PMID- 10607596
OWN - NLM
STAT- MEDLINE
DCOM- 20000216
LR  - 20190728
IS  - 0960-9822 (Print)
IS  - 0960-9822 (Linking)
VI  - 9
IP  - 24
DP  - 1999 Dec 16-30
TI  - The nonhomologous DNA end joining pathway is important for chromosome stability
      in primary fibroblasts.
PG  - 1501-4
AB  - There are two types of chromosome instability, structural and numerical, and
      these are important in cancer. Many structural abnormalities are likely to
      involve double-strand DNA (dsDNA) breaks. Nonhomologous DNA end joining (NHEJ)
      and homologous recombination are the major pathways for repairing dsDNA breaks.
      NHEJ is the primary pathway for repairing dsDNA breaks throughout the G0, G1 and 
      early S phases of the cell cycle [1]. Ku86 and DNA ligase IV are two major
      proteins in the NHEJ pathway. We examined primary dermal fibroblasts from mice
      (wild type, Ku86(+/-), Ku86(-/-), and DNA ligase IV(+/-)) for chromosome breaks. 
      Fibroblasts from Ku86(+/-) or DNA ligase IV(+/-) mice have elevated frequencies
      of chromosome breaks compared with those from wild-type mice. Fibroblasts from
      Ku86(-/-) mice have even higher levels of chromosome breaks. Primary pre-B cells 
      from the same animals did not show significant accumulation of chromosome breaks.
      Rather the pre-B cells showed increased cell death. These studies demonstrate
      that chromosome breaks arise frequently and that NHEJ is required to repair this 
      constant spontaneous damage.
FAU - Karanjawala, Z E
AU  - Karanjawala ZE
AD  - Department of Pathology, Rooms 5420 and 5428, Norris Comprehensive Cancer Center,
      University of Southern California School of Medicine, Los Angeles 90033, USA.
FAU - Grawunder, U
AU  - Grawunder U
FAU - Hsieh, C L
AU  - Hsieh CL
FAU - Lieber, M R
AU  - Lieber MR
LA  - eng
GR  - T32 CA09569/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - Curr Biol
JT  - Current biology : CB
JID - 9107782
RN  - 0 (Antigens, Nuclear)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (LIG4 protein, human)
RN  - 0 (Nuclear Proteins)
RN  - 9007-49-2 (DNA)
RN  - EC 3.6.4.- (DNA Helicases)
RN  - EC 3.6.4.12 (XRCC5 protein, human)
RN  - EC 3.6.4.12 (Xrcc5 protein, mouse)
RN  - EC 3.6.4.12 (Xrcc6 protein, human)
RN  - EC 3.6.4.12 (Xrcc6 protein, mouse)
RN  - EC 4.2.99.- (Ku Autoantigen)
RN  - EC 6.5.1.- (DNA Ligases)
RN  - EC 6.5.1.1 (DNA Ligase ATP)
SB  - IM
MH  - Animals
MH  - *Antigens, Nuclear
MH  - Cell Cycle
MH  - Cell Death
MH  - Cell Division
MH  - Cells, Cultured
MH  - Chromosomes/genetics/*metabolism
MH  - DNA/genetics/*metabolism
MH  - DNA Damage
MH  - *DNA Helicases
MH  - DNA Ligase ATP
MH  - DNA Ligases/genetics/metabolism
MH  - DNA Repair
MH  - DNA-Binding Proteins/genetics/metabolism
MH  - Ku Autoantigen
MH  - Mice
MH  - Mice, Knockout
MH  - Nuclear Proteins/genetics/metabolism
MH  - Recombination, Genetic
EDAT- 1999/12/23 09:00
MHDA- 2000/02/19 09:00
CRDT- 1999/12/23 09:00
PHST- 1999/12/23 09:00 [pubmed]
PHST- 2000/02/19 09:00 [medline]
PHST- 1999/12/23 09:00 [entrez]
AID - S0960-9822(00)80123-2 [pii]
AID - 10.1016/s0960-9822(00)80123-2 [doi]
PST - ppublish
SO  - Curr Biol. 1999 Dec 16-30;9(24):1501-4. doi: 10.1016/s0960-9822(00)80123-2.