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antibodies against csp  (Developmental Studies Hybridoma Bank)


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    Developmental Studies Hybridoma Bank antibodies against csp
    Loss or reduction of Drosophila LRRK has no effect on axonal transport, but excess human LRRK disrupts transport causing axonal blockages. (A) Representative images from WT and larvae that are homozygous for dLRRK e03680−/− or heterozygous for dLRRK ex1−/+ show smooth staining as assayed using the cysteine string antibody <t>(CSP)</t> similar to WT. In contrast larvae expressing human LRRK2 (hLRRK2) show axonal blockages that contain CSP (arrows). Quantification of the average number of CSP blocks per larvae with excess hLRRK show a significant number of blocks compared to WT ( p = 0.004). N = 5 larvae per genotype. Bar = 10 μm. (B) Representative images of larval brains from WT, homozygous dLRRK e03680−/− , heterozygous for dLRRK ex1−/+ and excess hLRRK stained with the TUNEL assay to evaluate cell death. While homozygous dLRRK e03680−/− and excess hLRRK larval brains were comparable to WT brains, heterozygous dLRRK ex1−/+ show more TUNEL positive nuclei, but not to the extent seen in the positive control. Quantification of the average number of cell death per area of ventral ganglion show significant amount of cell death in dLRRK ex1−/+ compared to WT. N = 10 larvae per genotype, bar = 10 μm. Statistical significance was determined using the two-sample two-sided Student’s t -test. Data represented as mean ± SEM.
    Antibodies Against Csp, supplied by Developmental Studies Hybridoma Bank, used in various techniques. Bioz Stars score: 94/100, based on 82 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/antibodies against csp/product/Developmental Studies Hybridoma Bank
    Average 94 stars, based on 82 article reviews
    antibodies against csp - by Bioz Stars, 2026-02
    94/100 stars

    Images

    1) Product Images from "Genetic evidence for a functional association between Parkinson’s disease proteins leucine-rich repeat kinase 2 and α -synuclein during axonal transport"

    Article Title: Genetic evidence for a functional association between Parkinson’s disease proteins leucine-rich repeat kinase 2 and α -synuclein during axonal transport

    Journal: Frontiers in Molecular Neuroscience

    doi: 10.3389/fnmol.2025.1667839

    Loss or reduction of Drosophila LRRK has no effect on axonal transport, but excess human LRRK disrupts transport causing axonal blockages. (A) Representative images from WT and larvae that are homozygous for dLRRK e03680−/− or heterozygous for dLRRK ex1−/+ show smooth staining as assayed using the cysteine string antibody (CSP) similar to WT. In contrast larvae expressing human LRRK2 (hLRRK2) show axonal blockages that contain CSP (arrows). Quantification of the average number of CSP blocks per larvae with excess hLRRK show a significant number of blocks compared to WT ( p = 0.004). N = 5 larvae per genotype. Bar = 10 μm. (B) Representative images of larval brains from WT, homozygous dLRRK e03680−/− , heterozygous for dLRRK ex1−/+ and excess hLRRK stained with the TUNEL assay to evaluate cell death. While homozygous dLRRK e03680−/− and excess hLRRK larval brains were comparable to WT brains, heterozygous dLRRK ex1−/+ show more TUNEL positive nuclei, but not to the extent seen in the positive control. Quantification of the average number of cell death per area of ventral ganglion show significant amount of cell death in dLRRK ex1−/+ compared to WT. N = 10 larvae per genotype, bar = 10 μm. Statistical significance was determined using the two-sample two-sided Student’s t -test. Data represented as mean ± SEM.
    Figure Legend Snippet: Loss or reduction of Drosophila LRRK has no effect on axonal transport, but excess human LRRK disrupts transport causing axonal blockages. (A) Representative images from WT and larvae that are homozygous for dLRRK e03680−/− or heterozygous for dLRRK ex1−/+ show smooth staining as assayed using the cysteine string antibody (CSP) similar to WT. In contrast larvae expressing human LRRK2 (hLRRK2) show axonal blockages that contain CSP (arrows). Quantification of the average number of CSP blocks per larvae with excess hLRRK show a significant number of blocks compared to WT ( p = 0.004). N = 5 larvae per genotype. Bar = 10 μm. (B) Representative images of larval brains from WT, homozygous dLRRK e03680−/− , heterozygous for dLRRK ex1−/+ and excess hLRRK stained with the TUNEL assay to evaluate cell death. While homozygous dLRRK e03680−/− and excess hLRRK larval brains were comparable to WT brains, heterozygous dLRRK ex1−/+ show more TUNEL positive nuclei, but not to the extent seen in the positive control. Quantification of the average number of cell death per area of ventral ganglion show significant amount of cell death in dLRRK ex1−/+ compared to WT. N = 10 larvae per genotype, bar = 10 μm. Statistical significance was determined using the two-sample two-sided Student’s t -test. Data represented as mean ± SEM.

