W0393
Anti-WRN antibody, Mouse monoclonal
clone 195C, purified from hybridoma cell culture
Synonym(s):
Anti-RECQ3, Anti-RECQL2, Anti-RECQL3, Anti-Werner syndrome helicase, Anti-Werner syndrome protein
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About This Item
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biological source
mouse
conjugate
unconjugated
antibody form
purified immunoglobulin
antibody product type
primary antibodies
clone
195C, monoclonal
form
buffered aqueous solution
mol wt
antigen ~167 kDa
species reactivity
human
concentration
~1 mg/mL
technique(s)
immunohistochemistry: suitable
immunoprecipitation (IP): suitable
indirect ELISA: suitable
western blot: 2-4 μg/mL using nuclear cell extract of HeLa cells
isotype
IgG1
UniProt accession no.
shipped in
dry ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... WRN(7486)
General description
Anti-WRN antibody, Mouse monoclonal, (mouse IgG1 isotype) is derived from the hybridoma 195C produced by the fusion of mouse myeloma cells (p3-NS1/Ag4-1) and splenocytes from BALB/c mice immunized with a recombinant fusion protein fragment of human WRN. Werner syndrome ATP-dependent helicase (WRN) is located on chromosome 8 and is 167 kDa. The WRN protein belongs to the RecQ helicase family of DNA helicases.
Immunogen
recombinant fusion protein fragment of human WRN (amino acids 1074-1432).
Application
Anti-WRN antibody has been used in
- enzyme linked immunosorbent assay (ELISA)
- immunoblotting
- immunoprecipitation
- immunohistochemistry
- western blotting
Biochem/physiol Actions
Werner syndrome ATP-dependent helicase (WRN) protein has been demonstrated to possess three known catalytic activities: 3′-5′ helicase, exonuclease and ATPase activities. The C-terminal region of the protein contains a nuclear localization signal (NLS), thus targeting WRN protein to the nucleus, nucleolus and nucleoplasmic foci. The involvement of WRN in multiple DNA metabolic process suggests its function as a tumor suppressor. Mutations in the WRN protein results in Werner syndrome (WS). The epigenetic inactivation of WRN leads to loss of WRN-exonuclease activity, resulting in increased chromosomal instability and hypersensitivity to chemotherapeutic drugs.
Physical form
Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.
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
nwg
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Personal Protective Equipment
dust mask type N95 (US), Eyeshields, Gloves
Certificates of Analysis (COA)
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Bidisha Saha et al.
Molecular genetics & genomic medicine, 1(1), 7-14 (2013-08-13)
Werner syndrome is a rare autosomal recessive disorder characterized by multiple features consistent with accelerated aging. It is caused by mutations in the WRN gene, which encodes a RecQ type helicase. To date, more than 70 disease-causing mutations have been
Yuyao Tian et al.
Cell & bioscience, 14(1), 7-7 (2024-01-07)
Metabolic dysfunction is one of the main symptoms of Werner syndrome (WS); however, the underlying mechanisms remain unclear. Here, we report that loss of WRN accelerates adipogenesis at an early stage both in vitro (stem cells) and in vivo (zebrafish).
Class I histone deacetylase HDAC1 and WRN RECQ helicase contribute additively to protect replication forks upon hydroxyurea-induced arrest
Kehrli K, et al.
The Journal of Biological Chemistry, 291(47), 24487-24503 (2016)
Piri Welcsh et al.
Methods (San Diego, Calif.), 108, 99-110 (2016-05-01)
Functional studies of the roles that DNA helicases play in human cells have benefited immensely from DNA fiber (or single molecule) technologies, which enable us to discern minute differences in behaviors of individual replication forks in genomic DNA in vivo.
Linda J W Bosch et al.
Clinical cancer research : an official journal of the American Association for Cancer Research, 22(18), 4612-4622 (2016-04-29)
WRN promoter CpG island hypermethylation in colorectal cancer has been reported to increase sensitivity to irinotecan-based therapies. We aimed to characterize methylation of the WRN promoter, determine the effect of WRN promoter hypermethylation upon expression, and validate a previous report
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