PLK1 Antibody

• 产品编号：CST-4535S      品牌：CST       原厂货号：4535S
• 产品分类：抗体 > 一抗 > 蛋白特异性一抗
• 应用分类：

描述：

PLK1 Antibody 能够独立于磷酸化状态检测内源性PLK1蛋白。该多克隆抗体是由合成的人源的针对PLK1蛋白羧基末端的肽段免疫动物，采用蛋白A和多肽亲和层析技术纯化生产的。 哺乳动物细胞中至少存在四种polo样激酶：PLK1，PLK2，PLK3和PLK4/SAK(1)。PLK1在有丝分裂中发挥多种作用，尤其是调节有丝分裂的进入和离开。有丝分裂促进因子(MPF)，cdc2/cyclin B1，通过cdc25C介导的cdc2去磷酸化而被激活。PLK1能够磷酸化cdc25C的第198位丝氨酸和周期蛋白B1的第133位丝氨酸，从而导致这些蛋白从细胞质向细胞核转移(2-5)。PLK1磷酸化Myt1的第426位丝氨酸和495位苏氨酸被认为能够失活Myt1，它是一种可以磷酸化cdc2第14位和15位苏氨酸的蛋白激酶(6)。Polo样蛋白激酶也可以磷酸化粘连蛋白亚基SCC1，引起染色体臂的粘连蛋白移位，促进粘连蛋白的中心体适当定位(7)。有丝分裂的退出需要激活后期促进复合物(APC)，一种负责中心体粘连蛋白清除的泛素连接酶并能够降解分离酶抑制蛋白，周期蛋白A，周期蛋白B1，极光激酶A和cdc20(9)。体外研究已表明PLK1磷酸化APC亚基Apc1，cdc16和cdc27，且被认为是一种调节有丝分裂退出的机制(10,11)。

1. Nigg, E.A. (1998) Curr. Opin. Cell Biol. 10, 776-783.
2. Toyoshima-Morimoto, F. et al. (2002) EMBO Rep. 3, 341-348.
3. Toyoshima-Morimoto, F. et al. (2001) Nature 410, 215-220.
4. Peter, M. et al. (2002) EMBO Rep. 3, 551-556.
5. Jackman, M. et al. (2003) Nat. Cell Biol. 5, 143-148.
6. Nakajima, H. et al. (2003) J. Biol. Chem. 278, 25277-25280.
7. Sumara, I. et al. (2002) Mol. Cell 9, 515-525.
8. Hauf, S. et al. (2001) Science 293, 1320-1323.
9. Peters, J.M. (1999) Exp. Cell Res. 248, 339-349.
10. Kraft, C. et al. (2003) EMBO J. 22, 6598-6609.
11. Kotani, S. et al. (1998) Mol. Cell 1, 371-380.
12. Jang, Y.J. et al. (2002) J Biol Chem 277, 44115-20.
13. Smits, V.A. et al. (2000) Nat Cell Biol 2, 672-6.
14. Tsvetkov, L. and Stern, D.F. (2005) Cell Cycle 4, 166-71.

原厂资料：

Homology

Species predicted to react based on 100% sequence homology: Pig

Specificity / Sensitivity

PLK1 Antibody detects endogenous levels of PLK1 independent of phosphorylation.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human PLK1. Antibodies are purified by protein A and peptide affinity chromatography.

Background

At least 4 distinct polo-like kinases exist in mammalian cells: PLK1, PLK2, PLK3 and PLK4/SAK (1). PLK1 apparently plays many roles during mitosis, particularly in regulating mitotic entry and exit. The mitosis promoting factor (MPF), cdc2/cyclin B1, is activated by dephosphorylation of cdc2 (Thr14/Tyr15) by cdc25C. PLK1 phosphorylates cdc25C at Ser198 and cyclin B1 at Ser133 causing translocation of these proteins from the cytoplasm to the nucleus (2-5). PLK1 phosphorylation of Myt1 at Ser426 and Thr495 has been proposed to inactivate Myt1, one of the kinases known to phosphorylate cdc2 at Thr14/Tyr15 (6). Polo-like kinases also phosphorylate the cohesin subunit SCC1, causing cohesin displacement from chromosome arms that allow for proper cohesin localization to centromeres (7). Mitotic exit requires activation of the anaphase promoting complex (APC) (8), a ubiquitin ligase responsible for removal of cohesin at centromeres, and degradation of securin, cyclin A, cyclin B1, Aurora A and cdc20 (9). PLK1 phosphorylation of the APC subunits Apc1, cdc16 and cdc27 has been demonstrated in vitro and has been proposed as a mechanism by which mitotic exit is regulated (10,11). 

1. Nigg, E.A. (1998) Curr. Opin. Cell Biol. 10, 776-783.
2. Toyoshima-Morimoto, F. et al. (2002) EMBO Rep. 3, 341-348.
3. Toyoshima-Morimoto, F. et al. (2001) Nature 410, 215-220.
4. Peter, M. et al. (2002) EMBO Rep. 3, 551-556.
5. Jackman, M. et al. (2003) Nat. Cell Biol. 5, 143-148.
6. Nakajima, H. et al. (2003) J. Biol. Chem. 278, 25277-25280.
7. Sumara, I. et al. (2002) Mol. Cell 9, 515-525.
8. Hauf, S. et al. (2001) Science 293, 1320-1323.
9. Peters, J.M. (1999) Exp. Cell Res. 248, 339-349.
10. Kraft, C. et al. (2003) EMBO J. 22, 6598-6609.
11. Kotani, S. et al. (1998) Mol. Cell 1, 371-380.
12. Jang, Y.J. et al. (2002) J Biol Chem 277, 44115-20.
13. Smits, V.A. et al. (2000) Nat Cell Biol 2, 672-6.
14. Tsvetkov, L. and Stern, D.F. (2005) Cell Cycle 4, 166-71.

注意事项：

Storage: Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM
NaCl, 100 µg/ml BSA and 50% glycerol. Store at –20°C.
Do not aliquot the antibody.