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DNA Topoisomerase I Mouse anti-Human, Unlabeled, Clone: C-21.2, BD

Catalog No. BDB556597 Shop All BD Biosciences Products
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Catalog No. BDB556597 Supplier BD Biosciences Supplier No. 556597
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Description

Mouse Monoclonal Antibody

DNA damage may be caused by various environmental factors, including radiation, mutagenic chemicals and copy errors which occur during DNA replication. The correction of DNA damage, so called “proofreading” functions of the cell, is achieved by numerous excision-repair enzymes. Topoisomerases alter the helical structure of DNA by introducing the transient breaking and rejoining of DNA strands, allowing other excision-repair enzymes to correct DNA errors. Topoisomerase I (Topo I) is a ubiquitous, soluble enzyme whose expression is fairly constant throughout the cell cycle. The related enzyme, Topo II, is a primarily insoluble structural protein whose expression varies between cell types and during the cell cycle. In addition to its role in DNA mismatch repair, Topo I displays kinase activity, phosphorylating serine-arginine rich (SR) splicing factors, and perhaps regulating gene expression by changing the splicing pattern of structural genes. DNA Topo I migrates at a molecular weight of 100kDa in SDS-PAGE. Clone C-21 recognizes human DNA Topoisomerase I. The antibody is
routinely tested by western blot analysis of A-431 cell lysates.

Host Species: Mouse
Clone: C-21
Isotype: IgM
Species Reactivity: Human

Western Blotting

TRUSTED_SUSTAINABILITY

Specifications

Antigen DNA Topoisomerase I
Applications Western Blot
Classification Monoclonal
Clone C-21.2
Concentration 0.5mg/mL
Conjugate Unconjugated
Formulation Aqueous buffered solution containing ≤0.09% sodium azide.
Host Species Mouse
Purification Method Affinity Purified
Quantity 0.1 mg
Regulatory Status RUO
Research Discipline Cell Biology
Primary or Secondary Primary
Target Species Human
Content And Storage Store undiluted at 4°C
Isotype IgM
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Safety and Handling

WARNING: Reproductive Harm - www.P65Warnings.ca.gov

For Research Use Only.

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