Loss of Mitochondrial Localization of Human FANCG Causes Defective FANCJ Helicase | Zendy

Jagadeesh Chandra Bose | Zendy; Bishwajit Singh Kapoor | Zendy; Kamal Mandal | Zendy; Shubhrima Ghosh | Zendy; Raveendra B. Mokhamatam | Zendy; Sunil K. Manna | Zendy; Sudit S. Mukhopadhyay | Zendy

AI Assistant Blog Pricing

Home ZAIA Blog

Open Access

Loss of Mitochondrial Localization of Human FANCG Causes Defective FANCJ Helicase

Author(s) -

Jagadeesh Chandra Bose,

Bishwajit Singh Kapoor,

Kamal Mandal,

Shubhrima Ghosh,

Raveendra B. Mokhamatam,

Sunil K. Manna,

Sudit S. Mukhopadhyay

Publication year - 2020

Publication title -

molecular and cellular biology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.14

H-Index - 327

eISSN - 1067-8824

pISSN - 0270-7306

DOI - 10.1128/mcb.00306-20

Subject(s) - biology , genome instability , fanconi anemia , fancd2 , fanca , dna damage , dna repair , mitochondrion , helicase , mitochondrial dna , mutation , microbiology and biotechnology , rna helicase a , genetics , gene , dna , rna

Fanconi anemia (FA) is a unique DNA damage repair pathway. To date, 22 genes have been identified that are associated with the FA pathway. A defect in any of those genes causes genomic instability, and the patients bearing the mutation become susceptible to cancer. In our earlier work, we identified that Fanconi anemia protein G (FANCG) protects the mitochondria from oxidative stress. In this report, we have identified eight patients having a mutation (C.65G>C), which converts arginine at position 22 to proline (p.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research