200 000 cells plated in 12-well dish were transfected with siRNA using Lullaby reagent for 48H.
This article demonstrates the high efficiency of Lullaby and the low toxicity of Lullaby, a transfection reagent from OZ Biosciences to induce gene silencing into Mouse Embryonic Fibroblasts.article reference: DNA Repair, 26 September 2014
ATMIN is required for the ATM-mediated signaling and recruitment of 53BP1 to DNA damage sites upon replication stress
Luisa Schmidt, Marc Wiedner, Georgia Velimezi, Jana Prochazkova, Michel Owusu, Sabine Bauer, Joanna I. Loizou
Abstract
Unresolved
replication intermediates can block the progression of replication
forks and become converted into DNA lesions, hence exacerbating genomic
instability. The p53-binding protein 1 (53BP1) forms nuclear bodies at
sites of unrepaired DNA lesions to shield these regions against erosion,
in a manner dependent on the DNA damage kinase ATM. The molecular
mechanism by which ATM is activated upon replicative stress to localize
the 53BP1 protection complex is unknown. Here we show that the ATM-INteracting
protein ATMIN (also known as ASCIZ) is partially required for 53BP1
localization upon replicative stress. Additionally, we demonstrate that
ATM activation is impaired in cells lacking ATMIN and we define that
ATMIN is required for initiating ATM signaling following replicative
stress. Furthermore, loss of ATMIN leads to chromosomal segregation
defects. Together these data reveal that chromatin integrity depends on
ATMIN upon exposure to replication-induced stress.
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