G2/M Cell Cycle Checkpoint Antibody

Panyue (Penny) Hao

Panyue (Penny) Hao
Apr 9, 2019 3:16:32 PM

The G2/M cycle checkpoint prevents cells with genomic DNA damage from entering mitosis (M phase). The main safeguards conferred by this checkpoint is to ensure that DNA is free of major lesions or replication errors, and there are enough organelles, metabolites, and other cellular cargo in the parent cell prior to division so the daughter cells can be adequately provided for once mitosis is complete. Failures at this checkpoint are associated with aberrant cellular growth and cancer progression.

 

The Cyclin B-CDK1 complex plays an important regulatory role during the G2 transition, at which time CDK1 is maintained inactivated by the tyrosine kinases Wee1 and Myt1. When the cells enter the M phase, the kinase Aurora A and the cofactor Bora act together to activate PLK1, which in turn activates the activity of phosphatase CDC25 and downstream CDC2, effectively driving the cells into mitosis. When the DNA is damaged, it activates the DNA-PK/ATM/ATR kinase and eventually inactivates the Cyclin B-CDK1 complex. Stopping cell cycle progression allows the cell enough time to attempt to repair any DNA or cellular damage, and if all else fails, to induce apoptosis to prevent risk to the entire organism.

 

ABclonal Technology provides a wide selection of cell cycle checkpoint antibody products for every phase of a cell's life. Please see a small sample of our offerings below.

 

CDK1 Polyclonal Antibody, CCNB1 Polyclonal Antibody, PLK1 Polyclonal Antibody

CDK1 western blot          Cyclin B1 immunofluorescence          PLK1 Western blot

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CDC25C Polyclonal Antibody, Phospho-ATM-S1981 Polyclonal Antibody

CDC25C immunofluorescence          Phospho-ATM immunofluorescence

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Tags: Antibodies, Featured Product Weekly, DNA Damage & Repair, Cell Cycle Checkpoint

Panyue (Penny) Hao

Panyue (Penny) Hao

Content creator, knowledge craver, all-around food fanatic thriving to survive in the fascinating yet uncharted world of biology.