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How To Repair P53 Gene

Review

. 2016 May 2;half-dozen(5):a026070.

doi: ten.1101/cshperspect.a026070.

p53 in the Deoxyribonucleic acid-Damage-Repair Process

Affiliations

  • PMID: 27048304
  • PMCID: PMC4852800
  • DOI: ten.1101/cshperspect.a026070

Gratis PMC article

Review

p53 in the Dna-Damage-Repair Process

Ashley B Williams  et al. Common cold Spring Harb Perspect Med. .

Free PMC article

Abstract

The cells in the human body are continuously challenged by a variety of genotoxic attacks. Erroneous repair of the Deoxyribonucleic acid tin can atomic number 82 to mutations and chromosomal aberrations that can alter the functions of tumor suppressor genes or oncogenes, thus causing cancer evolution. As a central tumor suppressor, p53 guards the genome past orchestrating a variety of Deoxyribonucleic acid-damage-response (DDR) mechanisms. Already early in metazoan evolution, p53 started controlling the apoptotic demise of genomically compromised cells. p53 plays a prominent role equally a facilitator of Dna repair by halting the cell cycle to permit time for the repair machineries to restore genome stability. In addition, p53 took on various roles to as well directly bear upon the activity of various Dna-repair systems. It thus appears as if p53 is multitasking in providing protection from cancer development by maintaining genome stability.

Figures

Figure 1.
Figure 1.

Examples of p53 interactions with DNA-repair pathways. (AC) Simplified representations of canonical Deoxyribonucleic acid-repair pathways: nucleotide excision repair (NER), base of operations excision repair (BER), and mismatch repair (MMR). Factors with transcription-related interactions are highlighted in orange and factors with nontranscriptional interactions are highlighted in blue. Note that OGG1 has both transcription-dependent and -independent interactions with p53 during base excision repair. Red arrows point regulatory effects on p53.

Figure 2.
Figure 2.

Examples of p53 interactions with double-strand pause repair pathways (left) and p53 checkpoint signaling (correct). (A,B) Simplified representations of double-strand pause repair via homologous recombination (HR) and nonhomologous terminate joining (NHEJ). (C) Simplified representation of p53 signaling at double-strand breaks. Factors with transcription-related interactions are highlighted in orange and factors with nontranscriptional interactions are highlighted in blue. Annotation that RAD51 has both transcription-dependent and -independent interactions with p53 during base excision repair. Cherry labels and blood-red arrows bespeak regulatory furnishings on p53.

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Source: https://pubmed.ncbi.nlm.nih.gov/27048304/

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