Product Pathways - Translational Control
PERK (D11A8) Rabbit mAb #5683
|W IP IHC-P||H||Endogenous||140||Rabbit IgG|
Reactivity Key: H=Human
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.
Specificity / Sensitivity
PERK (D11A8) Rabbit mAb recognizes endogenous levels of total PERK protein. Staining of red blood cells has been observed. The specificity of this staining is unknown.
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu156 of human PERK protein.
Western blot analysis of extracts from various cell lines using PERK (D11A8) Rabbit mAb.
Protein kinase-like endoplasmic reticulum kinase (PERK) is an eIF2α kinase and transmembrane protein resident in the endoplasmic reticulum (ER) membrane that couples ER stress signals to translation inhibition (1-3). ER stress increases the activity of PERK, which then phosphorylates eIF2α to promote reduced translation. Research studies have demonstrated that PERK-deficient mice have defects in pancreatic β cells several weeks after birth, suggesting a role for PERK-mediated translational control in protecting secretory cells from ER stress (4). PERK activation during ER stress correlates with autophosphorylation of its cytoplasmic kinase domain (1-3). Phosphorylation of PERK at Thr980 serves as a marker for its activation status.
- Harding, H. et al. (1999) Nature 397, 271-274.
- Shi, Y. et al. (1998) Mol. Cell. Biol. 18, 7499-7509.
- Harding, H. et al. (2000) Mol. Cell 5, 897-904.
- Harding, H. et al. (2001) Mol. Cell 7, 1153-1163.
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For Research Use Only. Not For Use In Diagnostic Procedures.