Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptome profiling of Gastrocnemius from mice following supplementation with the combination of nicotinamide and pyridoxine (NAM/PN)

ABSTRACT: Transcriptome profiling of Gastrocnemius from mice following supplementation with the combination of nicotinamide and pyridoxine (NAM/PN)

PROVIDER: PRJNA1101866 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR28732720.fastq.gz	Fastqsanger.gz
	SRR28732721.fastq.gz	Fastqsanger.gz
	SRR28732722.fastq.gz	Fastqsanger.gz
	SRR28732723.fastq.gz	Fastqsanger.gz
	SRR28732724.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 76

Similar Datasets

Transcriptome profiling of Gastrocnemius from mice following supplementation with the combination of nicotinamide and pyridoxine (NAM/PN)

Project description:Nicotinamide and pyridoxine have been identified in an in vitro screening as potent modulators of Muscel Stem cell activity. To test the in vivo efficacy (of NAM/PN) on muscle regneration, we used a mouse model of muscle injury and regeneration. Transcriptomic analyses on whole muscles harvested 5 days after muscle injury were performed to better understand the effect of NAM/PN.

2024-11-18 | GSE264284 | GEO

Transcriptome profiling of Muscle Stem cells from aged mice following treatment with the combination of nicotinamide (NAM) and pyridoxine (PN) for 3 days.

Project description:Nicotinamide and pyridoxine have been identified as potent modulators of Muscle Stem cell activity. We characterized genome-wide expression profiles of NAM/PN-treated MuSC and Vehicle to verify if NAM/PN supplementation reverses MuSC dysfunction during Aging.

2024-11-18 | GSE269250 | GEO

Transcriptome profiling of human myogenic progenitors following treatment with nicotinamide (NAM) or pyridoxine (PN) or the combination (NAM/PN).

Project description:Working with primary human myogenic progenitors (hMPs), we developed a high-content screen to discover molecules that enhanced myogenic function and identified NAM and PN as modulators of myogenic proliferation and differentiation. We characterized genome-wide expression profiles of NAM-, PN-treated and NAM/PN-treated hMPs with the goal to uncover the mechanisms of action of NAM and PN and the potential additivity from the combination at the molecular level in hMPs.

2024-11-18 | GSE264285 | GEO

Transcriptome profiling of human myogenic progenitors following treatment with nicotinamide (NAM) or pyridoxine (PN) or the combination (NAM/PN).

Project description:Transcriptome profiling of human myogenic progenitors following treatment with nicotinamide (NAM) or pyridoxine (PN) or the combination (NAM/PN).

| PRJNA1101870 | ENA

Transcriptome profiling of Muscle Stem cells from aged mice following treatment with the combination of nicotinamide (NAM) and pyridoxine (PN) for 3 days.

Project description:Transcriptome profiling of Muscle Stem cells from aged mice following treatment with the combination of nicotinamide (NAM) and pyridoxine (PN) for 3 days.

| PRJNA1120821 | ENA

Expression data for hiPSC-derived RPE treated with 10mM Nicotinamide or vehicle

Project description:We did the RNA-seq analysis to examine the global impact of Nicotinamide (NAM) on hiPSC-derived RPE transcriptome in order to better understand the mechanism of action of NAM. NAM inhibited the expression of Age related Macular degeneration (AMD) associated protein transcripts in hiPSC-derived RPE.

2017-01-25 | GSE90889 | GEO

Expression data for hiPSC-derived RPE treated with 10mM Nicotinamide or vehicle

Project description:Nicotinamide (NAM) inhibited the expression of Age related macular degeneration (AMD) associated proteins in hiPSC-derived retinal pigment epithelium (RPE). We did the microarray analysis to examine the global impact of NAM on hiPSC-derived RPE transcriptome in order to better understand the mechanism of action of NAM.

2018-01-15 | GSE76923 | GEO

Nicotinamide regulates LPS-induced HIF-1alpha responses through post-translational modifications in human macrophages

Project description:Mechanisms to control the immune response are important to pathogen evasion and host defense. Gram-negative bacteria are common pathogens that can activate host immune responses through their outer membrane component, lipopolysaccharide (LPS). Macrophages activated by LPS induce cell signals that promote hypoxic metabolism, phagocytosis, and antigen presentation. Nicotinamide (NAM) is a vitamin B3 derivative and precursor in the formation of nicotinamide adenine dinucleotide (NAD), which is a required co-factor in cellular function. In this study, treatment of human monocyte derived macrophages with NAM antagonized LPS-induced responses by altering the expression of ubiquitin genes, increasing HIF-1alpha and p65/RelA ubiquitination, decreasing p65/RelA acetylation and promoting the formation of the proteasome. NAM also elevated intracellular NAD levels and altered the genetic expression of sirtuins and poly(ADP-ribose) polymerases. These NAM responses highlight post-translational events in regulating the host response to pathogens and identify the ubiquitome as a target in pathogen evasion and host defense.

2023-05-01 | GSE188206 | GEO

SLC29A1 and SLC29A2 are human nicotinamide cell membrane transporters

Project description:Nicotinamide, a main precursor of NAD+, is essential for cellular fuel respiration, energy production, and other cellular processes. Transporters for other precursors of NAD+ such as nicotinic acid and nicotinamide mononucleotide have been identified, but the cellular transporter of nicotinamide has not been elucidated. Here, we demonstrated that equilibrative nucleoside transporters 1 and 2 (ENT1 and 2, encoded by SLC29A1/2) drove cellular nicotinamide uptake and set nicotinamide metabolism homeostasis. In addition, ENT1/2 exhibited a strong capacity to change the composition of cellular metabolites and the profile of transcripts, especially those related to nicotinamide. Then, we further found that ENT1/2 could regulate cellular respiration and senescence, which are universally acknowledged as nicotinamide biological functions, to which the NAD+ pool level and mitochondrial status influenced by ENT1/2 made important contributions. Together, ENT1 and ENT2 act as both cellular nicotinamide-level keepers and nicotinamide biological regulators through their NAM transport functions.

2025-01-01 | GSE251776 | GEO

Aged Mouse Muscle and Serum: Sedentary or Exercised Animals with or without Nicotinamide N-methyltransferase Inhibitor Treatment

Project description:Epigenomic profiling mouse gastrocnemius muscle and serum in aged female mice with/without exercise, with/without nicotinamide N-methyltransferase inhibitor treatment

2024-07-13 | GSE267903 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data