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Key Documents

WH0000993M1

Sigma-Aldrich

Monoclonal Anti-CDC25A antibody produced in mouse

clone 3D5, purified immunoglobulin, buffered aqueous solution

Synonym(s):

Anti-CDC25A2, Anti-cell division cycle 25A

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About This Item

MDL number:
UNSPSC Code:
12352203
NACRES:
NA.41

biological source

mouse

Quality Level

conjugate

unconjugated

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

3D5, monoclonal

form

buffered aqueous solution

species reactivity

human

technique(s)

indirect ELISA: suitable
proximity ligation assay: suitable
western blot: 1-5 μg/mL

isotype

IgG2aκ

GenBank accession no.

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... CDC25A(993)

General description

CDC25A is a member of the CDC25 family of phosphatases. CDC25A is required for progression from G1 to the S phase of the cell cycle. It activates the cyclin-dependent kinase CDC2 by removing two phosphate groups. CDC25A is specifically degraded in response to DNA damage, which prevents cells with chromosomal abnormalities from progressing through cell division. CDC25A is an oncogene, although its exact role in oncogenesis has not been demonstrated. Two transcript variants encoding different isoforms have been found for this gene. (provided by RefSeq)
The cell division cycle 25A (CDC25A) is a potent human oncogene, mapped to chromosome 3p21.31. The gene codes for a member of Cdc25 phosphatase family.

Immunogen

CDC25A (AAH07401, 151 a.a. ~ 250 a.a) partial recombinant protein with GST tag. MW of the GST tag alone is 26 KDa.

Sequence
PVRPVSRGCLHSHGLQEGKDLFTQRQNSAPARMLSSNERDSSEPGNFIPLFTPQSPVTATLSDEDDGFVDLLDGENLKNEEETPSCMASLWTAPLVMRTT

Biochem/physiol Actions

Cell division cycle 25A (CDC25A) plays a crucial role at the Gl/S-phase transition. The protein also facilitates G2 arrest caused by DNA damage or in the presence of unreplicated DNA. CDC25A controls cell cycle progression by dephosphorylating and activating cyclin-CDK complexes. Elevated expression of the gene increases the G1/S and G2/M transitions, which subsequently lead to genomic instability and tumorigenesis. CDC25A expression might be associated with the pathogenesis and progression of hepatocellular carcinoma (HCC).

Physical form

Solution in phosphate buffered saline, pH 7.4

Legal Information

GenBank is a registered trademark of United States Department of Health and Human Services

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Storage Class Code

10 - Combustible liquids

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Personal Protective Equipment

dust mask type N95 (US), Eyeshields, Gloves

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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CyclinD-CDK4/6 complexes phosphorylate CDC25A and regulate its stability
Dozier C
Oncogene, 36, 3781-3788 (2017)
Alterations of 3p21.31 tumor suppressor genes in head and neck squamous cell carcinoma: Correlation with progression and prognosis
Ghosh S
International Journal of Cancer. Journal International Du Cancer, 123, 2594-2604 (2008)
Identification of key genes in hepatocellular carcinoma and validation of the candidate gene, cdc25a, using gene set enrichment analysis, meta-analysis and cross-species comparison
Lu X
Molecular Medicine Reports, 13, 1172-1178 (2016)
Cell cycle regulation by the Cdc25 phosphatase family
Nilsson I and Hoffmann I
Progress in Cell Cycle Research, 4, 107-114 (2000)
Zijun Zhou et al.
International journal of oncology, 57(3), 697-706 (2020-06-26)
Retinoblastoma (RB) is one of the most aggressive malignancies affecting infants and children. Platinum drugs are commonly used in the treatment of RB; however, their efficacy is often compromised by drug resistance and severe toxicity. The present study aimed to

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