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Histone Modification02:32

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The histone proteins have a flexible N-terminal tail extending out from the nucleosome. These histone tails are often subjected to post-translational modifications such as acetylation, methylation, phosphorylation, and ubiquitination. Particular combinations of these modifications form “histone codes” that influence the chromatin folding and tissue-specific gene expression.
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The histone proteins in the nucleosomes are post-translationally modified (PTM) to increase or decrease access to DNA. The commonly observed PTMs are methylation, acetylation, phosphorylation, and ubiquitination of lysine amino acids in the histone H3 tail region. These histone modifications have specific meaning for the cell. Hence, they are called "histone code". The protein complex involved in histone modification is termed as "reader-writer" complex.
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Translesion (TLS) polymerases rescue stalled DNA polymerases at sites of damaged bases by replacing the replicative polymerase and installing a nucleotide across the damaged site. Doing so, TLS allows additional time for the cell to repair the damage before resuming regular DNA replication.
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Behavioral approaches have often been criticized for ignoring mental processes and focusing solely on observable behavior. However, these approaches provide an optimistic perspective for individuals seeking to change their behaviors. Rather than concentrating on intrinsic personality traits, behavioral approaches suggest that even longstanding habits can be modified by changing the reward contingencies that maintain them.
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DNA Methylation: Bisulphite Modification and Analysis
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DNA methylation modifications induced by hexavalent chromium.

Xinnian Guo1, Lingfang Feng1, Bernardo Lemos2

  • 1a Institute of Occupation Diseases, Zhejiang Academy of Medical Sciences , Hangzhou , Zhejiang , P.R. China.

Journal of Environmental Science and Health. Part C, Environmental Carcinogenesis & Ecotoxicology Reviews
|May 16, 2019
PubMed
Summary

Hexavalent chromium (Cr VI) exposure poses health risks, potentially causing cancer. This review explores how Cr VI affects DNA methylation, a key epigenetic factor in cancer development.

Keywords:
DNA methylationhexavalent chromiumhypermethylationhypomethylation

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Area of Science:

  • Environmental Health
  • Toxicology
  • Epigenetics

Background:

  • Hexavalent chromium (Cr VI) is a known human carcinogen.
  • The precise mechanisms of Cr VI carcinogenesis are not fully understood.
  • Epigenetic alterations, particularly DNA methylation, are increasingly implicated in Cr VI-induced cancers.

Purpose of the Study:

  • To review the current understanding of Cr VI's impact on DNA methylation.
  • To summarize findings on both global and gene-specific methylation changes induced by Cr VI exposure.

Main Methods:

  • Literature review of studies investigating Cr VI and DNA methylation.
  • Analysis of research on epigenetic modifications in Cr VI carcinogenesis.

Main Results:

  • Cr VI exposure is associated with alterations in global DNA methylation patterns.
  • Specific genes show altered methylation levels in response to Cr VI exposure, potentially affecting cellular functions.
  • DNA methylation changes may mediate the carcinogenic effects of Cr VI.

Conclusions:

  • Epigenetic modifications, specifically DNA methylation, are crucial in Cr VI-induced carcinogenesis.
  • Further research is needed to elucidate the precise role of DNA methylation in Cr VI toxicity and cancer development.