Cell Signaling Technology

Product Pathways - PI3K / Akt Signaling

Phospho-FoxO1 (Thr24)/FoxO3a (Thr32)/FoxO4 (Thr28) (4G6) Rabbit mAb #2599

FKHR   FKHRL-1   Fox-01   Fox-03   Fox-04   foxo 1a   FoxO-1   foxo-1a   FoxO-3   foxo-3a   FoxO-4   foxo1 a   foxo1a   foxo3-a   sc-22161  

No. Size Price
2599S 100 µl ( 10 western blots ) ¥3,900.00 现货查询 购买询价
2599T 20 µl ( 2 western blots ) ¥1,500.00 现货查询 购买询价
2599 carrier free & custom formulation / quantityemail request
Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
W 1:1000 Human,Mouse,Monkey, Endogenous 65, 78 to 82, 95 Rabbit

Species cross-reactivity is determined by western blot.

Applications Key: W=Western Blotting,

Specificity / Sensitivity

Phospho-FoxO1 (Thr24)/FoxO3a (Thr32)/Fox04 (Thr28) (4G6) Rabbit mAb detects endogenous levels of FoxO1 when phosphorylated at Thr24, of FoxO3a when phosphorylated at Thr32 or FoxO4 when phosphorylated at Thr28.

Phospho-FoxO1 (Thr24)/FoxO3a (Thr32)/Fox04 (Thr28) (4G6) Rabbit mAb兔单抗能够检测内源性的Thr24位点磷酸化的FoxO1 蛋白和Thr32位点磷酸化的FoxO3a蛋白或Thr28位点磷酸化的FoxO4蛋白。

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Thr28 of human Fox04.

该单克隆抗体是采用合成的与人FoxO4 蛋白Thr28周围序列相对应的磷酸化肽段免疫动物而生产的。

Western Blotting

Western Blotting

Western blot analysis of extracts from Jurkat cells treated with either Calyculin A (#9902) or LY294002 (#9901), NIH3T3 and COS-7 cells using Phospho-FoxO1 (Thr24)/(FoxO3a (Thr32)/FoxO4 (Thr28) (4G6) Rabbit mAb to detect FoxO1, FoxO3a and FoxO4 when phosphorylated at the Thr24, Thr32, and Thr28 positions, respectively (left panel). Total FoxO1, FoxO3a and FoxO4 were detected using FoxO1 (C29H4) Rabbit mAb (#2880), FoxO3a (75D8) Rabbit mAb (#2497) and FoxO4 Antibody (#9472), respectively (right panel).Western blot 检测分析分别用 Calyculin A (#9902) 和LY294002 (#9901)处理的Jurkat细胞,NIH3T3 细胞和 COS-7 细胞提取物,使用的抗体是 Phospho-FoxO1 (Thr24)/(FoxO3a (Thr32)/FoxO4 (Thr28) (4G6) Rabbit mAb检测分别在24,32和28位点的苏氨酸磷酸化修饰的 FoxO1, FoxO3a 和 FoxO4蛋白(左图)。用FoxO1 (C29H4) Rabbit mAb (#2880), FoxO3a (75D8) Rabbit mAb (#2497) 和FoxO4 Antibody (#9472), 检测 FoxO1, FoxO3a 和 FoxO4 的总蛋白(右图).

Western Blotting

Western Blotting

Western blot analysis of extracts from Jurkat cells treated with either Calyculin A (#9902) or LY294002 (#9901) using Phospho-FoxO1 (Thr24)/(FoxO3a (Thr32)/FoxO4 (Thr28) (4G6) Rabbit mAb. The phospho-specificity of the antibody was verified by treating the membrane in the absence (-) or presence (-) of calf intestinal phosphatase (CIP) after western transfer.Western blot 检测分析分别用 Calyculin A (#9902) 和LY294002 (#9901)处理的Jurkat细胞,提取物,使用的抗体是 Phospho-FoxO1 (Thr24)/(FoxO3a (Thr32)/FoxO4 (Thr28) (4G6) Rabbit mAb。Western转膜后,分别用小牛肠碱性磷酸酶 (CIP) 处理和不处理的膜确认抗体识别磷酸化蛋白的特异性。

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).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)。

  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.

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

U.S. Patent No. 5,675,063.

Cell Signaling Technology is a trademark of Cell Signaling Technology, Inc.

Cell Signaling Technology® is a trademark of Cell Signaling Technology, Inc.

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