    Techniques Used: Staining, Expressing, TUNEL Assay, Positive Control



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    Loss or reduction of Drosophila LRRK has no effect on axonal transport, but excess human LRRK disrupts transport causing axonal blockages. (A) Representative images from WT and larvae that are homozygous for dLRRK e03680−/− or heterozygous for dLRRK ex1−/+ show smooth staining as assayed using the cysteine string antibody <t>(CSP)</t> similar to WT. In contrast larvae expressing human LRRK2 (hLRRK2) show axonal blockages that contain CSP (arrows). Quantification of the average number of CSP blocks per larvae with excess hLRRK show a significant number of blocks compared to WT ( p = 0.004). N = 5 larvae per genotype. Bar = 10 μm. (B) Representative images of larval brains from WT, homozygous dLRRK e03680−/− , heterozygous for dLRRK ex1−/+ and excess hLRRK stained with the TUNEL assay to evaluate cell death. While homozygous dLRRK e03680−/− and excess hLRRK larval brains were comparable to WT brains, heterozygous dLRRK ex1−/+ show more TUNEL positive nuclei, but not to the extent seen in the positive control. Quantification of the average number of cell death per area of ventral ganglion show significant amount of cell death in dLRRK ex1−/+ compared to WT. N = 10 larvae per genotype, bar = 10 μm. Statistical significance was determined using the two-sample two-sided Student’s t -test. Data represented as mean ± SEM.
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    Loss or reduction of Drosophila LRRK has no effect on axonal transport, but excess human LRRK disrupts transport causing axonal blockages. (A) Representative images from WT and larvae that are homozygous for dLRRK e03680−/− or heterozygous for dLRRK ex1−/+ show smooth staining as assayed using the cysteine string antibody <t>(CSP)</t> similar to WT. In contrast larvae expressing human LRRK2 (hLRRK2) show axonal blockages that contain CSP (arrows). Quantification of the average number of CSP blocks per larvae with excess hLRRK show a significant number of blocks compared to WT ( p = 0.004). N = 5 larvae per genotype. Bar = 10 μm. (B) Representative images of larval brains from WT, homozygous dLRRK e03680−/− , heterozygous for dLRRK ex1−/+ and excess hLRRK stained with the TUNEL assay to evaluate cell death. While homozygous dLRRK e03680−/− and excess hLRRK larval brains were comparable to WT brains, heterozygous dLRRK ex1−/+ show more TUNEL positive nuclei, but not to the extent seen in the positive control. Quantification of the average number of cell death per area of ventral ganglion show significant amount of cell death in dLRRK ex1−/+ compared to WT. N = 10 larvae per genotype, bar = 10 μm. Statistical significance was determined using the two-sample two-sided Student’s t -test. Data represented as mean ± SEM.
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    Loss or reduction of Drosophila LRRK has no effect on axonal transport, but excess human LRRK disrupts transport causing axonal blockages. (A) Representative images from WT and larvae that are homozygous for dLRRK e03680−/− or heterozygous for dLRRK ex1−/+ show smooth staining as assayed using the cysteine string antibody <t>(CSP)</t> similar to WT. In contrast larvae expressing human LRRK2 (hLRRK2) show axonal blockages that contain CSP (arrows). Quantification of the average number of CSP blocks per larvae with excess hLRRK show a significant number of blocks compared to WT ( p = 0.004). N = 5 larvae per genotype. Bar = 10 μm. (B) Representative images of larval brains from WT, homozygous dLRRK e03680−/− , heterozygous for dLRRK ex1−/+ and excess hLRRK stained with the TUNEL assay to evaluate cell death. While homozygous dLRRK e03680−/− and excess hLRRK larval brains were comparable to WT brains, heterozygous dLRRK ex1−/+ show more TUNEL positive nuclei, but not to the extent seen in the positive control. Quantification of the average number of cell death per area of ventral ganglion show significant amount of cell death in dLRRK ex1−/+ compared to WT. N = 10 larvae per genotype, bar = 10 μm. Statistical significance was determined using the two-sample two-sided Student’s t -test. Data represented as mean ± SEM.
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    Image Search Results


