SLC29A1 and SLC29A2 are human nicotinamide cell membrane transporters
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1055465 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27318361_1.fastq.gz | Fastqsanger.gz | |||
| SRR27318361_2.fastq.gz | Fastqsanger.gz | |||
| SRR27318362_1.fastq.gz | Fastqsanger.gz | |||
| SRR27318362_2.fastq.gz | Fastqsanger.gz | |||
| SRR27318363_1.fastq.gz | Fastqsanger.gz |
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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.
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Project description:Nicotinamide (NAM), 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 (NMN) have been identified, but the cellular transporter of nicotinamide has not been elucidated. Here, we demonstrate that equilibrative nucleoside transporter 1 and 2 (ENT1 and 2, encoded by SLC29A1 and 2) drive cellular nicotinamide uptake and establish nicotinamide metabolism homeostasis. In addition, ENT1/2 exhibits a strong capacity to change the cellular metabolite composition and the transcript, especially those related to nicotinamide. We further observe that ENT1/2 regulates cellular respiration and senescence, contributing by altering the NAD+ pool level and mitochondrial status. Changes to cellular respiration, mitochondrial status and senescence by ENT1/2 knockdown are reversed by NMN supplementation. Together, ENT1 and ENT2 act as both cellular nicotinamide-level keepers and nicotinamide biological regulators through their NAM transport functions.
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Project description:We examined the effect of nicotinamide on cell survival and differentiation in human pluripotent stem cells. Nicotinamide inhibited the phosphorylation of myosin light chain, suppressed actomyosin contraction, and led to improved cell survival after individualization. Then we analyzed the global gene expression profile after 24 hours of nicotinamide and ROCK inhibitor treatment, and found that the gene expression profile of human embryonic stem cell (hESC) treated with nicotinamide was much different from that of ROCK inhibitor treatment. Further analysis demonstrates that nicotinamide is an inhibitor of multiple kinases, including ROCK and CK1. We demonstrated that nicotinamide affected human embryonic stem cell (hESC) pluripotency and differentiation as a selective kinase inhibitor.
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