Exact(2)
CDK/cyclin complexes are often involved in these checkpoints.
On cohesin depletion, checkpoint kinase 2 (CHK2) activation is impaired not only in these checkpoints but also in G1.
Similar(58)
In lupus, these checkpoints appear to be defective, resulting in the emergence of higher numbers of B cells expressing autoreactive BCRs than normal.
The complexes of various cyclins and cyclin dependent kinases (CDKs) play a crucial role in exceeding these checkpoints and CDKs should be activated by phosphorylation in order to work as positive regulators of the cell cycle (Sherr, 1994).
Defects in many of these checkpoints have been reported in murine models of lupus; thus, each appears necessary to stave off pathogenic autoreactivity [10], [11], [12], [13].
"How was the car able to get in there while these checkpoints have all these technical devices?" asked Mr. Faleh, who was also wounded.
The CDKs play an important role in the regulation of these checkpoints.
Since ATM and CHK2 are amongst the main activators of these checkpoints in response to DNA-damage, we sought to determine whether cell cycle checkpoints could be triggered by Nutlin-3 treatment.
Thus, the function of cohesin in these two checkpoints is cohesion-independent.
In healthy individuals, the B cell repertoire is purged of potentially pathogenic autoreactive B cells at multiple developmental checkpoints; however, in SLE patients, many of these checkpoints are breached and autoreactive B cells become part of the mature, immunocompetent and activated B cell repertoire [2] [4].
These checkpoints function in concert to control the mitochondrion's and thus the cell's proper function.
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