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Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
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In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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DNA Damage Can Stall the Cell Cycle

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Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
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Yeast As a Chassis for Developing Functional Assays to Study Human P53
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Published on: August 4, 2019

dNTP Supply Gene Expression Patterns after P53 Loss.

Tomas Radivoyevitch1, Yogen Saunthararajah, John Pink

  • 1Departments of Epidemiology and Biostatistics, General Medical Sciences (Oncology), and Pathology, Case Western Reserve School of Medicine, Cleveland, OH 44106, USA.

Cancers
|December 4, 2012
PubMed
Summary
This summary is machine-generated.

Loss of p53 transcription factor causes losses in p53R2 mRNA. Other genes in the deoxyribonucleotide triphosphate (dNTP) supply system compensate for these losses, maintaining DNA synthesis.

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Area of Science:

  • Molecular Biology
  • Genetics
  • Biochemistry

Background:

  • The transcription factor p53 regulates numerous genes, including p53R2, a subunit of human ribonucleotide reductase (RNR).
  • Loss of p53 function can lead to decreased expression of its target genes, potentially impacting DNA synthesis.
  • The deoxyribonucleotide triphosphate (dNTP) supply system is crucial for DNA replication and repair.

Purpose of the Study:

  • To investigate whether other genes within the dNTP supply system compensate for the loss of p53R2.
  • To analyze compensatory mechanisms in both de novo and salvage dNTP synthesis pathways following p53 loss.
  • To elucidate the distinct roles of mitochondrial and cytosolic salvage enzymes in maintaining dNTP pools.

Main Methods:

  • Analysis of gene expression data from personal experiments and the Gene Expression Omnibus (GEO) database.
  • Quantification of mRNA levels for various dNTP supply enzymes.
  • Comparison of gene expression profiles in the presence and absence of functional p53.

Main Results:

  • The de novo dNTP supply system compensates for p53R2 loss through increased expression of RNR subunits R1 and R2.
  • Compensatory upregulation of cytosolic salvage enzymes deoxycytidine kinase (dCK) and thymidine kinase 1 (TK1), and mitochondrial deoxyguanosine kinase (dGK) was observed.
  • Conversely, mitochondrial thymidine kinase 2 (TK2) expression decreased upon p53 loss.

Conclusions:

  • The dNTP supply system exhibits compensatory mechanisms to counteract p53-mediated losses of p53R2.
  • Mitochondrial TK2 may be primarily dedicated to mitochondrial dNTP demands, while dGK might support cytosolic dNTP supply for nuclear DNA.
  • These findings highlight the intricate regulation of dNTP pools and the specialized roles of salvage enzymes.