Dataset Information

Protein response of lncRNA-DRC to HU treatment

ABSTRACT: protein response of lncRNA-DRC overexpression (mec1Δ sml1Δ-lncRNA-DRC-OE) to HU treatment

ORGANISM(S): Saccharomyces Cerevisiae

SUBMITTER: Zewen Wen

PROVIDER: PXD056715 | iProX | Thu Oct 10 00:00:00 BST 2024

REPOSITORIES: iProX

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Publications

A novel lncRNA YIL163C enhances genomic stability and antifungal resistance via the DNA damage response in <i>Saccharomyces cerevisiae</i>.

Wang Xueting X Li Xuemei X Li Duoyun D Zhang Yiying Y Bai Bing B Chai Bao B Wen Zewen Z

Frontiers in microbiology 20250501

<h4>Introduction</h4>Long non-coding RNAs (lncRNAs) are increasingly recognized as key regulators in cellular processes, including the DNA damage response (DDR). In <i>Saccharomyces cerevisiae</i>, DDR is critical for maintaining genomic integrity under stress, mediated by proteins like Mec1 and Rad53. However, the involvement of lncRNAs in DDR pathways, remains largely unexplored. This study investigates the function of a novel lncRNA, YIL163C, in promoting cell survival and genomic stability u ...[more]

PMID: 40376465

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Project description:Inflammatory response plays a bidirectional regulatory role in myocardial infarction (MI). TLR signaling pathway plays an important role in the development of inflammation. Additionally, we discovered that CCRR is an anti-arrhythmic lncRNA in a prior work. Here we show, it is decreased in mice with 3-day MI followed by a sharp increase of pro-inflammatory cytokines and activation of the TLR pathway. Overexpression of CCRR could effectively inhibit the inflammatory response, reduce the infarct area, and improve cardiac function. And also reduced hypoxia-induced inflammation in cardiomyocytes and macrophages induced by IFN and LPS. It produced a similar protective effect in cardiomyocytes co-cultured with macrophages. Through microarray analysis, RNA-binding protein immunoprecipitation analysis, and other related experiments verification, TLR2 and TLR4 may be as potential targets of CCRR after MI. Our findings provide the evidence that lncRNA CCRR plays a key cardioprotective role against MI injury by targeting the TLR signaling pathway. nflammatory response plays a bidirectional regulatory role in myocardial infarction (MI). TLR signaling pathway plays an important role in the development of inflammation. Additionally, we discovered that CCRR is an anti-arrhythmic lncRNA in a prior work. Here we show, it is decreased in mice with 3-day MI followed by a sharp increase of pro-inflammatory cytokines and activation of the TLR pathway. Overexpression of CCRR could effectively inhibit the inflammatory response, reduce the infarct area, and improve cardiac function. And also reduced hypoxia-induced inflammation in cardiomyocytes and macrophages induced by IFN and LPS. It produced a similar protective effect in cardiomyocytes co-cultured with macrophages. Through microarray analysis, RNA-binding protein immunoprecipitation analysis, and other related experiments verification, TLR2 and TLR4 may be as potential targets of CCRR after MI. Our findings provide the evidence that lncRNA CCRR plays a key cardioprotective role against MI injury by targeting the TLR signaling pathway.

Dataset Information

Protein response of lncRNA-DRC to HU treatment

Publications

A novel lncRNA YIL163C enhances genomic stability and antifungal resistance via the DNA damage response in <i>Saccharomyces cerevisiae</i>.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

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Dataset Information

Protein response of lncRNA-DRC to HU treatment

Publications

A novel lncRNA YIL163C enhances genomic stability and antifungal resistance via the DNA damage response in &lt;i&gt;Saccharomyces cerevisiae&lt;/i&gt;.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets

A novel lncRNA YIL163C enhances genomic stability and antifungal resistance via the DNA damage response in <i>Saccharomyces cerevisiae</i>.