Biology, 05.10.2019 22:30 kaylaamberd

1. explain why neither cyclins not kinases alone can cause a cell to progress along in the cell cycle.
2. how do controls on the cell cycle protect multicellular organisms from accumulating large numbers of damaged or defective cells?
3. what is the difference between cancerous tumor and metastasis?
4. what are the functions of tumor-suppressive genes and proto-oncogenes in noncancerous cells?

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1. Explain why neither cyclins nor kinases alone can cause a cell to progress through the cell cycle.

As cyclin accumulates, it activates their kinases that turn on the pathway to mitotic spindle formation, and so on.

2. How do controls of the cell cycle protect multi-cellular organisms from accumulating large numbers of damaged or defective cells?

The checkpoint control is responsible for multi-cellular organisms for not accumulating large numbers of damaged or defective cells. Checkpoint controls consist of proteins that detect mistakes and damage and quickly halt the cell cycle until repairs are made. When this occurs, the cell is said to be in cell-cycle arrest.

3. What is the difference between a cancerous tumor and metastasis?
Cancer is cause by mutations in the genes that encode these proteins can lead to uncontrolled growth. Cancer is when there is uncontrolled cell growth and reproduction. Metastasis is caused by tumors when they grow and interfere with the surrounding tissue or cells and break off and spread around the body. Cancerous tumors cause metastasis, and tumors are caused by mutations in genes that lead to uncontrolled growth.
4. What are the functions of tumor-suppressor genes and protoncogenes in noncancerous cells?
The genes that encode the checkpoint proteins are called tumor suppressors because they suppress the development of cells into tumors. If mutations inactivate these genes, the cell-cycle break is removed with or without a signal from the outside. Proto-oncogene’s are involved in promoting cell division, mutations can cause them to become oncogenes, or cancer genes which stimulate cells to leave G0 and divide whether or not it is a signal.

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