NTH1 (12T15) Rabbit Monoclonal Antibody

NTH1 (12T15) Rabbit Monoclonal Antibody

Size1:50μl Price1:$128
Size2:100μl Price2:$230
Size3:500μl Price3:$980
SKU: AMRe14928 Category: Rabbit Monoclonal Antibody Tags: , , , , ,

Datasheet

Summary

Production Name

NTH1 (12T15) Rabbit Monoclonal Antibody

Description

Rabbit Monoclonal Antibody

Host

Rabbit

Application

WB

Reactivity

Human,Mouse,Rat

 

Performance

Conjugation

Unconjugated

Modification

Unmodified

Isotype

IgG

Clonality

Monoclonal

Form

Liquid

Storage

Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles.

Buffer

Supplied in 50mM Tris-Glycine(pH 7.4), 0.15M NaCl, 40%Glycerol, 0.01% New type preservative N and 0.05% BSA.

Purification

Affinity purification

 

Immunogen

Gene Name

NTHL1 {ECO:0000255|HAMAP-Rule:MF_03183}

Alternative Names

hNTH1; NTH1; Nthl1; OCTS3;

Gene ID

4913

SwissProt ID

P78549

 

Application

Dilution Ratio

WB: 1:1000

Molecular Weight

34kDa

 

Background

Has both an apurinic and/or apyrimidinic endonuclease activity and a DNA N-glycosylase activity. Incises damaged DNA at cytosines, thymines and guanines. Acts on a damaged strand, 5' from the damaged site. Required for the repair of both oxidative DNA damage and spontaneous mutagenic lesions. Bifunctional DNA N-glycosylase with associated apurinic/apyrimidinic (AP) lyase function that catalyzes the first step in base excision repair (BER), the primary repair pathway for the repair of oxidative DNA damage (PubMed:9927729). The DNA N-glycosylase activity releases the damaged DNA base from DNA by cleaving the N- glycosidic bond, leaving an AP site. The AP-lyase activity cleaves the phosphodiester bond 3' to the AP site by a beta-elimination. Primarily recognizes and repairs oxidative base damage of pyrimidines. Has also 8-oxo-7,8-dihydroguanine (8-oxoG) DNA glycosylase activity. Acts preferentially on DNA damage opposite guanine residues in DNA. Is able to process lesions in nucleosomes without requiring or inducing nucleosome disruption.

 

Research Area