Phospho-PERK(T981) Monoclonal Antibody

Shipped with Ice Packs
In Stock

Description

Antibody Characteristics

Target: Phosphorylated PERK (Thr981) in humans, mice, and rats .
Host Species: Mouse or Rabbit , depending on the product.
Clonality: Monoclonal (single epitope specificity) .
Immunogen: Synthesized peptide derived from human PERK around Thr981 .
Reactivity: Human, Mouse, Rat .
Applications:

ApplicationDilution RangeKey Validations (Sources)
Western Blot1:500–1:2000Detected 125 kDa band in ER-stressed cells .
Immunofluorescence1:50–1:200Localized to ER membrane in HeLa cells .
Immunohistochemistry1:100–1:300Stained paraffin-embedded tissues (e.g., rat lung, human prostate) .
ELISA1:40,000Specificity confirmed via phosphopeptide assays .

Specificity: Binds exclusively to PERK phosphorylated at Thr981, validated via peptide blocking assays .

Key Findings from Experimental Use:

  • Western Blot: Detected PERK phosphorylation in HeLa, AD293, and 453 cell lines under ER stress . Thapsigargin and tunicamycin treatments increased phosphorylation levels .

  • Immunofluorescence: Showed ER membrane localization in cervical carcinoma cells, consistent with PERK’s role in ER stress .

  • Tissue Staining: Positive signals in rat heart, kidney, and human prostate carcinoma tissues .

Cross-Reactivity:

Species ReactivityValidation MethodSource
HumanIF, IHC, WB
MouseIHC (kidney tissue)
RatWB, IHC (lung/heart)

Disease Associations:

  • Wolcott-Rallison Syndrome: Linked to EIF2AK3 (PERK) mutations .

  • Cancer: Overexpression observed in cervical and prostate carcinomas .

  • Diabetes: ER stress in pancreatic β-cells correlates with PERK activation .

Key Publications:

  • Brain and Pancreas: PERK expression confirmed via PubMed IDs 14702039 and 10677345 .

  • Liver and Testis: Detected in studies (PubMed ID: 10026192) .

Technical Considerations

  • Fixation: Paraformaldehyde (PFA) recommended for optimal epitope preservation .

  • Controls: Include non-phosphopeptide blocks to confirm specificity .

  • Secondary Antibodies: Compatible with HRP-, AP-, or fluorophore-conjugated reagents .

Product Specs

Buffer
Preservative: 0.03% Proclin 300
Constituents: 50% Glycerol, 0.01M PBS, pH 7.4
Form
Liquid
Lead Time
Generally, we can ship the products within 1-3 business days after receiving your order. Delivery time may vary depending on the purchasing method or location. Please consult your local distributor for specific delivery timeframes.
Synonyms
DKFZp781H1925 antibody; E2AK3_HUMAN antibody; EC 2.7.11.1 antibody; Eif2ak3 antibody; Eukaryotic translation initiation factor 2 alpha kinase 3 antibody; Eukaryotic translation initiation factor 2-alpha kinase 3 antibody; Heme regulated EIF2 alpha kinase antibody; HRI antibody; HsPEK antibody; Pancreatic eIF2 alpha kinase antibody; Pancreatic eIF2-alpha kinase antibody; PEK antibody; PRKR like endoplasmic reticulum kinase antibody; PRKR-like endoplasmic reticulum kinase antibody; WRS antibody
Target Names
Uniprot No.

