癌症的基本特征包括细胞增殖、血管生成、迁移、凋亡逃避机制和细胞永生等。找到癌症发生过程中这些通路的关键标记物和对应的抗体用于检测至关重要。
为您推荐一个泛素化位点预测神器——泛素化分析工具，可以为您的蛋白的泛素化位点作出预测和评分。
细胞自噬受体图形绘图工具为你的蛋白的细胞受体结合位点作出预测和评分，识别结合到自噬通路中的蛋白是非常重要的，便于让我们理解自噬在正常生理、病理过程中的作用，如发育、细胞分化、神经退化性疾病、压力条件下、感染和癌症。
PERK Antibody
Purified Rabbit Polyclonal Antibody (Pab)
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Application 
| WB, IP, ICC, IHC-P |
|---|---|
| Primary Accession | Q9NZJ5 |
| Reactivity | Human |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 125216 Da |
| Gene ID | 9451 |
|---|---|
| Other Names | Eukaryotic translation initiation factor 2-alpha kinase 3, PRKR-like endoplasmic reticulum kinase, Pancreatic eIF2-alpha kinase, HsPEK, EIF2AK3, PEK, PERK |
| Dilution | WB~~1:1000 IP~~N/A ICC~~N/A IHC-P~~1:50~200 |
| Format | 0.01M PBS, pH 7.2, 0.09% (W/V) Sodium azide, Glycerol 50% |
| Storage | Store at -20 °C.Stable for 12 months from date of receipt |
| Name | EIF2AK3 {ECO:0000303|PubMed:10932183, ECO:0000312|HGNC:HGNC:3255} |
|---|---|
| Function | 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, such as unfolded protein response (UPR) (PubMed:10026192, PubMed:10677345, PubMed:11907036, PubMed:12086964, PubMed:25925385, PubMed:31023583). Key effector of the integrated stress response (ISR) to unfolded proteins: EIF2AK3/PERK specifically recognizes and binds misfolded proteins, leading to its activation and EIF2S1/eIF-2-alpha phosphorylation (PubMed:10677345, PubMed:27917829, PubMed:31023583). EIF2S1/eIF-2-alpha phosphorylation in response to stress converts EIF2S1/eIF-2-alpha in a global protein synthesis inhibitor, leading to a global attenuation of cap-dependent translation, while concomitantly initiating the preferential translation of ISR-specific mRNAs, such as the transcriptional activators ATF4 and QRICH1, and hence allowing ATF4- and QRICH1-mediated reprogramming (PubMed:10026192, PubMed:10677345, PubMed:31023583, PubMed:33384352). The EIF2AK3/PERK- mediated unfolded protein response increases mitochondrial oxidative phosphorylation by promoting ATF4-mediated expression of COX7A2L/SCAF1, thereby increasing formation of respiratory chain supercomplexes (PubMed:31023583). In contrast to most subcellular compartments, mitochondria are protected from the EIF2AK3/PERK-mediated unfolded protein response due to EIF2AK3/PERK inhibition by ATAD3A at mitochondria-endoplasmic reticulum contact sites (PubMed:39116259). In addition to EIF2S1/eIF-2-alpha, also phosphorylates NFE2L2/NRF2 in response to stress, promoting release of NFE2L2/NRF2 from the BCR(KEAP1) complex, leading to nuclear accumulation and activation of NFE2L2/NRF2 (By similarity). Serves as a critical effector of unfolded protein response (UPR)-induced G1 growth arrest due to the loss of cyclin-D1 (CCND1) (By similarity). Involved in control of mitochondrial morphology and function (By similarity). |
| Cellular Location | Endoplasmic reticulum membrane {ECO:0000250|UniProtKB:Q9Z2B5}; Single-pass type I membrane protein. Note=Localizes to the Localizes to endoplasmic reticulum membrane (By similarity). Also present at mitochondria-endoplasmic reticulum contact sites; where it interacts with ATAD3A (PubMed:39116259). {ECO:0000250|UniProtKB:Q9Z2B5, ECO:0000269|PubMed:39116259} |
| Tissue Location | Ubiquitous. A high level expression is seen in secretory tissues. |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
Phosphorylates the alpha subunit of eukaryotic translation-initiation factor 2 (EIF2), leading to its inactivation and thus to a rapid reduction of translational initiation and repression of global protein synthesis. Serves as a critical effector of unfolded protein response (UPR)-induced G1 growth arrest due to the loss of cyclin-D1 (CCND1) (By similarity).
REFERENCES
Shi Y.,et al.J. Biol. Chem. 274:5723-5730(1999).
Sood R.,et al.Biochem. J. 346:281-293(2000).
Delepine M.,et al.Nat. Genet. 25:406-409(2000).
Ota T.,et al.Nat. Genet. 36:40-45(2004).
Hillier L.W.,et al.Nature 434:724-731(2005).
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