ArticleThe Journal of clinical investigation2004
Distal renal tubular acidosis in mice that lack the forkhead transcription factor Foxi1.
Article in The Journal of clinical investigation, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 papers.
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Who cites it
119 citing papers in PubMed, 203 citations in OpenAlex.
- The SLC-ome of membrane transport: from molecular discovery to physiology and clinical applications.Physiological reviews · 2026Review
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- Kidney Cyst Epithelia in Tuberous Sclerosis Complex (TSC) Exhibit Propagation and Expansion of A-Intercalated, but Loss of B-Intercalated and Principal Cells: The Role of FOXI1, FOXP1, and DMRT2 Transcription Factors.International journal of molecular sciences · 2026Article
- Molecular Basis of Rare Inherited Tubulopathies of the Kidney: A Primer for Clinicians.International journal of molecular sciences · 2026Review
- The landscape of gene mutations in a cohort of 3353 Han Chinese children with nonsyndromic hearing loss.EBioMedicine · 2026Article
- Hmx2 and Dmrt2 Coordinate the Differentiation of Intercalated Cell Subtypes in Kidney.Journal of the American Society of Nephrology : JASN · 2026Article
- The critical role of the proto-oncogene c-Kit in TSC renal cystogenesis.EMBO molecular medicine · 2026Article
- Foxi1 regulates multipotent mucociliary progenitors and ionocyte specification through transcriptional and epigenetic mechanisms.PLoS biology · 2026Article
- Foxi1 regulates multipotent mucociliary progenitors and ionocyte specification through transcriptional and epigenetic mechanisms.bioRxiv : the preprint server for biology · 2025Article
- The role and mechanism of TSC in kidney diseases: a literature review.BMC nephrology · 2025Review
- Dmrt2 and Hmx2 direct intercalated cell diversity in the mammalian kidney through antagonistic and supporting regulatory processes.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Developmental and Cell Fate Analyses Support a Postnatal Origin for the Cortical Collecting System in the Mouse Kidney.Journal of the American Society of Nephrology : JASN · 2025Article
- Integrated single-cell transcriptomic map of pig kidney cells across various periods and anatomical sites.Zoological research · 2025Article
- A case report and literature review of primary distal renal tubular acidosis resulting from a mutation inFrontiers in pediatrics · 2025Article
- Comparative genomic profiling of SLC26A4-expressing cells in the inner ear and other organs.PloS one · 2025Article
- A Possible Link between Cell Plasticity and Renin Expression in the Collecting Duct: A Narrative Review.International journal of molecular sciences · 2024Review
- Homozygous Missense Variants in FOXI1 and TMPRSS3 Genes Associated with Non-syndromic Deafness in Moroccan Families.Biochemical genetics · 2024Article
- Deletion of the prorenin receptor in the ureteric bud in mice inhibits Dot1/H3K79 pathway.Pediatric research · 2024Article
- Carbonic Anhydrase 2 Deletion Delays the Growth of Kidney Cysts Whereas Foxi1 Deletion Completely Abrogates Cystogenesis in TSC.International journal of molecular sciences · 2024Article
- Generation ofAmerican journal of physiology. Renal physiology · 2023Article
59 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
While macro- and microscopic kidney development appear to proceed normally in mice that lack Foxi1, electron microscopy reveals an altered ultrastructure of cells lining the distal nephron. Northern blot analyses, cRNA in situ hybridizations, and immunohistochemistry demonstrate a complete loss of expression of several anion transporters, proton pumps, and anion exchange proteins expressed by intercalated cells of the collecting ducts, many of which have been implicated in hereditary forms of distal renal tubular acidosis (dRTA). In Foxi1-null mutants the normal epithelium with its two major cell types - principal and intercalated cells - has been replaced by a single cell type positive for both principal and intercalated cell markers. To test the functional consequences of these alterations, Foxi1(-/-) mice were compared with WT littermates in their response to an acidic load. This revealed an inability to acidify the urine as well as a lowered systemic buffer capacity and overt acidosis in null mutants. Thus, Foxi1(-/-) mice seem to develop dRTA due to altered cellular composition of the distal nephron epithelium, thereby denying this epithelium the proper gene expression pattern needed for maintaining adequate acid-base homeostasis.
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