ArticleJournal of the American Society of Nephrology : JASN2013
LMX1B is essential for the maintenance of differentiated podocytes in adult kidneys.
Article in Journal of the American Society of Nephrology : JASN, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 70 citations in OpenAlex.
- Proteasome inhibition alleviates proteinuria in Lmx1b knock-in mice with dysfunctional LIM domains.Nature communications · 2026Article
- Clinicopathological characteristics and cyclosporine-responsive proteinuria in nail-patella syndrome with a novel LMX1B mutation.Pediatric nephrology (Berlin, Germany) · 2026Article
- Chromatin dynamics identifies 78 genes at loci associated with elevated intraocular pressure and primary open-angle glaucoma.bioRxiv : the preprint server for biology · 2026Article
- Horns, nails, and leaky kidneys: A rare case of congenital nephrotic syndrome.Clinical nephrology. Case studies · 2026Article
- Orthopedic manifestations and management of nail-patella syndrome: a narrative review.Frontiers in pediatrics · 2026Review
- Emerging genetic mechanisms of glomerular proteinuria: a podocyte-centered multi-layer network perspective.Frontiers in genetics · 2026Review
- Characterisation of lmx1b paralogues in zebrafish reveals divergent roles in skeletal, kidney and muscle development.Biology open · 2025Article
- When should the nephrologist think about genetics in patients with glomerular diseases?Clinical kidney journal · 2025Review
- Non-dialyzable uremic toxins and renal tubular cell damage in CKD patients: a systems biology approach.European journal of medical research · 2024Article
- Single-Cell Transcriptome Analysis Reveals Development-Specific Networks at Distinct Synchronized Antral Follicle Sizes in Sheep Oocytes.International journal of molecular sciences · 2024Article
- Single-cell transcriptomics and chromatin accessibility profiling elucidate the kidney-protective mechanism of mineralocorticoid receptor antagonists.The Journal of clinical investigation · 2024Article
- ATG8-dependent LMX1B-autophagy crosstalk shapes human midbrain dopaminergic neuronal resilience.The Journal of cell biology · 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
- LMX1B-associated nephropathy that showed myelin figures on electron microscopy.CEN case reports · 2021Article
- Identification of limb-specific Lmx1b auto-regulatory modules with Nail-patella syndrome pathogenicity.Nature communications · 2021Article
- Zebrafish Models for Human Skeletal Disorders.Frontiers in genetics · 2021Review
- Case Report: Corneal Leucoma as a Novel Clinical Presentation of Nail-Patella Syndrome in a 5-Year-Old Girl.Frontiers in pediatrics · 2021Article
- Nail-Patella syndrome with early onset end-stage renal disease in a child with a novel heterozygous missense mutation in the LMX1B homeodomain: A case report.Biomedical reports · 2020Article
- Myelin bodies in LMX1B-associated nephropathy: potential for misdiagnosis.Pediatric nephrology (Berlin, Germany) · 2020Article
- Epigenetic transcriptional reprogramming by WT1 mediates a repair response during podocyte injury.Science advances · 2020Article
Corrections and comments
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Authors and funding
23 authors at 7 institutions in 3 countries.
Funding
Abstract
Mutations of the LMX1B gene cause nail-patella syndrome, a rare autosomal-dominant disorder affecting the development of the limbs, eyes, brain, and kidneys. The characterization of conventional Lmx1b knockout mice has shown that LMX1B regulates the development of podocyte foot processes and slit diaphragms, but studies using podocyte-specific Lmx1b knockout mice have yielded conflicting results regarding the importance of LMX1B for maintaining podocyte structures. In order to address this question, we generated inducible podocyte-specific Lmx1b knockout mice. One week of Lmx1b inactivation in adult mice resulted in proteinuria with only minimal foot process effacement. Notably, expression levels of slit diaphragm and basement membrane proteins remained stable at this time point, and basement membrane charge properties also did not change, suggesting that alternative mechanisms mediate the development of proteinuria in these mice. Cell biological and biophysical experiments with primary podocytes isolated after 1 week of Lmx1b inactivation indicated dysregulation of actin cytoskeleton organization, and time-resolved DNA microarray analysis identified the genes encoding actin cytoskeleton-associated proteins, including Abra and Arl4c, as putative LMX1B targets. Chromatin immunoprecipitation experiments in conditionally immortalized human podocytes and gel shift assays showed that LMX1B recognizes AT-rich binding sites (FLAT elements) in the promoter regions of ABRA and ARL4C, and knockdown experiments in zebrafish support a model in which LMX1B and ABRA act in a common pathway during pronephros development. Our report establishes the importance of LMX1B in fully differentiated podocytes and argues that LMX1B is essential for the maintenance of an appropriately structured actin cytoskeleton in podocytes.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.