Target Background

Function
PERK is a metabolic-stress sensing protein kinase that phosphorylates the alpha subunit of eukaryotic translation initiation factor 2 (EIF2S1/eIF-2-alpha) in response to various stress conditions. It serves as a key activator of the integrated stress response (ISR), which is crucial for adaptation to various stressors, including the unfolded protein response (UPR) and low amino acid availability. Upon stress, phosphorylation of EIF2S1/eIF-2-alpha by PERK transforms EIF2S1/eIF-2-alpha into a global protein synthesis inhibitor, leading to a general suppression of cap-dependent translation. Simultaneously, this phosphorylation initiates the preferential translation of ISR-specific mRNAs, such as the transcriptional activators ATF4 and QRICH1. This allows ATF4- and QRICH1-mediated cellular reprogramming in response to stress. PERK plays a critical role in unfolded protein response (UPR)-induced G1 growth arrest due to the loss of cyclin-D1 (CCND1). It is also involved in regulating mitochondrial morphology and function.
Gene References Into Functions
  1. Phosphorylated PERK and ATF4 were found to be upregulated in Orexin neurons in Sudden Infant Death Syndrome (SIDS) compared to non-SIDS. PMID: 27796753
  2. This research evaluates the clinical features of patients with the W522X mutation in the PERK gene and compares them to other reported cases. While diabetes mellitus and epiphyseal dysplasia are characteristic features, all individuals with Wolcott-Rallison syndrome, including those with the W522X mutation, exhibit extensive phenotypic variability that does not strongly correlate with genotype. PMID: 30204972
  3. PERK acts as a master regulator, dictating pancreatic beta cell homeostasis during development and in the context of diabetes. (Review) PMID: 29168198
  4. Evidence suggests that PERK activation is part of a protective response to mutant rhodopsin, ultimately limiting photoreceptor cell death. PMID: 29036441
  5. Three branches of the Unfolded Protein Response (UPR) have been characterized, including the activation of the inositol-requiring enzyme 1 (IRE1), the pancreatic ER kinase (PKR)-like ER kinase (PERK), and the activating transcription factor 6 (ATF6). PMID: 28105371
  6. This study demonstrates that adaptation to endoplasmic reticulum (ER) stress in cancer cells produces a multidrug resistance phenotype. The PERK/Nrf2/MRP1 axis is responsible for resistance to ER stress and chemotherapy, and may represent a promising therapeutic target in aggressive and resistant tumors. PMID: 28499449
  7. miR-204 targets PERK and regulates UPR signaling and beta-cell apoptosis. PMID: 27384111
  8. Novel findings indicate that HMGB1 triggers EPC apoptosis through a mechanism involving RAGE-mediated activation of the PERK/eIF2alpha pathway. PMID: 28251435
  9. PERK plays a role in mediating the internal ribosome entry site-dependent translational activation of mRNAs encoding angiogenic growth factors following ischemic stress. PMID: 27141928
  10. This research reveals for the first time that the adaptation to endoplasmic reticulum (ER) stress in cervical cancer cells (HeLa and CaSki) results in a survival advantage through coordinated IRE1 and PERK signaling. PMID: 28358375
  11. NDRG2 is a novel ERS-responsive protein that acts as a PERK co-factor to facilitate PERK pathway activation, contributing to ERS-induced apoptosis. PMID: 28948615
  12. To elucidate the mechanism by which the PERK luminal domain interacts with misfolded proteins, the crystal structure of the human PERK luminal domain was determined at 3.2 A resolution. The structure reveals two dimers of the PERK luminal domain forming a tetramer in the asymmetric unit. PMID: 27917829
  13. These findings suggest that dual targeting of the PI3K and PERK pathways may improve clinical prognosis and enhance the treatment of ESCC patients. PMID: 28867195
  14. The study reports the role of neutrophil elastase in the activation of unfolded protein response effector molecules via PERK and CHOP. PMID: 28507169
  15. High PERK expression is associated with gastrointestinal neuroendocrine tumors. PMID: 28423496
  16. The PERK-eIF2alpha-ATF4-CHOP signaling pathway plays a critical role in tumor progression during endoplasmic reticulum stress. (Review) PMID: 27211800
  17. This research uncovers a new aspect of PERK function and previously unknown roles for Claspin and Chk1 as negative regulators of DNA replication in the absence of genotoxic stress. PMID: 27375025
  18. These data indicate that PERK regulates radioresistance in oropharyngeal carcinoma through NF-kB activation-mediated phosphorylation of eIF2alpha. PMID: 28418119
  19. The actin regulator FLNA interacts with the endoplasmic reticulum stress kinase PERK, and this interaction is essential for the efficient formation of ER-plasma membrane contact sites. PMID: 28238652
  20. SLC30A10 plays a protective role in 1-methyl-4-phenylpyridinium-induced toxicity via the PERK-ATF4 pathway. PMID: 28688763
  21. This research reveals distinct binding affinities between binary and ternary complexes, suggesting a preference for the PERK signaling branch under stress conditions and a predilection for the GRP78-UPR sensor complex formation upon stressor removal. These findings imply a gated UPR mechanism that fine-tunes overall cellular behavior in response to the accumulation of unfolded proteins. PMID: 28416388
  22. PERK is involved in multivesicular body information during endoplasmic reticulum stress. PMID: 27725157
  23. This research suggests that PERK signaling promotes medulloblastoma tumorigenesis by attenuating apoptosis of premalignant granule cell precursors during malignant transformation. PMID: 27181404
