Cell Signaling Technology

Product Pathways - Protein Translation

Phospho-PERK (Thr980) (16F8) Rabbit mAb #3179


No. Size Price
3179L 300 µl ( 30 western blots ) ¥8,992.00 现货查询 购买询价 防伪查询
3179S 100 µl ( 10 western blots ) ¥4,050.00 现货查询 购买询价 防伪查询
3179 carrier free & custom formulation / quantityemail request
Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
W 1:1000 Rat, Endogenous 170 Rabbit IgG

Species cross-reactivity is determined by western blot.

Applications Key: W=Western Blotting,


Species predicted to react based on 100% sequence homology: Mouse,

Specificity / Sensitivity

Phospho-PERK (Thr980) (16F8) Rabbit mAb detects endogenous levels of PERK phosphorylated at Thr980.

Phospho-PERK (Thr980) (16F8) Rabbit mAb兔单抗可识别内源性的Thr980磷酸化的PERK。

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Thr980 of mouse PERK.


Western Blotting

Western Blotting

Western blot analysis of extracts from AR42J cells untreated (-) or treated with 1 μM thapsigargin (Tg) for 20 minutes (+), using Phospho-PERK (Thr980) (16F8) Rabbit mAb.

对AR42J细胞(未处理(-),或1uM thapsigargin (Tg) (+) 处理20分钟),使用Phospho-PERK (Thr980) (16F8) Rabbit mAb兔单抗进行Western blot分析。


PERK (protein kinase-like endoplasmic reticulum kinase) 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. 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.

蛋白激酶类似的内质网激酶(PERK)是一种eIF2α激酶并且为一种定位在endoplasmic reticulum (ER) 膜上的跨膜蛋白,能够传导ER应激信号从而抑制翻译(1-3)。ER应激会提高PERK的活性,然后使eIF2α磷酸化从而增加翻译水平的降低。研究证实PERK缺失的小鼠在出生后的几周内其胰岛β细胞会出现缺陷,这也暗示着PERK介导的翻译控制在ER应激时保护分泌细胞的重要作用(4)。ER应激时PERK的活化与其胞内激酶结构域的自身磷酸化相关联(1-3)。PERK Thr980位点的磷酸化是其自身活化状态的一个标志。

  1. Harding, H. et al. (1999) Nature 397, 271-274.
  2. Shi, Y. et al. (1998) Mol. Cell. Biol. 18, 7499-7509.
  3. Harding, H. et al. (2001) Mol. Cell 7, 1153-1163.

Application References

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Companion Products

For Research Use Only. Not For Use In Diagnostic Procedures.

U.S. Patent No. 5,675,063.

Cell Signaling Technology is a trademark of Cell Signaling Technology, Inc.

Cell Signaling Technology® is a trademark of Cell Signaling Technology, Inc.

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