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产品信息
PEP-0425
| 应用 | 建议稀释比 | 已发表文章 |
|---|---|---|
对照试剂 (Ctrl) |
Assay-dependent | - |
阻断反应 (BLOCK) |
Assay-dependent | - |
| 产品规格 | |
|---|---|
种属反应 |
Human |
宿主/亚型 |
Not Applicable |
分类 |
Synthetic |
类型 |
Peptide |
偶联物 |
Unconjugated |
形式 |
Liquid |
浓度 |
200 µg/mL |
纯化类型 |
purified |
保存液 |
PBS, pH 7.2, with 0.1% BSA |
内含物 |
0.02% sodium azide |
保存条件 |
-20°C |
产品详细信息
This peptide corresponds to 19 amino acids near the carboxy terminus of human PDCD4.
PEP-0425 can be used as a blocking peptide with polyclonal antibody PA5-20309.
靶标信息
Apoptosis, also known as programmed cell death, plays major roles in development and normal tissue turnover in addition to tumor formation. During this process, the expression patterns of numerous genes are radically altered. One such gene is the programmed cell death protein 4 (PDCD4), whose expression was found to be upregulated in all cell lines following the onset of apoptosis. PDCD4 encodes a tumor suppressor protein whose expression is lost in carcinomas of breast, colon, lung and prostate. It can bind to and inhibit the helicase activity of the eukaryotic translation initiation factor 4A and inhibit the transactivation and transformation mediated by the transcription factor AP-1. The kinase Akt regulates PDCD4 by phosphorylation, decreasing the ability of PDCD4 to interfere with the transactivation of AP-1-responsive promoter by c-Jun. There are two known isoforms of PDCD4.
仅用于科研。不用于诊断过程。未经明确授权不得转售。
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生物信息学
蛋白别名: MGC33046; MGC33047; Neoplastic transformation inhibitor protein; nuclear antigen H731; Nuclear antigen H731-like; Programmed cell death protein 4; Protein 197/15a; RP11-348N5.4
基因别名: H731; PDCD4
UniProt ID: (Human) Q53EL6
Entrez Gene ID: (Human) 27250
分子生物学功能:
translation factor
translational protein
apoptotic process
cell aging
positive regulation of smooth muscle cell apoptotic process
negative regulation of apoptotic process
negative regulation of JUN kinase activity
negative regulation of cell cycle
negative regulation of transcription, DNA-templated
negative regulation of myofibroblast differentiation
