Phospho-cdc25C (Ser216) Antibody [D12E13]

Catalog No.: F0406

Application: Reactivity: Human, Monkey

Lane 1: HT29, Lane 2: HT29 (nocodazole-treated), Lane 3: HT29 (nocodazole-treated; λ phosphotase-treated)

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代表番号: 045-509-1970|電子メール：sales@selleck.co.jp

使用情報

Dilution
WB1:1000 IP1:50 IHC1:100

Application
WB, IP, IHC

Source
Rabbit Monoclonal Antibody

Reactivity
Human, Monkey

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW
60 kDa

Datasheet & SDS

生物学的記述

Specificity
Phospho-cdc25C (Ser216) Antibody [D12E13] detects endogenous levels of total cdc25C protein only when it is phosphorylated at Ser216.

Clone
D12E13

Synonym(s)
M-phase inducer phosphatase 3; Dual specificity phosphatase Cdc25C; CDC25C

Background
Phospho-cdc25C (Ser216) refers to the cdc25C phosphatase phosphorylated at Ser216, a crucial regulatory event that controls the G2/M cell cycle transition. cdc25C has an N-terminal regulatory domain with multiple phosphorylation sites and a C-terminal catalytic domain containing the conserved dual-specificity phosphatase motif, with Ser216 located in a flexible loop. Under normal conditions, cdc25C activates cyclin B1-CDK1 by dephosphorylating CDK1, thereby promoting mitotic entry. However, phosphorylation of Ser216 by c-TAK1 (in interphase) or by Chk1/Chk2 (following DNA damage) creates a binding site for 14-3-3 proteins, sequestering cdc25C in the cytoplasm and preventing premature mitosis. This checkpoint mechanism integrates DNA damage response signaling (ATM/ATR→Chk1/2) with cell cycle arrest, allowing time for repair, while Plk1 and CDK1 can counteract this inhibition to permit mitotic progression when appropriate. Dysregulation of phospho-cdc25C(Ser216) can override cell cycle checkpoints, contributing to genomic instability and cancer progression, with cdc25C overexpression linked to poor prognosis in several cancers.

Background

Phospho-cdc25C (Ser216) refers to the cdc25C phosphatase phosphorylated at Ser216, a crucial regulatory event that controls the G2/M cell cycle transition. cdc25C has an N-terminal regulatory domain with multiple phosphorylation sites and a C-terminal catalytic domain containing the conserved dual-specificity phosphatase motif, with Ser216 located in a flexible loop. Under normal conditions, cdc25C activates cyclin B1-CDK1 by dephosphorylating CDK1, thereby promoting mitotic entry. However, phosphorylation of Ser216 by c-TAK1 (in interphase) or by Chk1/Chk2 (following DNA damage) creates a binding site for 14-3-3 proteins, sequestering cdc25C in the cytoplasm and preventing premature mitosis. This checkpoint mechanism integrates DNA damage response signaling (ATM/ATR→Chk1/2) with cell cycle arrest, allowing time for repair, while Plk1 and CDK1 can counteract this inhibition to permit mitotic progression when appropriate. Dysregulation of phospho-cdc25C(Ser216) can override cell cycle checkpoints, contributing to genomic instability and cancer progression, with cdc25C overexpression linked to poor prognosis in several cancers.

References
[1] Sur S, et al. Mol Cell Biochem. 2016 May;416(1-2):33-46. [2] Liu K, et al. Cancer Cell Int. 2020 Jun 3;20:213.

PVDFメンブレン孔径参考表

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%