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What are oncogenes? How were tumor retroviruses used to discover oncogenes? What are tumor suppressors? What...

What are oncogenes? How were tumor retroviruses used to discover oncogenes?

What are tumor suppressors?

What are the differences between tumor suppressors and oncogenes?

How does p53 function to induce cell cycle arrest and apoptosis in response to stress?

Solutions

Expert Solution

1.What are oncogene

Oncogenes are genes that have more probability of causing cancer.when we take tumour cells these oncogenes are highly mutated.

2.How were tumor retroviruses used to discover oncogenes?

The first oncogenes were identified using retroviruses .The RNA tumor viruses genomes were reverse-transcribed into the DNA of the infected animal cells. During the time of the infection, retroviral DNA was inserted into the chromosomes of host cells.

3.What are tumor suppressors?

It regulates the gene during cell division and control the cell division by blocking uncontrollable division of the cells.

4.What are the differences between tumor suppressors and oncogenes?

The main difference between the oncogenes and tumor suppressor genes is that the oncogenes result from the activation or(turning on) of proto-oncogenes, but the tumor suppressor genes cause cancer when they are inactivated.So this is the major difference.

5.How does p53 function to induce cell cycle arrest and apoptosis in response to stress?

p53 mainly induces aptosis and cell arrest in response to stress it does this by the below mechanisms

In the normal cells, p53 protein level is low. DNA damage and other stress signals may increase  p53 proteins, which have three major functions: growth arrest, DNA repair and apoptosis (cell death). The growth arrest stops the progression of cell cycle, preventing replication of damaged DNA.

P53 induces apoptosis in nontransformed cells by directionl transcriptional activation of the pro-apoptotic BH3-only proteins PUMA and NOXA. Combined loss of the p53 effectors of apoptosis (PUMA plus NOXA) and cell cycle arrest/cell senescence (p21) and itdoes not cause spontaneous tumour development.So this is how it induces apoptosis.


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