Basic Information
Gene ID
Atru.chr13.535.g
Position
chr13:4065395-4069065 (+)
3670bp
Gene Type
gene
Gene Description (Protein Product)
Methyladenine glycosylase
Organism
Also AS AT1G75090

Gene Structure

upstream:

Domain
Database EntryID E-Value Start end InterPro ID Description

Regulation&Interaction
Protein-protein interaction (PPI)
Atru.chr3.135.g HMG1 2-like
Atru.chr8.2229.g High mobility group B protein
Atru.chr3.1534.g 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. 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
Regulatory gene
Atru.chr1.1136.g Agamous-like MADS-box protein
Atru.chr1.254.g transcription factor
Atru.chr1.2813.g AP2-like ethylene-responsive transcription factor

Load All Networks

Annotation

Orthologous Group
Orthologous ID Species Number All hits in PereRegDB Hits of this species Orthologous Detail


Pathway
KEGG Term Name Description
map03410 Base excision repair Base excision repair (BER) is the predominant DNA damage repair pathway for the processing of small base lesions, derived from oxidation and alkylation damages. BER is normally defined as DNA repair initiated by lesion-specific DNA glycosylases and completed by either of the two sub-pathways: short-patch BER where only one nucleotide is replaced and long-patch BER where 2-13 nucleotides are replaced. Each sub-pathway of BER relies on the formation of protein complexes that assemble at the site of the DNA lesion and facilitate repair in a coordinated fashion. This process of complex formation appears to provide an increase in specificity and efficiency to the BER pathway, thereby facilitating the maintenance of genome integrity by preventing the accumulation of highly toxic repair intermediates.