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P0073

Sigma-Aldrich

Anti-PERK (N-terminal) antibody produced in rabbit

IgG fraction of antiserum, buffered aqueous solution

Synonym(s):

Anti-E2AK3, Anti-EIF2AK3, Anti-HsPEK, Anti-PEK, Anti-PRKR-like endoplasmic reticulum kinase, Anti-Pancreatic eIF2α kinase, Anti-WRS

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

Quality Level

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

General description

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.

Specificity

Anti-PERK (N-terminal) specifically recognizes mouse and rat PERK.

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

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.

Target 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

Physical form

Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.

Storage and Stability

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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Certificates of Analysis (COA)

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Perk gene dosage regulates glucose homeostasis by modulating pancreatic ?-cell functions.
Wang R et al
PLoS ONE, 9(6), e99684-e99684 (2014)
Perk Ablation Ameliorates Myelination in S63del-Charcot-Marie-Tooth 1B Neuropathy.
Musner N et al
ASN Neuro, 8(2) (2016)
PERK inhibition prevents tau-mediated neurodegeneration in a mouse model of frontotemporal dementia.
Radford H et al
Acta Neuropathologica, 130(5), 633-642 (2015)
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)
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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