Rabbit Anti-NTHL1 Recombinant Antibody (
22H10) (V2LY-0725-LY1399)

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Datasheet Target References Q & As Review & reward Protocols Associated Products

Basic Information

Host Animal
Rabbit
Clone
22H10
Application
ELISA, WB, IHC, IF, FC
Immunogen
A synthesized peptide derived from human NTHL1.
Host Species
Rabbit
Specificity
Human
Antibody Isotype
IgG
Clonality
Monoclonal Antibody
Application Notes
ApplicationNote
WB1:500-1:2,000
IHC1:50-1:200
IF1:50-1:200
FC1:50-1:200

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Buffer
PBS, glycerol
Preservative
Sodium azide
Concentration
Batch dependent
Purity
> 95% Purity determined by SDS-PAGE.
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freezethaw cycles.
More Infomation

Target

Full Name
Nth Like Dna Glycosylase 1
Entrez Gene ID
UniProt ID
Function
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.
Biological Process
Base-excision repair, AP site formationManual Assertion Based On ExperimentIDA:UniProtKB
DepyrimidinationTAS:Reactome
Nucleotide-excision repair, DNA incision, 5'-to lesionManual Assertion Based On ExperimentIDA:UniProtKB
Cellular Location
Nucleus
Mitochondrion
Involvement in disease
Familial adenomatous polyposis 3 (FAP3):
A form of familial adenomatous polyposis, a condition characterized by the development of multiple colorectal adenomatous polyps, benign neoplasms derived from glandular epithelium. Some affected individuals may develop colorectal carcinoma.

Salo-Mullen, E. E., Maio, A., Mukherjee, S., Bandlamudi, C., Shia, J., Kemel, Y., ... & Stadler, Z. K. (2021). Prevalence and characterization of biallelic and monoallelic NTHL1 and MSH3 variant carriers from a pan-cancer patient population. JCO precision oncology, 5, 455-465.

Magrin, L., Fanale, D., Brando, C., Fiorino, A., Corsini, L. R., Sciacchitano, R., ... & Bazan, V. (2021). POLE, POLD1, and NTHL1: The last but not the least hereditary cancer-predisposing genes. Oncogene, 40(40), 5893-5901.

Carroll, B. L., Zahn, K. E., Hanley, J. P., Wallace, S. S., Dragon, J. A., & Doublié, S. (2021). Caught in motion: human NTHL1 undergoes interdomain rearrangement necessary for catalysis. Nucleic Acids Research, 49(22), 13165-13178.

Das, L., Quintana, V. G., & Sweasy, J. B. (2020). NTHL1 in genomic integrity, aging and cancer. DNA repair, 93, 102920.

Kuiper, R. P., Nielsen, M., De Voer, R. M., & Hoogerbrugge, N. (2020). NTHL1 tumor syndrome.

Grolleman, J. E., De Voer, R. M., Elsayed, F. A., Nielsen, M., Weren, R. D., Palles, C., ... & Kuiper, R. P. (2019). Mutational signature analysis reveals NTHL1 deficiency to cause a multi-tumor phenotype. Cancer cell, 35(2), 256-266.

Belhadj, S., Quintana, I., Mur, P., Munoz-Torres, P. M., Alonso, M. H., Navarro, M., ... & Valle, L. (2019). NTHL1 biallelic mutations seldom cause colorectal cancer, serrated polyposis or a multi-tumor phenotype, in absence of colorectal adenomas. Scientific Reports, 9(1), 9020.

Terradas, M., Munoz‐Torres, P. M., Belhadj, S., Aiza, G., Navarro, M., Brunet, J., ... & Valle, L. (2019). Contribution to colonic polyposis of recently proposed predisposing genes and assessment of the prevalence of NTHL1‐and MSH3‐associated polyposes. Human Mutation, 40(11), 1910-1923.

Groves, A., Gleeson, M., & Spigelman, A. D. (2019). NTHL1-associate polyposis: first Australian case report. Familial cancer, 18(2), 179-182.

Altaraihi, M., Gerdes, A. M., & Wadt, K. (2019). A new family with a homozygous nonsense variant in NTHL1 further delineated the clinical phenotype of NTHL1-associated polyposis. Human Genome Variation, 6(1), 46.

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For research use only. Not intended for any clinical use.

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