recognizes mouse and rat PERK.
Protein kinase RNA-like endoplasmic reticulum kinase (PERK) is an ER stress sensor which phosphorylates eukaryotic initiation factor 2 α (eIF2α), thereby reducing the translation of most messenger RNAs (mRNAs). This results in reduction of protein load in the ER lumen. In S63del-Charcot-Marie-Tooth 1B neuropathy mice model, the suppression of PERK results in improved myelination. In mice models of frontotemporal dementia, the suppression of translation in a PERK-eIF2α-dependent manner plays a key role in neuronal loss. Administration of GSK2606414, a PERK inhibitor, results in suppression of tau-mediated neurodegeneration. PERK confers protection to heart against pressure overload-induced congestive heart failure. Mutations in this gene are linked with Wolcott-Rallison syndrome (WRS) in humans, which is characterized by permanent neonatal diabetes, exocrine-deficient pancreas, growth retardation, and osteopenia.
Physical form
Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.
Preparation Note
For continuous use, store at 2-8 °C for up to one month. For extended storage, freeze in working aliquots. Repeated freezing and thawing, or storage in “frost-free” freezers is also not recommended. If slight turbidity occurs upon prolonged storage, clarify the solution by centrifugation before use. Working dilutions should be discarded if not used within 12 hours.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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存储类别
10 - Combustible liquids
wgk
WGK 2
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)
法规信息
常规特殊物品
常规特殊物品
低风险生物材料
此项目有
Perk gene dosage regulates glucose homeostasis by modulating pancreatic ?-cell functions.
Wang R et al
PLoS ONE, 9(6), e99684-e99684 (2014)
The eIF2a kinase PERK limits the expression of hippocampal metabotropic glutamate receptor-dependent long-term depression.
Trinh MA et al
Learning & Memory, 21(5), 298-304 (2014)
PERK inhibition prevents tau-mediated neurodegeneration in a mouse model of frontotemporal dementia.
Radford H et al
Acta Neuropathologica, 130(5), 633-642 (2015)
Perk Ablation Ameliorates Myelination in S63del-Charcot-Marie-Tooth 1B Neuropathy.
Musner N et al
ASN Neuro, 8(2) (2016)
Mohamad A Zaini et al.
Scientific reports, 7, 42603-42603 (2017-02-16)
An important part of the beneficial effects of calorie restriction (CR) on healthspan and lifespan is mediated through regulation of protein synthesis that is under control of the mechanistic target of rapamycin complex 1 (mTORC1). As one of its activities
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