  24. This study demonstrates that small molecule PERK inhibitors exhibit single-agent efficacy against BrafV600E-dependent tumors, highlighting the clinical value of targeting PERK. PMID: 27977682
  25. A novel homozygous nonsense mutation (p.Q333) in exon 5 of the eukaryotic translation initiation factor 2-alpha kinase 3 (EIF2AK3) gene was identified in a Wolcott-Rallison syndrome patient. Notably, her parents were first-degree cousins with heterozygous mutations in the EIF2AK3 gene. PMID: 27145240
  26. BiP/GRP78 and PERK were found to be highly expressed. PMID: 27502501
  27. The PERK-eIF2alpha-ATF4 signaling pathway mediated by endoplasmic reticulum stress is involved in osteoblast differentiation of periodontal ligament cells under cyclic mechanical force. PMID: 27079961
  28. ER stress assessed by the expression of PERK and p-eIF2alpha was significantly associated with tumor infiltrating lymphocytes in HER2-positive breast cancer. PMID: 27272779
  29. Influenza A virus downregulates the host unfolded protein response mediated by the PERK protein. PMID: 27094326
  30. Using drugs that specifically inhibit or activate the PERK or IRE1alpha sensors, this research demonstrates that signaling through the PERK axis activates expression through a transcriptional mechanism. PMID: 26634309
  31. Data show that CGK733 induced microtubule associated protein LC3B formation upstream of AMP-activated protein kinase and protein kinase RNA-like endoplasmic reticulum kinase/CCAAT-enhancer-binding protein homologous protein pathways and p21 Cip1 expression. PMID: 26486079
  32. Nitric oxide can S-nitrosylate the endoplasmic reticulum stress sensors IRE1alapha and PERK. PMID: 26446798
  33. Data from two consanguineous families suggest that EIF2AK3 mutations (c.1337_1338insT/p.K346*; c.3009C>T/p.R903*) are responsible for Wolcott-Rallison syndrome. Ultrastructural features of autopsy materials suggest endoplasmic reticulum dysfunction. [CASE STUDIES] PMID: 25131821
  34. Data indicated that CGK733-induced intracellular calcium sequestration in pancreatic tumor cells is correlated with the PERK/CHOP signaling pathway and may also be involved in the dysregulations of calcium-binding proteins. PMID: 26259235
  35. Data indicated that the relative timing of IRE1 and PERK signaling determines the shift from cell survival to apoptosis. PMID: 25633195
  36. In human alveolar epithelial A549 cells, Lipopolysaccharide induces autophagic cell death that depends on the activation of the PERK branch of the unfolded protein response upon endoplasmic reticulum (ER) stress. PMID: 26279443
  37. This review focuses on the novel, intriguing, and complex role of PERK in ER stress-decided cell fate and also discusses additional roles of PERK in restoring cellular homeostasis. PMID: 26225772
  38. This study demonstrates a new role for CREB as a regulator of ER stress, which is required to properly respond to stressful conditions, such as hypoxia. PMID: 26642955
  39. PERK-activated osteosarcomatous autophagy via inhibition of the mTORC1 pathway prevents cell apoptosis. PMID: 26078722
  40. These results reveal that PERK activation is involved in glioma glycolysis regulation and may be a potential molecular target for glioma treatment. PMID: 25761777
  41. These findings confirm that HIV infection activates stress-response components and that antiretroviral therapy contributes to changes in the unfolded protein response activation profile. PMID: 25976933
  42. This research discovers that BiP is a dual-functional UPR sensor, sensing unfolded proteins through canonical binding to substrates and transducing this event to noncanonical, signaling interactions with Ire1 and Perk. PMID: 25692299
  43. ER stress-induced apoptosis was important in the development of SPE, especially in early-onset SPE, and was likely due to the activation of the PERK signaling pathway. PMID: 25675914
  44. ER stress-PERK-GSK3alpha/beta signaling promotes proatherogenic macrophage lipid accumulation. PMID: 25183803
  45. Interface mutations that disrupt tetramer formation in vitro reduce phosphorylation of PERK and its target eIF2alpha in cells. PMID: 25925385
  46. TBL2 interacts with PERK via the N-terminus proximal region and also associates with eIF2a via the WD40 domain, thus modulating stress-signaling and cell survival during endoplasmic reticulum stress. PMID: 25393282
  47. In erythroid cells, pull-down experiments identified the presence of a novel complex formed by HDAC5, GATA1, EKLF, and pERK, which was instead undetectable in cells of the megakaryocytic lineage. PMID: 24594363
  48. To enable a detailed study of PERK signaling, an analog-sensitive PERK allele was generated that accepts N(6)-alkylated ATP analogs. PMID: 24846185
  49. Neoplastic de-differentiation confers multidrug resistance via non-canonical PERK-Nrf2 signaling. PMID: 25203443
  50. This study demonstrates that excessive NO generation in RPE cells can have an unanticipated effect by activating PERK pathways in ECs, resulting in a novel mechanism for vascular endothelium to avoid injury from prolonged hyperglycemia. PMID: 24813399

Show More

Hide All

Database Links

HGNC: 3255

OMIM: 226980

KEGG: hsa:9451

STRING: 9606.ENSP00000307235

UniGene: Hs.591589

Involvement In Disease
Wolcott-Rallison syndrome (WRS)
Protein Families
Protein kinase superfamily, Ser/Thr protein kinase family, GCN2 subfamily
Subcellular Location
Endoplasmic reticulum membrane; Single-pass type I membrane protein.
Tissue Specificity
Ubiquitous. A high level expression is seen in secretory tissues.

Quick Inquiry

Personal Email Detected
Please use an institutional or corporate email address for inquiries. Personal email accounts ( such as Gmail, Yahoo, and Outlook) are not accepted. *
© Copyright 2025 TheBiotek. All Rights Reserved.