Cell Signaling Technology

Product Pathways - PI3K / Akt Signaling

Phospho-FoxO3a (Ser294) Antibody #5538

AFX   FKHR   FKHRL-1   FoxO   foxo-3a   foxo3-a  

No. Size Price
5538S 100 µl ( 10 western blots ) ¥3,900.00 现货查询 购买询价
5538 carrier free & custom formulation / quantityemail request
Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
W 1:1000 Human,Mouse,Rat,Monkey, Endogenous 82 to 97 Rabbit
IP 1:50

Species cross-reactivity is determined by western blot.

Applications Key: W=Western Blotting, IP=Immunoprecipitation,

Homology

Species predicted to react based on 100% sequence homology: Chicken,

Specificity / Sensitivity

Phospho-FoxO3a (Ser294) Antibody detects exogenous and endogenous levels of FoxO3a protein only when phosphorylated at serine 294.

Phospho-FoxO3a (Ser294) Antibody可以检测出在serine 294位点磷酸化的内源性和外源的FoxO3a蛋白。

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide surrounding Ser294 of human FoxO3a. Antibodies are purified by protein A and peptide affinity chromatography.

多克隆抗体是采用合成的与人类FoxO3a蛋白Ser294周围序列相对应的肽段免疫动物生产的,抗体采用蛋白A和肽亲和层析法纯化。

Western Blotting

Western Blotting

Western blot analysis of extracts from C2C12 cells, untreated or H2O2 treated, using Phospho-FoxO3a (Ser294) Antibody (upper) or FoxO3a (75D8) Rabbit mAb #2497 (lower).

Western blot 分析C2C12细胞提取物,未处理组和双氧水处理组,所用抗体为Phospho-FoxO3a (Ser294) Antibody (上) 或 FoxO3a (75D8) Rabbit mAb 兔单抗#2497 (下).

Western Blotting

Western Blotting

Western blot analysis of extracts from 293T cells, transfected with tagged FoxO3a, using Phospho-FoxO3a (Ser294) Antibody.

Western blot 分析293T细胞提取物,采用FoxO3a转染,所用抗体为Phospho-FoxO3a (Ser294) Antibody

Background

The Forkhead family of transcription factors is involved in tumorigenesis of rhabdomyosarcoma and acute leukemias (1-3). Within the family, three members (FoxO1, FoxO4, and FoxO3a) have sequence similarity to the nematode orthologue DAF-16, which mediates signaling via a pathway involving IGFR1, PI3K, and Akt (4-6). Active forkhead members act as tumor suppressors by promoting cell cycle arrest and apoptosis. Increased expression of any FoxO member results in the activation of the cell cycle inhibitor p27 Kip1. Forkhead transcription factors also play a part in TGF-β-mediated upregulation of p21 Cip1, a process negatively regulated through PI3K (7). Increased proliferation results when forkhead transcription factors are inactivated through phosphorylation by Akt at Thr24, Ser256, and Ser319, which results in nuclear export and inhibition of transcription factor activity (8). Forkhead transcription factors can also be inhibited by the deacetylase sirtuin (SirT1) (9).Erk phosphorylates FoxO3a at Ser294, Ser344 and Ser425, resulting in degradation of FoxO3a through the MDM2-mediated ubiquitin-proteasome pathway. Thus, Erk promotes proliferation and tumor progression by inhibiting FoxO3a (10).。The Forkhead family of transcription factors is involved in tumorigenesis of rhabdomyosarcoma and acute leukemias (1-3). Within the family, three members (FoxO1, FoxO4, and FoxO3a) have sequence similarity to the nematode orthologue DAF-16, which mediates signaling via a pathway involving IGFR1, PI3K, and Akt (4-6). Active forkhead members act as tumor suppressors by promoting cell cycle arrest and apoptosis. Increased expression of any FoxO member results in the activation of the cell cycle inhibitor p27 Kip1. Forkhead transcription factors also play a part in TGF-β-mediated upregulation of p21 Cip1, a process negatively regulated through PI3K (7). Increased proliferation results when forkhead transcription factors are inactivated through phosphorylation by Akt at Thr24, Ser256, and Ser319, which results in nuclear export and inhibition of transcription factor activity (8). Forkhead transcription factors can also be inhibited by the deacetylase sirtuin (SirT1) (9).Erk phosphorylates FoxO3a at Ser294, Ser344 and Ser425, resulting in degradation of FoxO3a through the MDM2-mediated ubiquitin-proteasome pathway. Thus, Erk promotes proliferation and tumor progression by inhibiting FoxO3a (10).。

Forkhead转录因子家族参与横纹肌肉瘤和急性白血病的发生(1-3)。在这个家族中,三个成员(FoxO1,FoxO4和FoxO3a)与线虫的同源基因DAF-16具有序列相似度,而DAF-16介导包括IGFR1,PI3K和Akt在内的信号通路(4-6)。活化的forkhead成员作为肿瘤抑制因子,促进细胞周期阻滞和凋亡。FOXO家族任何成员的表达上调都会激活细胞周期抑制剂p27 Kip1。Forkhead转录因子也参与TGF-β介导的p21 CIP1上调,而这个上调过程可以被PI3K负调控(7)。forkhead转录因子被Akt在Thr24,Ser256以及Ser319磷酸化后而失活,导致出核转运与转录因子的活性的抑制(8),最终导致增殖增加。Forkhead转录因子活性也可以被去乙酰化酶sirtuin(SIRT1)抑制(9)。ERK在 Ser294, Ser344 和Ser425位磷酸化 FoxO3后, 导致FoxO3通过MDM2介导的泛素化-蛋白酶信号通路被降解。因此Erk通过抑制FoxO3a促进了肿瘤的增殖和发展(10)。ERK在 Ser294, Ser344 和Ser425位点磷酸化 FoxO3后, 导致FoxO3通过MDM2介导的泛素化-蛋白酶体信号通路被降解。因此Erk通过抑制FoxO3a促进了肿瘤的增殖和发展(10)。

  1. Anderson, M.J. et al. (1998) Genomics 47, 187-99.
  2. Galili, N. et al. (1993) Nat Genet 5, 230-5.
  3. Borkhardt, A. et al. (1997) Oncogene 14, 195-202.
  4. Nakae, J. et al. (1999) J Biol Chem 274, 15982-5.
  5. Rena, G. et al. (1999) J Biol Chem 274, 17179-83.
  6. Guo, S. et al. (1999) J Biol Chem 274, 17184-92.
  7. Seoane, J. et al. (2004) Cell 117, 211-23.
  8. Arden, K.C. (2004) Mol Cell 14, 416-8.
  9. Yang, Y. et al. (2005) EMBO J 24, 1021-32.
  10. Yang, J.Y. et al. (2008) Nat Cell Biol 10, 138-48.

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