Methyltransferase Set7/9 as a Multifaceted Regulator of ROS Response.

Daks, Alexandra; Shuvalov, Oleg; Fedorova, Olga; Parfenyev, Sergey; Simon, Hans-Uwe; Barlev, Nickolai A (2023). Methyltransferase Set7/9 as a Multifaceted Regulator of ROS Response. International journal of biological sciences, 19(8), pp. 2304-2318. 10.7150/ijbs.83158

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Reactive oxygen species (ROS) induce multiple signaling cascades in the cell and hence play an important role in the regulation of the cell's fate. ROS can cause irreversible damage to DNA and proteins resulting in cell death. Therefore, finely tuned regulatory mechanisms exist in evolutionarily diverse organisms that are aimed at the neutralization of ROS and its consequences with respect to cellular damage. The SET domain-containing lysine methyltransferase Set7/9 (KMT7, SETD7, SET7, SET9) post-translationally modifies several histones and non-histone proteins via monomethylation of the target lysines in a sequence-specific manner. In cellulo, the Set7/9-directed covalent modification of its substrates affects gene expression, cell cycle, energy metabolism, apoptosis, ROS, and DNA damage response. However, the in vivo role of Set7/9 remains enigmatic. In this review, we summarize the currently available information regarding the role of methyltransferase Set7/9 in the regulation of ROS-inducible molecular cascades in response to oxidative stress. We also highlight the in vivo importance of Set7/9 in ROS-related diseases.

Item Type:

Journal Article (Review Article)

Division/Institute:

04 Faculty of Medicine > Pre-clinic Human Medicine > Institute of Pharmacology

UniBE Contributor:

Simon, Hans-Uwe

Subjects:

600 Technology > 610 Medicine & health

ISSN:

1449-2288

Language:

English

Submitter:

Pubmed Import

Date Deposited:

23 May 2023 10:21

Last Modified:

24 May 2023 15:36

Publisher DOI:

10.7150/ijbs.83158

PubMed ID:

37215983

Uncontrolled Keywords:

ROS metabolism Set7/9 chromatin diabetes myocardial ischemic injury nephropathy oxidative stress p53

BORIS DOI:

10.48350/182806

URI:

https://boris.unibe.ch/id/eprint/182806

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