Cell Signaling Technology

Product Pathways - Apoptosis

Phospho-Mcl-1 (Ser159/Thr163) Antibody #4579

No. Size Price
4579S 100 µl ( 10 western blots ) ¥3,900.00 现货查询 购买询价
4579 carrier free & custom formulation / quantityemail request
Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
W 1:1000 Human, Endogenous 42 Rabbit

Species cross-reactivity is determined by western blot.

Applications Key: W=Western Blotting,

Specificity / Sensitivity

Phospho-Mcl-1 (Ser159/Thr163) Antibody detects endogenous levels of human Mcl-1 only when phosphorylated at either Ser159 or Thr163. It also recognizes transfected levels of phosphorylated mouse Mcl-1.

Phospho-Mcl-1 (Ser159/Thr163) Antibody 能够检测内源性的Ser159或Thr163磷酸化的人源Mcl-1蛋白。该抗体也能够检测转染后表达的小鼠磷酸化Mcl-1蛋白。

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding human Ser159/Thr163. Antibodies were purified by peptide affinity chromatography.

该多克隆抗体是采用合成的人源蛋白Ser159/Thr163周围残基相对应的磷酸化多肽免疫动物而制备的。抗体由protein A和肽亲和层析技术纯化。

Western Blotting

Western Blotting

Western blot analysis of extracts from HeLa cells transfected with human Mcl-1, untreated or treated with λ-phosphatase, using Phospho-Mcl-1 (Ser159/Thr163) Antibody (upper) or with total Mcl-1 Antibody #4572 (lower).

Western blot方法检测HeLa细胞转染人Mcl-1后的提取物,未经处理(左)或λ-磷酸酶处理(右),使用抗体为Phospho-Mcl-1 (Ser159/Thr163) Antibody(上图)或total Mcl-1 Antibody #4572(下图)。

Western Blotting

Western Blotting

Western blot analysis of extracts from H929 cells, untreated or treated with the proteasome inhibitor MG132 for 2 hrs, using Phospho-Mcl-1 (Ser159/Thr163) Antibody (upper) or total Mcl-1 Antibody #4572 (lower).

Western blot方法检测 H929 细胞提取物,未经处理或蛋白酶抑制剂MG132处理2hr,使用抗体为Phospho-Mcl-1 (Ser159/Thr163) Antibody(上图)或total Mcl-1 Antibody #4572(下图)。


Mcl-1 is an anti-apoptotic member of the Bcl-2 family originally isolated from the ML-1 human myeloid leukemia cell line during phorbol ester-induced differentiation along the monocyte/macrophage pathway (1). Similar to other Bcl-2 family members, Mcl-1 localizes to the mitochondria (2), interacts with and antagonizes pro-apoptotic Bcl-2 family members (3), and inhibits apoptosis induced by a number of cytotoxic stimuli (4). Mcl-1 differs from its other family members in its regulation at both the transcriptional and post-translational level. First, Mcl-1 has an extended amino-terminal PEST region, which is responsible for its relatively short half-life (1,2). Second, unlike other family members, Mcl-1 is rapidly transcribed via a PI3K/Akt dependent pathway, resulting in its increased expression during myeloid differentiation and cytokine stimulation (1,5-7). Mcl-1 is phosphorylated in response to treatment with phorbol ester, microtubule-damaging agents, oxidative stress, and cytokine withdrawal (8-11). Phosphorylation at Thr163, the conserved MAP kinase/ERK site located within the PEST region, slows Mcl-1 protein turnover (10) but may prime the GSK-3 mediated phosphorylation at Ser159 that leads to Mcl-1 destabilization (11). Mcl-1 deficiency in mice results in peri-implantation lethality (12). In addition, conditional disruption of the corresponding mcl-1 gene shows that Mcl-1 plays an important role in early lymphoid development and in the maintenance of mature lymphocytes (13).

Mcl-1 是Bcl-2抗凋亡家族的成员,在单核细胞/巨噬细胞通路佛波酯诱导分化时,首次从ML-1人髓系白血病细胞系被分离(1) 。类似于其他 Bcl-2 家族成员,Mcl-1定位于线粒体 (2),与促凋亡Bcl-2 家族成员互作和拮抗(3),抑制细胞毒性刺激诱导的细胞凋亡(4)。与其他家族成员不同,Mcl-1的调控同时涉及了转录和转录后修饰水平。首先,Mcl-1 有一个扩展的氨基末端PEST区域,负责其相对较短的半衰期 (1,2)。第二,与其他家族成员不同,Mcl-1通过PI3K/Akt依赖的通路是迅速被转录,从而在髓细胞分化和细胞因子刺激时表达量增加 (1,5-7)。Mcl-1 在应答佛波酯处理、微管损伤试剂、氧化应激和细胞因子停药时,会被磷酸化(8-11)。磷酸化Thr163,PEST区域内保守的MAP kinase/ERK位点,磷酸化将减慢 Mcl-1 蛋白质转化 (10),但可能会刺激GSK-3介导的Ser159磷酸化,导致Mcl-的不稳定 (11)。小鼠缺乏Mcl-1会导致围着床期致死(12)。此外,条件性中断相应的 mcl-1 基因显示了Mcl-1在早期淋巴组织发育和维持的成熟淋巴细胞中发挥了重要作用(13)。

  1. Kozopas, K.M. et al. (1993) Proc Natl Acad Sci USA 90, 3516-20.
  2. Yang, T. et al. (1995) J Cell Biol 128, 1173-84.
  3. Sato, T. et al. (1994) Proc Natl Acad Sci USA 91, 9238-42.
  4. Zhou, P. et al. (1997) Blood 89, 630-43.
  5. Wang, J.M. et al. (1999) Mol Cell Biol 19, 6195-206.
  6. Jourdan, M. et al. (2003) Oncogene 22, 2950-9.
  7. Chao, J.R. et al. (1998) Mol Cell Biol 18, 4883-98.
  8. Domina, A.M. et al. (2000) J Biol Chem 275, 21688-94.
  9. Inoshita, S. et al. (2002) J Biol Chem 277, 43730-4.
  10. Domina, A.M. et al. (2004) Oncogene 23, 5301-15.
  11. Maurer, U. et al. (2006) Mol Cell 21, 749-60.
  12. Rinkenberger, J.L. et al. (2000) Genes Dev 14, 23-7.
  13. Opferman, J.T. et al. (2003) Nature 426, 671-6.

Application References

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