PPGR - Gene Detail

Basic Information

Gene ID	FSB0153827 View in Genome Browser
Position	scaffold686_size182474:15618-23971 (-) 8353bp
Gene Type	gene
Gene Description (Protein Product)	Methyladenine glycosylase
Organism	Fagus sylvatica
Also AS	AT4G23160

upstream:

Domain

Database	EntryID	E-Value	Start	end	InterPro ID	Description

Regulation&Interaction

Protein-protein interaction (PPI)

FSB0155484 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

FSB0158539 Catalyzes the conversion of inosine 5'-phosphate (IMP) to xanthosine 5'-phosphate (XMP), the first committed and rate- limiting step in the de novo synthesis of guanine nucleotides, and therefore plays an important role in the regulation of cell growth

FSB0154227 PsbB mRNA maturation factor Mbb1

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Annotation

Orthologous Group

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

Expression Profile

DataSet	Number of Samples expressed(TPM>1)	Mean	Min	Max	Standard deviation(SD)	Coeffcient variation(CV)

Select Expression

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.