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Merck

P0074

Sigma-Aldrich

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

IgG fraction of antiserum, buffered aqueous solution

Sinónimos:

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

mol wt

antigen ~150 kDa

species reactivity

human (predicted), mouse, rat

technique(s)

western blot: 1:500-1:1,000 using whole cell lysate of HEK-293T expressing PERK cells

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

Categorías relacionadas

General description

Protein kinase RNA-like endoplasmic reticulum kinase (PERK) is one of the three mammalian unfolded protein response (UPR) transducers. It is a highly conserved eukaryotic initiation factor 2 α (eIF2α) kinase. The gene encoding this protein is localized on human chromosome 2p11.2.
Protein kinase RNA-like endoplasmic reticulum kinase (PERK) belongs to a family of eukaryotic initiation factor 2 α (eIF2α) kinases. It is a transmembrane kinase that is highly expressed in the pancreas. PERK contains two main domains: a kinase domain and an N-terminal domain like inositol- requiring enzyme-1 (IRE1), a protein involved in the unfolded protein response (UPR).

Specificity

Anti-PERK C-terminal specifically recognizes PERK.

Immunogen

synthetic peptide corresponding to amino acids 1078-1092 of mouse PERK, conjugated to KLH. This sequence is identical in rat and differs by one amino acid in human.

Application

Anti-PERK (C-terminal) antibody produced in rabbit has been used for western blotting and ERK (extracellular-signal-regulated kinase) phosphorylation assays.

Biochem/physiol Actions

Protein kinase RNA-like endoplasmic reticulum kinase (PERK) is an endoplasmic reticulum (ER) stress sensor which phosphorylates eukaryotic initiation factor 2 α (eIF2α), thereby reducing the translation of most messenger RNAs (mRNAs). In mice models of frontotemporal dementia, the suppression of translation in a PERK-eIF2α-dependent manner plays a key role in neuronal loss. PERK confers protection to heart against pressure overload-induced congestive heart failure. Mutations in this gene are linked with Wolcott-Rallison syndrome (WRS) which is characterized by permanent neonatal diabetes, exocrine-deficient pancreas, growth retardation and osteopenia.
Protein kinase RNA-like endoplasmic reticulum kinase (PERK) responds to distinct cellular stress signals.

Physical form

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

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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Storage Class

10 - Combustible liquids

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WGK 2

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The eIF2a kinase PERK limits the expression of hippocampal metabotropic glutamate receptor-dependent long-term depression.
Trinh MA
Learning & Memory (2014)
PERK inhibition prevents tau-mediated neurodegeneration in a mouse model of frontotemporal dementia.
Radford H
Acta Neuropathologica (2015)
Role of the C-terminal di-leucine motif of 5-HT1A and 5-HT1B serotonin receptors in plasma membrane targeting
Damien Carrel
Journal of Cell Science (2006)
Perk gene dosage regulates glucose homeostasis by modulating pancreatic ?-cell functions.
Perk gene dosage regulates glucose homeostasis by modulating pancreatic ?-cell functions.
Wang R
PLoS ONE (2014)
Endoplasmic reticulum stress sensor protein kinase R-like endoplasmic reticulum kinase (PERK) protects against pressure overload-induced heart failure and lung remodeling.
Hypertension (2014)

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