| First Author | Hudson BH | Year | 2018 |
| Journal | Proc Natl Acad Sci U S A | Volume | 115 |
| Issue | 12 | Pages | 3000-3005 |
| PubMed ID | 29507250 | Mgi Jnum | J:259846 |
| Mgi Id | MGI:6147942 | Doi | 10.1073/pnas.1715302115 |
| Citation | Hudson BH, et al. (2018) Modulation of intestinal sulfur assimilation metabolism regulates iron homeostasis. Proc Natl Acad Sci U S A 115(12):3000-3005 |
| abstractText | Sulfur assimilation is an evolutionarily conserved pathway that plays an essential role in cellular and metabolic processes, including sulfation, amino acid biosynthesis, and organismal development. We report that loss of a key enzymatic component of the pathway, bisphosphate 3''-nucleotidase (Bpnt1), in mice, both whole animal and intestine-specific, leads to iron-deficiency anemia. Analysis of mutant enterocytes demonstrates that modulation of their substrate 3''-phosphoadenosine 5''-phosphate (PAP) influences levels of key iron homeostasis factors involved in dietary iron reduction, import and transport, that in part mimic those reported for the loss of hypoxic-induced transcription factor, HIF-2alpha. Our studies define a genetic basis for iron-deficiency anemia, a molecular approach for rescuing loss of nucleotidase function, and an unanticipated link between nucleotide hydrolysis in the sulfur assimilation pathway and iron homeostasis. |
