Abstract
ATM, Rad50 and Mre11 have been shown to prevent telomere fusion in Drosophila, thereby extending the protective role of DNA damage checkpoint proteins to non-canonical telomeres formed without telomerase. How do these proteins help chromosomal termini escape fusion through 'repair' while promoting repair of induced DNA breaks?
MeSH terms
-
Acid Anhydride Hydrolases
-
Ataxia Telangiectasia Mutated Proteins
-
Cell Cycle Proteins / metabolism
-
Chromosomal Instability*
-
DNA Damage / physiology
-
DNA Repair Enzymes / metabolism
-
DNA Repair*
-
DNA-Binding Proteins / metabolism
-
Protein Serine-Threonine Kinases / metabolism
-
Telomerase / metabolism
-
Telomere / metabolism*
-
Telomere-Binding Proteins / metabolism*
-
Tumor Suppressor Proteins
Substances
-
Cell Cycle Proteins
-
DNA-Binding Proteins
-
Telomere-Binding Proteins
-
Tumor Suppressor Proteins
-
ATM protein, human
-
Ataxia Telangiectasia Mutated Proteins
-
Protein Serine-Threonine Kinases
-
Telomerase
-
Acid Anhydride Hydrolases
-
RAD50 protein, human
-
DNA Repair Enzymes