ArticleAmerican journal of physiology. Renal physiology2008
Nephrin binds to the COOH terminus of a large-conductance Ca2+-activated K+ channel isoform and regulates its expression on the cell surface.
Article in American journal of physiology. Renal physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 52 citations in OpenAlex.
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- TRPC6 effects on albumin permeation, nephrin shedding, and apoptosis in podocytes: Role of calcineurin and metalloproteases.Physiological reports · 2025Article
- Revisiting nephrin signaling and its specialized effects on the uniquely adaptable podocyte.The Biochemical journal · 2025Review
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- Reduced Nephrin Tyrosine Phosphorylation Enhances Insulin Secretion and Increases Glucose Tolerance With Age.Endocrinology · 2024Article
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- Ion channels and channelopathies in glomeruli.Physiological reviews · 2023Review
- RAGE and αVβ3-integrin are essential for suPAR signaling in podocytes.Biochimica et biophysica acta. Molecular basis of disease · 2021Article
- Upregulated LRRC55 promotes BK channel activation and aggravates cell injury in podocytes.The Journal of experimental medicine · 2021Article
- Prompt apoptotic response to high glucose in SGLT-expressing renal cells.American journal of physiology. Renal physiology · 2019Article
- Mechanism of Regulation of Big-Conductance CaFrontiers in physiology · 2019Article
- Nephrin Signaling in the Podocyte: An Updated View of Signal Regulation at the Slit Diaphragm and Beyond.Frontiers in endocrinology · 2018Review
- Changes in podocyte TRPC channels evoked by plasma and sera from patients with recurrent FSGS and by putative glomerular permeability factors.Biochimica et biophysica acta. Molecular basis of disease · 2017Article
- Article
- 20-Hydroxyeicosatetraenoic Acid (20-HETE) Modulates Canonical Transient Receptor Potential-6 (TRPC6) Channels in Podocytes.Frontiers in physiology · 2016Article
- Large-Conductance Calcium-Activated Potassium Channels in Glomerulus: From Cell Signal Integration to Disease.Frontiers in physiology · 2016Review
- Deficiency of fibroblast growth factor-inducible 14 (Fn14) preserves the filtration barrier and ameliorates lupus nephritis.Journal of the American Society of Nephrology : JASN · 2015Article
- Podocytes … What's Under Yours? (Podocytes and Foot Processes and How They Change in Nephropathy).Frontiers in endocrinology · 2015Review
- The inhibitory effect of angiotensin II on BKCa channels in podocytes via oxidative stress.Molecular and cellular biochemistry · 2015Article
- ATP acting through P2Y receptors causes activation of podocyte TRPC6 channels: role of podocin and reactive oxygen species.American journal of physiology. Renal physiology · 2014Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
We carried out a yeast two-hybrid screen to identify proteins that interact with large-conductance Ca2+-activated K+ (BKCa) channels encoded by the Slo1 gene. Nephrin, an essential adhesion and scaffolding molecule expressed in podocytes, emerged in this screen. The Slo1-nephrin interaction was confirmed by coimmunoprecipitation from the brain and kidney, from HEK-293T cells expressing both proteins, and by glutathione S-transferase pull-down assays. We detected nephrin binding to the Slo1 VEDEC splice variant, which is typically retained in intracellular stores, and to the beta4-subunit. However, we did not detect significant binding of nephrin to the Slo1 QEERL or Slo1 EMVYR splice variants. Coexpression of nephrin with Slo1 VEDEC increased expression of functional BKCa channels on the surface of HEK-293T cells but did not affect steady-state surface expression of the other COOH-terminal Slo1 variants. Nephrin did not affect the kinetics or voltage dependence of channel activation in HEK-293T cells expressing Slo1. Stimulation of Slo1 VEDEC surface expression in HEK-293T cells was also observed by coexpressing a small construct encoding only the distal COOH-terminal domains of nephrin that interact with Slo1. Reduction of endogenous nephrin expression by application of small interfering RNA to differentiated cells of an immortalized podocyte cell line markedly reduced the steady-state surface expression of Slo1 as assessed by electrophysiology and cell-surface biotinylation assays. Nephrin therefore plays a role in organizing the surface expression of ion channel proteins in podocytes and may play a role in outside-in signaling to allow podocytes to adapt to mechanical or neurohumoral stimuli originating in neighboring cells.
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