◀ Back to ABL1
ABL1 — PRKDC
Pathways - manually collected, often from reviews:
-
OpenBEL Selventa BEL large corpus:
PRKDC
→
ABL1
(directlyIncreases, PRKDC Activity)
Evidence: c-Abl phosphorylates DNA-PK in the C-terminal region (amino acids 3414?3850) (Jin et al., 1997). c-Abl-dependent phosphorylation of DNA-PK is stimulated by IR (Kharbanda et al., 1997). c-Abl does not phosphorylate Ku (Kharbanda et al., 1997).
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Shangary et al., J Biol Chem 2000
(Ataxia Telangiectasia) :
To unravel the
role of ATM and
DNA-PK in the activation of
Abl , we assayed Abl, ATM, and DNA-PK activity in ATM- and DNA-PKcs-deficient cells after irradiation ... Conversely, normal activation of both ATM and c-Abl occurs in DNA-PKcs-deficient cells, indicating that ATM but not
DNA-PK is
required for activation of
Abl in response to IR treatment ... Examination of DNA-PK activity in response to IR treatment in Abl-deficient cells expressing mutant forms of Abl or in normal cells exposed to an inhibitor of Abl suggests an in vivo
role for
Abl in the down-regulation of
DNA-PK activity
Tang et al., Chembiochem 2012
:
Our findings show that nuclear and cytoplasmic Abl kinase is activated early on ( within 5 min ) in response to IR by both ATM and
DNAPK , and that although one or the other of these kinases is required, either one is
sufficient to activate
Abl
Kharbanda et al., Nature 1997
:
We show that
DNA-PK phosphorylates and
activates c-Abl in vitro
Kharbanda et al., Oncogene 1998
:
The
DNA dependent protein kinase (DNA-PK) and the ataxia telangiectasia mutated (ATM) gene product, effectors in the DNA damage response,
contribute to the induction of
c-Abl activity
Kharbanda et al., Oncogene 1998
:
c-Abl associates with the DNA dependent protein kinase (DNA-PK) and is
activated by
DNA-PK dependent phosphorylation