ArticleNature communications2026
NAPRT-mediated deamidated NAD biosynthesis enhances colon tissue resiliency and suppresses tumorigenesis.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- NAPRT loss promotes lung tumor initiation and growth through AKT signaling independently of NADMolecular oncology · 2026Article
- Identification and functional analysis of NADFrontiers in genetics · 2026Article
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Authors and funding
23 authors.
Funding
Abstract
Nicotinamide adenine dinucleotide (NAD) is synthesized through both amidated salvage and deamidated pathways. Although NAD-producing enzymes are often overexpressed in cancer cells to meet the high metabolic demands of rapid proliferation and are considered oncogenic, we report that physiological levels of nicotinic acid phosphoribosyl transferase (NAPRT), the first enzyme in the Preiss-Handler arm of the deamidated pathways, suppress tumorigenesis. We show that NAPRT is enriched in gut epithelial cells, where it sustains the NAD pool for an efficient response to stress-induced acute NAD depletion. Consequently, NAPRT deficiency impairs the activity of poly-(ADP-ribose) polymerases and DNA repair, sensitizes mice to chemical-induced colitis and tumorigenesis, as well as to age-associated spontaneous tumor development. Moreover, low NAPRT expression correlates with poor prognosis in several human cancer types. Thus, homeostatic levels of deamidated NAD biosynthesis contribute to tumor suppression, and boosting this pathway may offer a strategy for cancer prevention.
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