Teri bhen di sallaa kutta kamina penchod.<-df is that ignore it, If there are mutations in checkpoint proteins (such as in cancer cells), mitosis may proceed but the chromosomes may not be separated normally (resulting in "aneuploidy").
I am answering my own question here I'm afraid, but I have since found the answer. Basically, a checkpoint (otherwise known as the DNA damage checkpoint) response is a stage in DNA replication where the cell cycle stops owing to DNA damage and becomes more susceptible to apoptosis ( programmed cell death). a more detailed answer is shown in the paragraph below. "In response to DNA damage, eukaryotic cells activate a set of surveillance systems that interrupt cell cycle progression to allow time for repair. These surveillance systems are called checkpoints and have been given an empirical definition. The DNA damage checkpoint acts in three stages in the cell cycle, one at the G1-S phase transition (G1 checkpoint), one at S phase (S-phase checkpoint), and one at the G2-M boundary (G2 checkpoint. With checkpoint failure, the immediate consequence is that the cells increase their sensitivity to being killed, and the long-term consequence is that the cells increase their susceptibility to tumor genesis. S-phase checkpoint monitors progression through S phase, which slows the rate of on-going DNA synthesis." Ref: http://cancerres.aacrjournals.org/cgi/content/full/62/6/1598
DNA endonucleases are used to cut the DNA. They are specific enzyme that recognize the particular site of the DNA and digest them. DNA polymerase and DNA ligase are also involved in repairing DNA damage.
DNA Lesions are sites of damage in the base-pairing or structure of DNA.
DNA polymerase can fill the gaps in the DNA that are left by removal of damage bases. DNA polymerase can help cancer cells to tolerate DNA damage.
Teri bhen di sallaa kutta kamina penchod.<-df is that ignore it, If there are mutations in checkpoint proteins (such as in cancer cells), mitosis may proceed but the chromosomes may not be separated normally (resulting in "aneuploidy").
I am answering my own question here I'm afraid, but I have since found the answer. Basically, a checkpoint (otherwise known as the DNA damage checkpoint) response is a stage in DNA replication where the cell cycle stops owing to DNA damage and becomes more susceptible to apoptosis ( programmed cell death). a more detailed answer is shown in the paragraph below. "In response to DNA damage, eukaryotic cells activate a set of surveillance systems that interrupt cell cycle progression to allow time for repair. These surveillance systems are called checkpoints and have been given an empirical definition. The DNA damage checkpoint acts in three stages in the cell cycle, one at the G1-S phase transition (G1 checkpoint), one at S phase (S-phase checkpoint), and one at the G2-M boundary (G2 checkpoint. With checkpoint failure, the immediate consequence is that the cells increase their sensitivity to being killed, and the long-term consequence is that the cells increase their susceptibility to tumor genesis. S-phase checkpoint monitors progression through S phase, which slows the rate of on-going DNA synthesis." Ref: http://cancerres.aacrjournals.org/cgi/content/full/62/6/1598
DNA endonucleases are used to cut the DNA. They are specific enzyme that recognize the particular site of the DNA and digest them. DNA polymerase and DNA ligase are also involved in repairing DNA damage.
DNA Lesions are sites of damage in the base-pairing or structure of DNA.
Cell cycle checkpoints are used by the cell to monitor and regulate the progress of the cell cycle. Checkpoints prevent cell cycle progression at specific points, allowing verification of necessary phase processes and repair of DNA damage. The cell cannot proceed to the next phase until checkpoint requirements have been met. Several checkpoints are designed to ensure that damaged or incomplete DNA is not passed on to daughter cells. Two main checkpoints exist: the G1/S checkpoint and the G2/M checkpoint. G1/S transition is a rate-limiting step in the cell cycle and is also known as restriction point. An alternative model of the cell cycle response to DNA damage has also been proposed, known as the postreplication checkpoint. p53 plays an important role in triggering the control mechanisms at both G1/S and G2/M checkpoints. Impaired spindle checkpoint function has been found in many forms of cancer. The BRCA1 tumor suppressor plays a role in the activation of human chk1, therefore the posreplication checkpoint may prevent the genetic changes that lead to cancer. Mutations in factors contributing to cell cycle arrest at the restriction point are thought to be the main contributors of cancer. hope this helps!
DNA polymerase can fill the gaps in the DNA that are left by removal of damage bases. DNA polymerase can help cancer cells to tolerate DNA damage.
DNA is copied (or replicated) by an enzyme called DNA polymerase. This enzyme generally operates in the 3' to 5' direction. However, this enzyme also has a 5' to 3' exonuclease activity, which enables it to remove certain wrong bases and insert correct ones. This ensure that the DNA is copied correctly
DNA replication occurs during the S phase of mitosis. Once the checkpoint S is passed in the cell cycle, the cell is committed to division.
Check for large healthy cell, proper DNA replication, and nuclear cytoplasmic division.
receptor proteins
checkpoint
No, vigorous vortexing can damage the DNA