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Identification And Characterization Of Histone Mark Isonicotinylation That Is Induced By Anti-tuberculosis First-line Drug Isoniazid

ABSTRACT: Identification And Characterization Of Histone Mark Isonicotinylation That Is Induced By Anti-tuberculosis First-line Drug Isoniazid

PROVIDER: PRJNA707505 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13890622_1.fastq.gz	Fastqsanger.gz
	SRR13890622_2.fastq.gz	Fastqsanger.gz
	SRR13890623_1.fastq.gz	Fastqsanger.gz
	SRR13890623_2.fastq.gz	Fastqsanger.gz
	SRR13890624_1.fastq.gz	Fastqsanger.gz

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Identification And Characterization Of Histone Mark Isonicotinylation That Is Induced By Anti-tuberculosis First-line Drug Isoniazid

Project description:We identified and characterized a previously undescribed histone mark, lysine isonicotinylation. This histone mark could be modulated by isoniazid (INH), aa preferred and widely used drug for the treatment of latent tuberculosis (TB), via generation of isonicotyl CoA. By RNA-seq analysis, we demonstrate that histone lysine isonicotinylation marks are involved in regulation of gene expression and associated with diverse biological processes. Thereby,enhanced isonicotinylation may represent a mechanism underlying side effects in patients who taking long-term isoniazid and may also increase risk for cancers.

2021-08-11 | GSE168473 | GEO

Isonicotinylation is Isonicotinylation is a histone mark induced by the anti-tuberculosis first-line drug isoniazida histone mark induced by the anti-tuberculosis first-line drug isoniazid

Project description:Isoniazid (INH) is the first-line anti-tuberculosis drug used for nearly seventy years. Metabolites of INH showed hepatotoxicity in human and tumorigenicity in rodents. However, mechanism underlying the side effects of INH is elusive. Histone acylation is known to be modulated by intracellular metabolites. Here, we report INH and its metabolites induces a novel post-translational modification (PTM) on histones, the lysine isonicotinylation (Kinic), also called 4-picolinylation, in cells and mice. INH functions as a donor to promote biosynthesis of isonicotinyl-CoA that is used for a co-factor of intracellular isonicotinylation reaction. Twenty-six isonicotinylation sites were identified on histones in HepG2 cells by mass spectrometry. Acetyltransferases CREB-binding protein (CBP) and P300 were found to catalyze histone Kinic, whilst histone deacetylase HDAC3 functions as a deisonicotinylase. MNase sensitivity assay and RNA-seq analysis showed that histone Kinic relaxes chromatin structure and promotes gene transcription. Importantly, INH-mediated histone Kinic upregulates PIK3R1 gene expression and activates PI3K/Akt/mTOR signaling pathway in liver cancer cells, linking INH to the tumorigenicity in liver. Further, Kinic was found increased in liver cancer patients with concomitant raised PIK3R1 protein level. In addition, histone Kinic also affects TNF and GABAergic synapse signaling pathways that are closely related to INH-caused side effects. Taken together, we demonstrated that lysine isonicotinylation represents the first histone acylation mark with the pyridine ring that may arise broad biological effects. Therefore, INH-induced isonicotinylation is likely a mechanism accounting for side effects in patients who taking long-term INH for anti-tuberculosis therapy and this modification may also increase cancer risk in human.

2021-08-20 | PXD025490 | Pride

Small RNAs in anti-tuberculosis drug-induced liver injury

Project description:The antimicrobials isoniazid and pyrazinamide, used for the treatment of tuberculosis are known to cause drug-induced liver injury in humans. This limits the effectiveness of tuberculosis treatment, resulting in incomplete cure, relapse and the development of antimicrobial resistance. MicroRNAs are known to be good biomarkers of disease, with the microRNA miR-122 being diagnostic for liver injury. In this study zebrafish larvae were exposed to the anti-tuberculosis drugs isoniazid and pyrazinamide at concentrations which demonstrated liver injury by microscopy and histology. The aim of this study is to understand small RNA changes occurring in anti-tuberculosis drug-induced liver injury and to attempt to identify novel microRNA biomarkers of liver injury.

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Expression profiling of extensively drug-resistant tuberculosis isolates and H37Rv exposed to anti-TB compounds

Project description:To explore the mechanism of drug resistance, most works focused on resistance associated genetic mutations, whereas concerns for resistance related gene expression are relatively low. Here a global expression analysis was performed between a reference strain H37Rv and two clinical extensively drug-resistant (XDR) strains with three anti-TB drug exposures {isoniazid (INH), capreomycin (CAP), rifampicin (RIF)} Strains were grown in Middlebrook 7H9 broth supplemented with ADC, 0.05% Tween 80 and 0.2% glycerol to an OD600 of 0.5-0.6, and then respectively treated with control (water), 10×MIC INH, 1×MIC RIF and CAP for 6hr.

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Project description:Genome wide DNA methylation profiling of normal and colon cancer and assosiation study between anti-cancer drug respond group and non-respond group. The Illumina Infinium 27k Human DNA methylation Beadchip v1.2 was used to obtain DNA methylation profiles across approximately 27,000 CpGs in 118 paired anti-cancer drug response tested colon cancer and adjacent normal tissues Bisulphite converted DNA from the 248 samples were hybridised to the Illumina Infinium 27k Human Methylation Beadchip v1.2

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Lysine benzoylation - Here we report the identification and characterization of a histone mark, lysine benzoylation (Kbz). Our study identifies 22 Kbz sites on histones from HepG2 and RAW cells. This type of histone mark can be stimulated by sodium benzoate (SB), a FDA-approved drug and a widely used chemical food preservative, via generation of benzoyl CoA.

Project description:Here we report the identification and characterization of a histone mark, lysine benzoylation (Kbz). Our study identifies 22 Kbz sites on histones from HepG2 and RAW cells. This type of histone mark can be stimulated by sodium benzoate (SB), a FDA-approved drug and a widely used chemical food preservative, via generation of benzoyl CoA.

2018-07-11 | PXD010332 | Pride

Isonicotinylation is a histone mark induced by the anti-tuberculosis first-line drug isoniazid.

Project description:Isoniazid (INH) is a first-line anti-tuberculosis drug used for nearly 70 years. However, the mechanism underlying the side effects of INH has remained elusive. Here, we report that INH and its metabolites induce a post-translational modification (PTM) of histones, lysine isonicotinylation (Kinic), also called 4-picolinylation, in cells and mice. INH promotes the biosynthesis of isonicotinyl-CoA (Inic-CoA), a co-factor of intracellular isonicotinylation. Mass spectrometry reveals 26 Kinic sites in histones in HepG2 cells. Acetyltransferases CREB-binding protein (CBP) and P300 catalyse histone Kinic, while histone deacetylase HDAC3 functions as a deisonicotinylase. Notably, MNase sensitivity assay and RNA-seq analysis show that histone Kinic relaxes chromatin structure and promotes gene transcription. INH-mediated histone Kinic upregulates PIK3R1 gene expression and activates the PI3K/Akt/mTOR signalling pathway in liver cancer cells, linking INH to tumourigenicity in the liver. We demonstrate that Kinic is a histone acylation mark with a pyridine ring, which may have broad biological effects. Therefore, INH-induced isonicotinylation potentially accounts for the side effects in patients taking INH long-term for anti-tuberculosis therapy, and this modification may increase the risk of cancer in humans.

| S-EPMC8452692 | biostudies-literature

2020-10-02 | MSV000086228 | MassIVE