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Key Documents

WH0000993M1

Sigma-Aldrich

Monoclonal Anti-CDC25A antibody produced in mouse

clone 3D5, purified immunoglobulin, buffered aqueous solution

Synonyme(s) :

Anti-CDC25A2, Anti-cell division cycle 25A

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About This Item

Numéro MDL:
Code UNSPSC :
12352203
Nomenclature NACRES :
NA.41

Source biologique

mouse

Conjugué

unconjugated

Forme d'anticorps

purified immunoglobulin

Type de produit anticorps

primary antibodies

Clone

3D5, monoclonal

Forme

buffered aqueous solution

Espèces réactives

human

Technique(s)

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

Isotype

IgG2aκ

Numéro d'accès GenBank

Numéro d'accès UniProt

Conditions d'expédition

dry ice

Température de stockage

−20°C

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... CDC25A(993)

Description générale

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.

Immunogène

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

Actions biochimiques/physiologiques

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).

Forme physique

Solution in phosphate buffered saline, pH 7.4

Informations légales

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

Clause de non-responsabilité

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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Code de la classe de stockage

10 - Combustible liquids

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

Équipement de protection individuelle

Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)


Certificats d'analyse (COA)

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Consulter la Bibliothèque de documents

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)
CyclinD-CDK4/6 complexes phosphorylate CDC25A and regulate its stability
Dozier C
Oncogene, 36, 3781-3788 (2017)
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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