Cell Signaling Technology

Product Pathways - Cell Cycle / Checkpoint

Rb Control Proteins #9303

retinoblastoma  

Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype

Species cross-reactivity is determined by western blot.

Applications Key:

Description

Nonphosphorylated Rb-C Fusion Protein (5 µg/ml): Rb-C is expressed as a recombinant fusion protein of Rb residues 701–928 and maltose binding protein, serves as a negative control. Supplied in SDS Sample Buffer. 
 Phosphorylated Rb-C Fusion Protein (5 µg/ml): Prepared by in vitro kinase reaction with cdc2, serves as a positive control. Supplied in SDS Sample Buffer.Nonphosphorylated Rb-C Fusion Protein (5 µg/ml)非磷酸化Rb-C融合蛋白(5 µg/ml) Rb-C是Rb蛋白的701-928氨基酸残基重组融合蛋白,是麦芽糖结合蛋白,作为阴性对照。供应于SDS样品缓冲液中。Phosphorylated Rb-C Fusion Protein (5 µg/ml) 磷酸化Rb-C融合蛋白(5 µg/ml)由cdc2发挥体外激酶反应制备,作为阳性对照。供应于SDS样品缓冲液中。

Directions for Use

These lysates are useful controls for total and Phospho-Rb antibodies. However, this truncated Rb recombinant protein is not recognized by Phospho-Rb (Ser608) Antibody #2181 or Rb (D20) Rabbit mAb #9313.这些裂解液是Rb总蛋白抗体和磷酸化Rb抗体的有用的对照。然而,截短的Rb重组蛋白不被Phospho-Rb (Ser608) Antibody #2181 或 Rb (D20) Rabbit mAb #9313识别。

Background

The retinoblastoma tumor suppressor protein, Rb, regulates cell proliferation by controlling progression through the restriction point within the G1-phase of the cell cycle (1). Rb has three functionally distinct binding domains and interacts with critical regulatory proteins including the E2F family of transcription factors, c-Abl tyrosine kinase and proteins with a conserved LXCXE motif (2-4). Cell cycle-dependent phosphorylation by a CDK inhibits Rb target binding and allows cell cycle progression (5). Rb inactivation and subsequent cell cycle progression likely requires an initial phosphorylation by cyclin D-CDK4/6 followed by cyclin E-CDK2 phosphorylation (6). Specificity of different CDK/cyclin complexes has been observed in vitro (6-8) and cyclin D1 is required for Ser780 phosphorylation in vivo (9). 视网膜母细胞瘤肿瘤抑制蛋白Rb通过控制细胞周期的G1期限制点的进程来调控细胞增殖(1)。Rb具有3个功能特异的结合结构域并能够与转录因子家族的关键调节蛋白E2F、c-Abl酪氨酸激酶和具有保守的LXCXE模体蛋白相互作用(2-4)。CDK介导的细胞周期依赖性磷酸化能够抑制Rb靶向结合并允许细胞周期进程(5)。Rb的失活和随后的细胞周期进程似乎需要伴随周期蛋白E-CDK2磷酸化的cyclin D-CDK4/6初始磷酸化(6)。离体已经观察到不同CDK/cyclin复合物的特异性(6-8),而且周期蛋白D1为第780位丝氨酸在体磷酸化所必需(9)。

  1. Sherr, C.J. (1996) Science 274, 1672-7.
  2. Nevins, J.R. (1992) Science 258, 424-9.
  3. Welch, P.J. and Wang, J.Y. (1993) Cell 75, 779-90.
  4. Hu, Q.J. et al. (1990) EMBO J 9, 1147-55.
  5. Knudsen, E.S. and Wang, J.Y. (1997) Mol Cell Biol 17, 5771-83.
  6. Lundberg, A.S. and Weinberg, R.A. (1998) Mol Cell Biol 18, 753-61.
  7. Connell-Crowley, L. et al. (1997) Mol Biol Cell 8, 287-301.
  8. Kitagawa, M. et al. (1996) EMBO J 15, 7060-9.
  9. Geng, Y. et al. (2001) Proc Natl Acad Sci USA 98, 194-9.

Application References

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

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