HPV Mutation Detail Information

Virus Mutation HPV Mutation F47R


Basic Characteristics of Mutations
Mutation Site F47R
Mutation Site Sentence To address this gap, a well-defined dominant negative HPV 16 E6 mutant (HPV16 E6 F47R) was expressed exogenously in HeLa cells.
Mutation Level Amino acid level
Mutation Type Nonsynonymous substitution
Gene/Protein/Region E6
Standardized Encoding Gene E6
Genotype/Subtype HPV16
Viral Reference -
Functional Impact and Mechanisms
Disease Uterine Cervical Neoplasms    
Immune -
Target Gene -
Clinical and Epidemiological Correlations
Clinical Information -
Treatment -
Location -
Literature Information
PMID 33374731
Title High Risk alpha-HPV E6 Impairs Translesion Synthesis by Blocking POLeta Induction
Author Wendel SO,Snow JA,Bastian T,Brown L,Hernandez C,Burghardt E,Kahn A,Murthy V,Neill D,Smith ZC,Ault K,Tawfik O,Wu C,Wallace NA
Journal Cancers
Journal Info 2020 Dec 23;13(1):28
Abstract High risk genus alpha human papillomaviruses (alpha-HPVs) express two versatile oncogenes (alpha-HPV E6 and E7) that cause cervical cancer (CaCx) by degrading tumor suppressor proteins (p53 and RB). alpha-HPV E7 also promotes replication stress and alters DNA damage responses (DDR). The translesion synthesis pathway (TLS) mitigates DNA damage by preventing replication stress from causing replication fork collapse. Computational analysis of gene expression in CaCx transcriptomic datasets identified a frequent increased expression of TLS genes. However, the essential TLS polymerases did not follow this pattern. These data were confirmed with in vitro and ex vivo systems. Further interrogation of TLS, using POLeta as a representative TLS polymerase, demonstrated that alpha-HPV16 E6 blocks TLS polymerase induction by degrading p53. This doomed the pathway, leading to increased replication fork collapse and sensitivity to treatments that cause replication stress (e.g., UV and Cisplatin). This sensitivity could be overcome by the addition of exogenous POLeta.
Sequence Data -
Mutation Information
Note
Basic Characteristics of Mutations
  • Mutation Site: The specific location in a gene or protein sequence where a change occurs.
  • Mutation Level: The level at which a mutation occurs, including the nucleotide or amino acid level.
  • Mutation Type: The nature of the mutation, such as missense mutation, nonsense mutation, synonymous mutation, etc.
  • Gene/Protein/Region: Refers to the specific region of the virus where the mutation occurs. Including viral genes, viral proteins, or a specific viral genome region. If the article does not specifically indicate the relationship between the mutation and its correspondence, the main
  • Gene/Protein/Region studied in the article is marked.
  • Genotype/Subtype: Refers to the viral genotype or subtype where the mutation occurs. If the article does not specifically indicate the relationship between the mutation and its correspondence, the main Genotype/Subtype studied in the article is marked.
  • Viral Reference: Refers to the standard virus strain used to compare and analyze viral sequences.
Functional Impact and Mechanisms
  • Disease: An abnormal physiological state with specific symptoms and signs caused by viral infection.
  • Immune: The article focuses on the study of mutations and immune.
  • Target Gene: Host genes that viral mutations may affect.
Clinical and Epidemiological Correlations
  • Clinical Information: The study is a clinical or epidemiological study and provides basic information about the population.
  • Treatment: The study mentioned a certain treatment method, such as drug resistance caused by mutations. If the study does not specifically indicate the relationship between mutations and their correspondence treatment, the main treatment studied in the article is marked.
  • Location: The source of the research data.
Literature Information
  • Sequence Data: The study provides the data accession number.