טוען...
Deletion of individual Ku subunits in mice causes an NHEJ-independent phenotype potentially by altering apurinic/apyrimidinic site repair.
Ku70 and Ku80 form a heterodimer called Ku that forms a holoenzyme with DNA dependent-protein kinase catalytic subunit (DNA-PKCS) to repair DNA double strand breaks (DSBs) through the nonhomologous end joining (NHEJ) pathway. As expected mutating these genes in mice caused a similar DSB repair-defec...
שמור ב:
Main Authors: | , , , , , , , , , , , , |
---|---|
פורמט: | Artigo |
שפה: | Inglês |
יצא לאור: |
Public Library of Science (PLoS)
2014-01-01
|
סדרה: | PLoS ONE |
גישה מקוונת: | http://europepmc.org/articles/PMC3900520?pdf=render |
תגים: |
הוספת תג
אין תגיות, היה/י הראשונ/ה לתייג את הרשומה!
|