SLC29A1 and SLC29A2 are human nicotinamide cell membrane transporters

Mingyang Chen, Luexiang Yuan, Binxin Chen, Hui Chang, Jun Luo, Hengbin Zhang, Zhongjian Chen, Jiao Kong, Yaodong Yi, Mengru Bai, Minlei Dong, Hui Zhou (zhouhui@zju.edu.cn) and Huidi Jiang (hdjiang@zju.edu.cn)
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Mingyang Chen: Zhejiang University
Luexiang Yuan: Zhejiang University
Binxin Chen: Zhejiang University
Hui Chang: Zhejiang University
Jun Luo: Zhejiang University
Hengbin Zhang: Zhejiang University
Zhongjian Chen: Chinese Academy of Sciences
Jiao Kong: Zhejiang University
Yaodong Yi: Zhejiang University
Mengru Bai: Westlake University
Minlei Dong: Zhejiang University
Hui Zhou: Zhejiang University
Huidi Jiang: Zhejiang University

Nature Communications, 2025, vol. 16, issue 1, 1-17

Abstract: Abstract 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.

Date: 2025
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DOI: 10.1038/s41467-025-56402-y

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