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Key Documents

HPA006748

Sigma-Aldrich

Anti-FEN1 antibody produced in rabbit

enhanced validation

Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution

Synonym(s):

Anti-DNase IV, Anti-FEN-1, Anti-Flap endonuclease 1, Anti-Flap structure-specific endonuclease 1, Anti-MF1, Anti-Maturation factor 1, Anti-hFEN-1

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About This Item

UNSPSC Code:
12352203
Human Protein Atlas Number:
NACRES:
NA.41

biological source

rabbit

Quality Level

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

product line

Prestige Antibodies® Powered by Atlas Antibodies

form

buffered aqueous glycerol solution

species reactivity

human, mouse, rat

enhanced validation

orthogonal RNAseq
Learn more about Antibody Enhanced Validation

technique(s)

immunoblotting: 0.04-0.4 μg/mL
immunohistochemistry: 1:50-1:200

immunogen sequence

CAALVKAGKVYAAATEDMDCLTFGSPVLMRHLTASEAKKLPIQEFHLSRILQELGLNQEQFVDLCILLGSDYCESIRGIGPKRAVDLIQKHKSIEEIVRRLDPNKYPVPENWLHKEAHQLFLEPEVLDPESVELKW

UniProt accession no.

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... FEN1(2237)

General description

Flap endonuclease 1 (FEN1) protein is a multifunctional and structure-specific nuclease. The FEN1 gene is located on the human chromosome at 11q12.2.

Immunogen

Flap endonuclease 1 recombinant protein epitope signature tag (PrEST)

Application

All Prestige Antibodies Powered by Atlas Antibodies are developed and validated by the Human Protein Atlas (HPA) project and as a result, are supported by the most extensive characterization in the industry.

The Human Protein Atlas project can be subdivided into three efforts: Human Tissue Atlas, Cancer Atlas, and Human Cell Atlas. The antibodies that have been generated in support of the Tissue and Cancer Atlas projects have been tested by immunohistochemistry against hundreds of normal and disease tissues and through the recent efforts of the Human Cell Atlas project, many have been characterized by immunofluorescence to map the human proteome not only at the tissue level but now at the subcellular level. These images and the collection of this vast data set can be viewed on the Human Protein Atlas (HPA) site by clicking on the Image Gallery link. We also provide Prestige Antibodies® protocols and other useful information.
Anti-FEN1 antibody produced in rabbit has been used in western blotting (1:250).

Biochem/physiol Actions

Flap endonuclease 1 (FEN1) is involved in the maturation of Okazaki fragments during the synthesis of DNA lagging strands and long-patch DNA-base excision repair due to its flap-specific endonuclease (FEN) activity. It possesses 5′ exonuclease activity for processing DNA ends during DNA recombination. FEN1 plays a role in maintaining genomic stability by preserving telomere stability. Overexpression of the FEN1 gene is observed in testis, brain, and lung tumors. Mutations in the FEN1 gene are associated with several human cancers.

Features and Benefits

Prestige Antibodies® are highly characterized and extensively validated antibodies with the added benefit of all available characterization data for each target being accessible via the Human Protein Atlas portal linked just below the product name at the top of this page. The uniqueness and low cross-reactivity of the Prestige Antibodies® to other proteins are due to a thorough selection of antigen regions, affinity purification, and stringent selection. Prestige antigen controls are available for every corresponding Prestige Antibody and can be found in the linkage section.

Every Prestige Antibody is tested in the following ways:
  • IHC tissue array of 44 normal human tissues and 20 of the most common cancer type tissues.
  • Protein array of 364 human recombinant protein fragments.

Linkage

Corresponding Antigen APREST71085

Physical form

Solution in phosphate-buffered saline, pH 7.2, containing 40% glycerol and 0.02% sodium azide

Legal Information

Prestige Antibodies is a registered trademark of Merck KGaA, Darmstadt, Germany

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

WGK

WGK 1

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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Li Zheng et al.
Nature medicine, 13(7), 812-819 (2007-06-26)
Functional deficiency of the FEN1 gene has been suggested to cause genomic instability and cancer predisposition. We have identified a group of FEN1 mutations in human cancer specimens. Most of these mutations abrogated two of three nuclease activities of flap
Xue-ren Gao et al.
Scientific reports, 4, 6183-6183 (2014-08-27)
Previous studies have investigated the associations between FEN1 -69G>A (rs174538) and 4150G>T (rs4246215) polymorphisms and cancer risk in Chinese population. However, the results were controversial. We therefore carried out a meta-analysis to derive a more precise estimation of the associations.
FEN1 is overexpressed in testis, lung and brain tumors.
Nikolova, et al.
Anticancer Research, 29, 2453-2459 (2018)
Masashi Takawa et al.
Cancer research, 72(13), 3217-3227 (2012-05-05)
Although the physiologic significance of lysine methylation of histones is well known, whether lysine methylation plays a role in the regulation of nonhistone proteins has not yet been examined. The histone lysine methyltransferase SETD8 is overexpressed in various types of
Viktoriya Peeva et al.
Nature communications, 9(1), 1727-1727 (2018-05-02)
Emerging gene therapy approaches that aim to eliminate pathogenic mutations of mitochondrial DNA (mtDNA) rely on efficient degradation of linearized mtDNA, but the enzymatic machinery performing this task is presently unknown. Here, we show that, in cellular models of restriction

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