NEIL2

Last update 08 May 2025

Basic Info

Synonyms

DNA glycosylase/AP lyase Neil2, DNA-(apurinic or apyrimidinic site) lyase Neil2, Endonuclease 8-like 2

+ [9]

Introduction

Involved in base excision repair of DNA damaged by oxidation or by mutagenic agents. Has DNA glycosylase activity towards 5-hydroxyuracil and other oxidized derivatives of cytosine with a preference for mismatched double-stranded DNA (DNA bubbles). Has low or no DNA glycosylase activity towards thymine glycol, 2-hydroxyadenine, hypoxanthine and 8-oxoguanine. Has AP (apurinic/apyrimidinic) lyase activity and introduces nicks in the DNA strand. Cleaves the DNA backbone by beta-delta elimination to generate a single-strand break at the site of the removed base with both 3'- and 5'-phosphates.

100 Clinical Results associated with NEIL2

100 Translational Medicine associated with NEIL2

0 Patents (Medical) associated with NEIL2

200

Literatures (Medical) associated with NEIL2

01 Jun 2025·Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease

Activation, interaction and intimation of Nrf2 pathway and their mutational studies causing Nrf2 associated cancer

Review

Author: Sahu, Mridul ; Jain, Utkarsh

Responses against infection trigger several signaling pathways that lead to the production of cytokines, these cytokines release ROS and RNS, damaging DNA and proteins turn into various diseases including cancer. To combat these harmful cytokines, the Nrf2 pathway is activated. The gene NFE2L2 encodes Nrf2, which is divided into seven conserved domains (Neh1-7). The DLG and ETGE motifs, conserved sequences of amino acid in the Neh2 domain of Nrf2, bind to the BTB domain of Keap1. BTB domain promotes Keap1's homodimerization resulting in Cul3 recruitment providing scaffold formation to E2 ubiquitin ligase to form ubiquitin complex. Under normal conditions, this complex regularly degrades Nrf2. However, once the cell is exposed to oxidative stress by ROS interaction with Keap1 resulting in conformational changes that stabilize the Nrf2. Nrf2 further concentrates on the nucleus where it binds with the transcriptional factor to perform the desired genes transcription for synthesizing SOD, GSH, CAT, and various other proteins which reduce the ROS levels preventing certain diseases. To prevent cells from oxidative stress, molecular hydrogen activates the Nrf2 pathway. To activate the Nrf2 pathway, molecular hydrogen oxidizes the iron porphyrin which acts as an electrophile and interacts with Keap1's cysteine residue.

01 Mar 2025·Archives of Toxicology

E-cigarettes increase the risk of adenoma formation in murine colorectal cancer model

Article

Author: Park, Kenneth ; Das, Soumita ; Dugan, Leanne ; Crotty Alexander, Laura E ; Chakraborty, Anirban ; Kasaraneni, Nikita ; Ma, Benjamin ; Sayed, Ibrahim M ; Inouye, Kaili ; Tocci, Stefania ; Gaboyan, Samvel ; Advani, Ira ; Hazra, Tapas K

E-cigarettes (E.cigs) cause inflammation and damage to human organs, including the lungs and heart. In the gut, E.cig vaping promotes inflammation and gut leakiness. Further, E.cig vaping increases tumorigenesis in oral and lung epithelial cells by inducing mutations and suppressing host DNA repair enzymes. It is well known that cigarette (cig) smoking increases the risk of colorectal cancer (CRC). To date, it is unknown whether E.cig vaping impacts CRC development. A mouse model of human familial adenomatous polyposis (CPC-APC) was utilized wherein a mutation in the adenomatous polyposis coli (APC) gene, CDX2-Cre-APC^Min/+, leads to the development of colon adenomas within 11-16 weeks. Mice were exposed to air (controls), E.cig vaping, cig, or both (dual exposure). After 4 weeks of 2 h exposures per day (1 h of each for dual exposures), the colon was collected and assessed for polyp number and pathology scores by microscopy. Expression of inflammatory cytokines and cancer stem cell markers were quantified. DNA damage such as double-strand DNA breaks was evaluated by immunofluorescence, western blot, and gene-specific long amplicon qPCR. DNA repair enzyme levels (NEIL-2, NEIL-1, NTH1, and OGG1) were quantified by western blot. Proliferation markers were assessed by RT-qPCR and ELISA. CPC-APC mice exposed to E.cig, cig, and dual exposure developed a higher number of polyps compared to controls. Inflammatory proteins, DNA damage, and cancer stemness markers were higher in E-cig, cig, and dual-exposed mice as well. DNA damage was found to be associated with the suppression of DNA glycosylases, particularly with NEIL-2 and NTH1. E.cig and dual exposure both stimulated cancer cell stem markers (CD44, Lgr-5, DCLK1, and Ki67). The effect of E.cigs on polyp formation and CRC development was less than that of cigs, while dual exposure was more tumorigenic than either of the inhalants alone. E.cig vaping promotes CRC by stimulating inflammatory pathways, mediating DNA damage, and upregulating transcription of cancer stem cell markers. Critically, combining E.cig vaping with cig smoking leads to higher levels of tumorigenesis. Thus, while the chemical composition of these two inhalants, E.cigs and cigs, is highly disparate, they both drive the development of cancer and when combined, a highly common pattern of use, they can have additive or synergistic effects.

01 Mar 2025·Free Radical Biology and Medicine

NEIL1: The second DNA glycosylase involved in action-at-a-distance mutations induced by 8-oxo-7,8-dihydroguanine

Article

Author: Suzuki, Tetsuya ; Kamiya, Hiroyuki ; Kawai, Hidehiko ; Fujikawa, Yoshihiro

8-Oxo-7,8-dihydroguanine (G^O, 8-hydroxyguanine), an oxidatively damaged base, induces mutations and is involved in cancer initiation. In addition to G:C→T:A transversions at the damaged site, it causes untargeted base substitution (action-at-a-distance) mutations at the G bases of 5'-GpA-3' sites in human cells. Paradoxically, OGG1, a DNA glycosylase involved in the base excision repair (BER) pathway, enhances the action-at-a-distance mutations by G^O. In this study, other DNA glycosylases, potential repair enzymes for the G^O base, were knocked down, and their effects on the untargeted mutations were examined using the supF reporter gene. The knockdown of NEIL1 decreased such mutations, while those of NTH1, NEIL2, and NEIL3 had no effects. The double knockdown of OGG1 and NEIL1 additively affected the mutation frequency. These results indicated that NEIL1 is another BER protein involved in the action-at-a-distance mutations triggered by the oxidized guanine base.

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NEIL2

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