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。
Anti-JMY (C-terminal region) Antibody
- 产品详情
- 实验流程
- 背景知识
Application 
| WB, ICC |
|---|---|
| Primary Accession | Q9QXM1 |
| Reactivity | Rat |
| Host | Rabbit |
| Clonality | Rabbit Polyclonal |
| Isotype | IgG |
| Calculated MW | 110586 Da |
| Gene ID | 57748 |
|---|---|
| Other Names | p53 cofactor, WHDC1L3; FLJ37870; MGC163496 |
| Target/Specificity | JMY (junction mediating and regulatory protein) is a transcription co-factor, originally identified as a p300-binding protein involved in p53-dependent transcription. Upon DNA damage, JMY is released from Mdm2 inhibition and forms a complex with Strap and p300. This complex recruits PRMT5 to activate the p53 response. Through regulation of p53-dependent transcription, JMY has important roles in the DNA damage response. In addition, JMY contains three carboxyl-terminal WH2 actin binding domains which are are commonly found in WASP family proteins. JMY can bind to actin and to the Arp2/3 complex, as well as direct the assembly of actin filaments in vitro. These actin-regulating effects of JMY may have important roles in cell migration. When slow migrating HL-60 cells are differentiated into highly motile neutrophil-like cells, JMY moves from the nucleus to the cytoplasm and is concentrated at the actin-rich leading edge of cells. The loss of JMY leads to decreased cell migration in HL-60 cells. Thus, JMY represents a new class of multifunctional actin assembly factors whose activity may be regulated by cellular localization. |
| Dilution | WB~~1:1000 ICC~~N/A |
| Storage | Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | Anti-JMY (C-terminal region) Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
| Shipping | Blue Ice |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
JMY (junction mediating and regulatory protein) is a transcription co-factor, originally identified as a p300-binding protein involved in p53-dependent transcription. Upon DNA damage, JMY is released from Mdm2 inhibition and forms a complex with Strap and p300. This complex recruits PRMT5 to activate the p53 response. Through regulation of p53-dependent transcription, JMY has important roles in the DNA damage response. In addition, JMY contains three carboxyl-terminal WH2 actin binding domains which are are commonly found in WASP family proteins. JMY can bind to actin and to the Arp2/3 complex, as well as direct the assembly of actin filaments in vitro. These actin-regulating effects of JMY may have important roles in cell migration. When slow migrating HL-60 cells are differentiated into highly motile neutrophil-like cells, JMY moves from the nucleus to the cytoplasm and is concentrated at the actin-rich leading edge of cells. The loss of JMY leads to decreased cell migration in HL-60 cells. Thus, JMY represents a new class of multifunctional actin assembly factors whose activity may be regulated by cellular localization.
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