Sentence examples for weakened checkpoint from inspiring English sources

Some authors have demonstrated that cells with compromised (or weakened) checkpoint machinery can progress to anaphase with one or more chromosomes unattached to microtubules, and these cells can arrest in the cell cycle but eventually finish the cell cycle, generating aneuploid cells [32], [33].

Anaphase is initiated in the presence of misaligned and lagging chromosomes, indicative of a weakened checkpoint and persistent merotelic attachments, respectively.

The cells with weakened checkpoint can generate chromosomal instability when a few chromosomes are not correctly attached to microtubules, and the cells complete metaphase, thus generating aneuploid cells [32].

A weakened checkpoint, on the other hand, is thought to result in infrequent losses and gains of chromosomes (known as chromosomal instability) that can be compatible with life.

Spindle checkpoint proteins are essential for survival in mammalian cells (10- 12), thus researchers have used either cancer cells with weakened checkpoint function or cultured cells with conditional expression of mutant checkpoint proteins or siRNA to investigate the correlation.

So in these TP53 mutant lines, the loss of p53 function and subsequent reduction or loss of p21 activity would undermine proper regulation of the G1/S and G2/M phase transitions, resulting in weakened checkpoints even in an unperturbed cell.

Mitotic catastrophe is considered an oncosuppressive pathway due to its association with absent or weakened checkpoints.

Two of the causes of CIN are weakened mitotic checkpoint signaling and persistent merotelic attachments that result in lagging chromosomes during anaphase.

Mps1 activity is indispensable for cell viability, but viability is maintained in CIN tumor cells that have a weakened mitotic checkpoint [5].

Reduced Mps1 kinase activity allows weakened mitotic checkpoint signaling as well as lagging chromosomes at anaphase, two major defects suggested to contribute to CIN in tumor cells [5], [10].

They are able to survive and proliferate because key checkpoints are weakened, thereby increasing the barrier for activation of DDR signalling [ 4].