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human cd2ap cdna  (OriGene)


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    Structured Review

    OriGene human cd2ap cdna
    Human monogenic Nephrotic Syndrome (NS) genes and their Drosophila orthologs
    Human Cd2ap Cdna, supplied by OriGene, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/cms/pmc06074792-331-10-16?v=OriGene
    Average 90 stars, based on 1 article reviews
    human cd2ap cdna - by Bioz Stars, 2026-08
    90/100 stars

    Images

    1) Product Images from "A Drosophila model system to assess the function of human monogenic podocyte mutations that cause nephrotic syndrome"

    Article Title: A Drosophila model system to assess the function of human monogenic podocyte mutations that cause nephrotic syndrome

    Journal: Human Molecular Genetics

    doi: 10.1093/hmg/ddw428

    Human monogenic Nephrotic Syndrome (NS) genes and their Drosophila orthologs
    Figure Legend Snippet: Human monogenic Nephrotic Syndrome (NS) genes and their Drosophila orthologs

    Techniques Used: Filtration, Binding Assay, Clinical Proteomics, Membrane, Glycoproteomics

    Cindr is required for nephrocyte function, fly survival, and nephrocyte cell ultrastructure; Cindr gene silencing can be rescued by a normal but not a patient-derived mutant allele of human CD2AP; Cindr interacts with Mec2 in nephrocytes. (A). ANF-RFP uptake visualized by fluorescence microscopy in nephrocytes of Control flies (genotype Hand-GFP; Dot-Gal4), Cindr (CD2AP)-KD flies in which Cindr expression was silenced in nephrocytes with a Cindr targeting RNAi construct (genotype Hand-GFP; Dot-Gal4; UAS-Cindr-RNAi), Cindr-KD + CD2AP-WT flies in which a transgenic wild type allele of human CD2AP was expressed simultaneously with Cindr -targeting RNAi (genotype Hand-GFP; Dot-Gal4; UAS-Cindr-RNAi; UAS-CD2AP), and Cindr-KD + CD2AP-K301M flies in which a transgenic mutant allele of human CD2AP was expressed simultaneously with Cindr -targeting RNAi (genotype Hand-GFP; Dot-Gal4; UAS-Cindr-RNAi; UAS-CD2AP-K301M). The panels show merged ANF-RFP (54) and GFP (green, mostly nuclear) fluorescence. (B) Quantification of nephrocyte RFP levels relative to Control flies. For quantification, ≥20 nephrocytes were analysed from each of three female flies per genotype. The results are presented as mean ± s.e.m. Statistical significance (*) was defined as P < 0.05. (C) Adult fly survival curves illustrating effects on longevity of Cindr silencing and extent of rescue from expression of WT and mutant alleles of human CD2AP. 50 flies of each genotype were maintained at 29°C (to increase Gal4 driven RNAi transgene expression) and mortality was recorded every 48 hours until all flies were dead. Triplicate samples were analysed. (D) Average adult lifespan showing effects of Cindr silencing and rescue by WT and mutant alleles of human CD2AP. 50 flies of each genotype were maintained at 29°C (to increase Gal4 driven RNAi transgene expression) and mortality was recorded every 48 hours until all flies were dead. Experiments were performed in triplicate. The results are presented as mean ± s.e.m. Statistical significance (*) was defined as P < 0.05. (E) Transmission electron microscopy showing effects on nephrocyte NSD (arrowheads) and lacunar channel (*) ultrastructure of Cindr gene silencing and the extent of rescue from expression of WT and mutant alleles of human CD2AP. In Control nephrocytes NSDs were regularly and precisely spaced along the entire circumference of the cell and spanned the
    Figure Legend Snippet: Cindr is required for nephrocyte function, fly survival, and nephrocyte cell ultrastructure; Cindr gene silencing can be rescued by a normal but not a patient-derived mutant allele of human CD2AP; Cindr interacts with Mec2 in nephrocytes. (A). ANF-RFP uptake visualized by fluorescence microscopy in nephrocytes of Control flies (genotype Hand-GFP; Dot-Gal4), Cindr (CD2AP)-KD flies in which Cindr expression was silenced in nephrocytes with a Cindr targeting RNAi construct (genotype Hand-GFP; Dot-Gal4; UAS-Cindr-RNAi), Cindr-KD + CD2AP-WT flies in which a transgenic wild type allele of human CD2AP was expressed simultaneously with Cindr -targeting RNAi (genotype Hand-GFP; Dot-Gal4; UAS-Cindr-RNAi; UAS-CD2AP), and Cindr-KD + CD2AP-K301M flies in which a transgenic mutant allele of human CD2AP was expressed simultaneously with Cindr -targeting RNAi (genotype Hand-GFP; Dot-Gal4; UAS-Cindr-RNAi; UAS-CD2AP-K301M). The panels show merged ANF-RFP (54) and GFP (green, mostly nuclear) fluorescence. (B) Quantification of nephrocyte RFP levels relative to Control flies. For quantification, ≥20 nephrocytes were analysed from each of three female flies per genotype. The results are presented as mean ± s.e.m. Statistical significance (*) was defined as P < 0.05. (C) Adult fly survival curves illustrating effects on longevity of Cindr silencing and extent of rescue from expression of WT and mutant alleles of human CD2AP. 50 flies of each genotype were maintained at 29°C (to increase Gal4 driven RNAi transgene expression) and mortality was recorded every 48 hours until all flies were dead. Triplicate samples were analysed. (D) Average adult lifespan showing effects of Cindr silencing and rescue by WT and mutant alleles of human CD2AP. 50 flies of each genotype were maintained at 29°C (to increase Gal4 driven RNAi transgene expression) and mortality was recorded every 48 hours until all flies were dead. Experiments were performed in triplicate. The results are presented as mean ± s.e.m. Statistical significance (*) was defined as P < 0.05. (E) Transmission electron microscopy showing effects on nephrocyte NSD (arrowheads) and lacunar channel (*) ultrastructure of Cindr gene silencing and the extent of rescue from expression of WT and mutant alleles of human CD2AP. In Control nephrocytes NSDs were regularly and precisely spaced along the entire circumference of the cell and spanned the "“mouth”" of each lacunar channel. Silencing Cindr gene expression led to fusion of NSDs and the loss of lacunar channels. Expression of WT human CD2AP significantly rescued the ultrastructural defects, while the mutant CD2AP allele had very little effect. (F). Functional interaction between Cindr and Mec2 in nephrocytes demonstrated by Cindr+/-; Mec2+/- double heterozygote synergistic enhancement of deleterious effect on uptake of fluorescent Dextran particles in comparison to Cindr+/- or Mec2+/- single heterozygotes. (G). Quantitative analysis of fluorescent Dextran levels in nephrocytes of the indicated genotype, expressed relative to Control. For quantification, ≥20 nephrocytes were analysed from each of three female flies per genotype. The results are presented as mean ± s.e.m. Statistical significance (*) was defined as P < 0.05.

    Techniques Used: Derivative Assay, Mutagenesis, Fluorescence, Microscopy, Control, Expressing, Construct, Transgenic Assay, Transmission Assay, Electron Microscopy, Gene Expression, Functional Assay, Comparison



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