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&nbsp;P53 is a [[Tumour|tumour]] suppressor [[Gene|gene]], which is accumulates when DNA becomes damaged beyond repair or the cell becomes stressed <ref>Bruce Alberts, Alexander Johnson, Julian Lewis, Martin Raff, Keith Roberts, Peter Walter, (2008) Molecular Biology of the Cell, 5th edition,  New York: Garland Science p.1123</ref> . In a normal cell in which DNA is not damaged or when the cell is not stressed, [[Mdm2|Mdm2]] binds to P53. [[Mdm2|Mdm2]] is a polyubiquitin ligase which labels P53 for degredation. However, when DNA is damaged, or when the cell is stressed, [[ATM|ATM]] becomes activated which [[Phosphorylation|phosporylates]] P53 preventing the binding of [[Mdm2|Mdm2]]&nbsp; <ref>Bruce Alberts, Alexander Johnson, Julian Lewis, Martin Raff, Keith Roberts, Peter Walter, (2008) Molecular Biology of the Cell, 5th edition,  New York: Garland Science p.1105</ref> . Consequently the levels of P53 increase, inducing the production of [[P21|p21]] resulting in the inhibition [[Cdk-Cyclin|Cdk-Cyclin]] complexs which arrest the cell division cycle <ref>Bruce Alberts, Alexander Johnson, Julian Lewis, Martin Raff, Keith Roberts, Peter Walter, (2008) Molecular Biology of the Cell, 5th edition,  New York: Garland Science p.1105-1107</ref> . However if P53 levels increase to a high level due to high levels of DNA damage, [[Apoptosis|apoptosis]] results. <br>Cancer cells accumulate more mutations due to the loss of P53 which allows the [[Cell division cycle|cell division cycle]] to progress even when DNA is damaged <ref>Bruce Alberts, Alexander Johnson, Julian Lewis, Martin Raff, Keith Roberts, Peter Walter, (2008) Molecular Biology of the Cell, 5th edition,  New York: Garland Science p.1106</ref> .  
P53 is a [[Tumour|tumour]] suppressor [[Gene|gene]], which is accumulates when [[DNA|DNA]] becomes damaged beyond repair or the [[Cell|cell]] becomes stressed <ref>Bruce Alberts, Alexander Johnson, Julian Lewis, Martin Raff, Keith Roberts, Peter Walter, (2008) Molecular Biology of the Cell, 5th edition,  New York: Garland Science p.1123</ref>. In a normal cell in which DNA is not damaged or when the cell is not stressed, [[Mdm2|Mdm2]] binds to P53. [[Mdm2|Mdm2]] is a [[polyubiquitin ligase|polyubiquitin ligase]] which labels P53 for degredation. However, when DNA is damaged, or when the cell is stressed, [[ATM|ATM]] becomes activated which [[Phosphorylation|phosporylates]] P53 preventing the binding of [[Mdm2|Mdm2]]&nbsp; <ref>Bruce Alberts, Alexander Johnson, Julian Lewis, Martin Raff, Keith Roberts, Peter Walter, (2008) Molecular Biology of the Cell, 5th edition,  New York: Garland Science p.1105</ref> . Consequently the levels of P53 increase, inducing the production of [[P21|p21]] resulting in the inhibition [[Cdk-Cyclin|Cdk-Cyclin]] complexs which arrest the [[Cell_cycle|cell division cycle]] <ref>Bruce Alberts, Alexander Johnson, Julian Lewis, Martin Raff, Keith Roberts, Peter Walter, (2008) Molecular Biology of the Cell, 5th edition,  New York: Garland Science p.1105-1107</ref> . However if P53 levels increase to a high level due to high levels of DNA damage, [[Apoptosis|apoptosis]] results. <br>Cancer cells accumulate more mutations due to the loss of P53 which allows the [[Cell division cycle|cell division cycle]] to progress even when DNA is damaged <ref>Bruce Alberts, Alexander Johnson, Julian Lewis, Martin Raff, Keith Roberts, Peter Walter, (2008) Molecular Biology of the Cell, 5th edition,  New York: Garland Science p.1106</ref> .  


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=== References ===


=== References  ===
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Revision as of 07:32, 15 November 2011

P53 is a tumour suppressor gene, which is accumulates when DNA becomes damaged beyond repair or the cell becomes stressed [1]. In a normal cell in which DNA is not damaged or when the cell is not stressed, Mdm2 binds to P53. Mdm2 is a polyubiquitin ligase which labels P53 for degredation. However, when DNA is damaged, or when the cell is stressed, ATM becomes activated which phosporylates P53 preventing the binding of Mdm2  [2] . Consequently the levels of P53 increase, inducing the production of p21 resulting in the inhibition Cdk-Cyclin complexs which arrest the cell division cycle [3] . However if P53 levels increase to a high level due to high levels of DNA damage, apoptosis results.
Cancer cells accumulate more mutations due to the loss of P53 which allows the cell division cycle to progress even when DNA is damaged [4] .

References

  1. ↑ Bruce Alberts, Alexander Johnson, Julian Lewis, Martin Raff, Keith Roberts, Peter Walter, (2008) Molecular Biology of the Cell, 5th edition, New York: Garland Science p.1123
  2. ↑ Bruce Alberts, Alexander Johnson, Julian Lewis, Martin Raff, Keith Roberts, Peter Walter, (2008) Molecular Biology of the Cell, 5th edition, New York: Garland Science p.1105
  3. ↑ Bruce Alberts, Alexander Johnson, Julian Lewis, Martin Raff, Keith Roberts, Peter Walter, (2008) Molecular Biology of the Cell, 5th edition, New York: Garland Science p.1105-1107
  4. ↑ Bruce Alberts, Alexander Johnson, Julian Lewis, Martin Raff, Keith Roberts, Peter Walter, (2008) Molecular Biology of the Cell, 5th edition, New York: Garland Science p.1106

  

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