ArticleThe Journal of clinical investigation2002
Transcriptional induction of slit diaphragm genes by Lmx1b is required in podocyte differentiation.
Article in The Journal of clinical investigation, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 149 citations in OpenAlex.
- Proteasome inhibition alleviates proteinuria in Lmx1b knock-in mice with dysfunctional LIM domains.Nature communications · 2026Article
- FOXC2 and WT1 regulate transcriptional reprogramming during the podocyte response to injury.JCI insight · 2026Article
- Clinicopathological characteristics and cyclosporine-responsive proteinuria in nail-patella syndrome with a novel LMX1B mutation.Pediatric nephrology (Berlin, Germany) · 2026Article
- Horns, nails, and leaky kidneys: A rare case of congenital nephrotic syndrome.Clinical nephrology. Case studies · 2026Article
- Identification of ARMH4 and WIPF3 as human podocyte proteins with potential roles in immunomodulation and cytoskeletal dynamics.PloS one · 2023Article
- Quality assessment and refinement of chromatin accessibility data using a sequence-based predictive model.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- A Novel Mutation in LMX1B (p.Pro219Ala) Causes Focal Segmental Glomerulosclerosis with Alport Syndrome-like Phenotype.Internal medicine (Tokyo, Japan) · 2021Article
- Case Report: Corneal Leucoma as a Novel Clinical Presentation of Nail-Patella Syndrome in a 5-Year-Old Girl.Frontiers in pediatrics · 2021Article
- Plateau iris syndrome and angle-closure glaucoma in a patient with nail-patella syndrome.American journal of ophthalmology case reports · 2020Article
- Focal Segmental Glomerulosclerosis and Scheduled Pretransplant Plasmapheresis: A Timely Diagnosis of Nail-Patella Syndrome Avoided More Futile Immunosuppression.Case reports in nephrology · 2020Article
- Foxc2 is essential for podocyte function.Physiological reports · 2019Article
- Modeling congenital kidney diseases inDisease models & mechanisms · 2019Review
- Novel missense mutation affecting the LIM-A domain of LMX1B in a family with Nail-Patella syndrome.Intractable & rare diseases research · 2019Article
- Podocyte-Specific Induction of Krüppel-Like Factor 15 Restores Differentiation Markers and Attenuates Kidney Injury in Proteinuric Kidney Disease.Journal of the American Society of Nephrology : JASN · 2018Article
- Lamellar projections in the endolymphatic sac act as a relief valve to regulate inner ear pressure.eLife · 2018Article
- Lmx1a is required for the development of the ovarian stem cell niche inDevelopment (Cambridge, England) · 2018Article
- Spectrum of LMX1B mutations: from nail-patella syndrome to isolated nephropathy.Pediatric nephrology (Berlin, Germany) · 2017Review
- Nail-patella syndrome.Pflugers Archiv : European journal of physiology · 2017Review
- Steroid-resistant nephrotic syndrome as the initial presentation of nail-patella syndrome: a case of a de novo LMX1B mutation.BMC nephrology · 2017Article
- Podocytes.F1000Research · 2016Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
LMX1B encodes a LIM-homeodomain transcription factor. Mutations in LMX1B cause nail-patella syndrome (NPS), an autosomal dominant disease with skeletal abnormalities, nail hypoplasia, and nephropathy. Expression of glomerular basement membrane (GBM) collagens is reduced in Lmx1b(-/-) mice, suggesting one basis for NPS nephropathy. Here, we show that Lmx1b(-/-) podocytes have reduced numbers of foot processes, are dysplastic, and lack typical slit diaphragms, indicating an arrest in development. Using antibodies to podocyte proteins important for podocyte function, we found that Lmx1b(-/-) podocytes express near-normal levels of nephrin, synaptopodin, ZO-1, alpha3 integrin, and GBM laminins. However, mRNA and protein levels for CD2AP and podocin were greatly reduced, suggesting a cooperative role for these molecules in foot process and slit diaphragm formation. We identified several LMX1B binding sites in the putative regulatory regions of both CD2AP and NPHS2 (podocin) and demonstrated that LMX1B binds to these sequences in vitro and can activate transcription through them in cotransfection assays. Thus, LMX1B regulates the expression of multiple podocyte genes critical for podocyte differentiation and function. Our results indicate that reduced levels of proteins associated with foot processes and the glomerular slit diaphragm likely contribute, along with reduced levels of GBM collagens, to the nephropathy associated with NPS.
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