    Loss or reduction of Drosophila LRRK has no effect on axonal transport, but excess human LRRK disrupts transport causing axonal blockages. (A) Representative images from WT and larvae that are homozygous for dLRRK e03680−/− or heterozygous for dLRRK ex1−/+ show smooth staining as assayed using the cysteine string antibody (CSP) similar to WT. In contrast larvae expressing human LRRK2 (hLRRK2) show axonal blockages that contain CSP (arrows). Quantification of the average number of CSP blocks per larvae with excess hLRRK show a significant number of blocks compared to WT ( p = 0.004). N = 5 larvae per genotype. Bar = 10 μm. (B) Representative images of larval brains from WT, homozygous dLRRK e03680−/− , heterozygous for dLRRK ex1−/+ and excess hLRRK stained with the TUNEL assay to evaluate cell death. While homozygous dLRRK e03680−/− and excess hLRRK larval brains were comparable to WT brains, heterozygous dLRRK ex1−/+ show more TUNEL positive nuclei, but not to the extent seen in the positive control. Quantification of the average number of cell death per area of ventral ganglion show significant amount of cell death in dLRRK ex1−/+ compared to WT. N = 10 larvae per genotype, bar = 10 μm. Statistical significance was determined using the two-sample two-sided Student’s t -test. Data represented as mean ± SEM.

    Journal: Frontiers in Molecular Neuroscience

    Article Title: Genetic evidence for a functional association between Parkinson’s disease proteins leucine-rich repeat kinase 2 and α -synuclein during axonal transport

    doi: 10.3389/fnmol.2025.1667839

    Figure Lengend Snippet: Loss or reduction of Drosophila LRRK has no effect on axonal transport, but excess human LRRK disrupts transport causing axonal blockages. (A) Representative images from WT and larvae that are homozygous for dLRRK e03680−/− or heterozygous for dLRRK ex1−/+ show smooth staining as assayed using the cysteine string antibody (CSP) similar to WT. In contrast larvae expressing human LRRK2 (hLRRK2) show axonal blockages that contain CSP (arrows). Quantification of the average number of CSP blocks per larvae with excess hLRRK show a significant number of blocks compared to WT ( p = 0.004). N = 5 larvae per genotype. Bar = 10 μm. (B) Representative images of larval brains from WT, homozygous dLRRK e03680−/− , heterozygous for dLRRK ex1−/+ and excess hLRRK stained with the TUNEL assay to evaluate cell death. While homozygous dLRRK e03680−/− and excess hLRRK larval brains were comparable to WT brains, heterozygous dLRRK ex1−/+ show more TUNEL positive nuclei, but not to the extent seen in the positive control. Quantification of the average number of cell death per area of ventral ganglion show significant amount of cell death in dLRRK ex1−/+ compared to WT. N = 10 larvae per genotype, bar = 10 μm. Statistical significance was determined using the two-sample two-sided Student’s t -test. Data represented as mean ± SEM.

    Article Snippet: Dissected larvae were fixed in 8% paraformaldehyde, washed with PBT (phosphate buffered saline supplemented with 0.1% Tween-20) and incubated overnight with antibodies against CSP (1:10, Developmental Studies Hybridoma Bank) or tubulin (1:100, Invitrogen).

    Techniques: Staining, Expressing, TUNEL Assay, Positive Control

    Journal: Cell Death & Disease

    Article Title: Opposing roles for GSK3β and ERK1-dependent phosphorylation of huntingtin during neuronal dysfunction and cell death in Huntington’s disease

    doi: 10.1038/s41419-025-07524-0

    Figure Lengend Snippet:

    Article Snippet: Mouse anti-DCSP-3 (1G12) , Developmental Studies Hybridoma Bank , Cat# DCSP-3 (1G12) RRID: AB_528184.

    Techniques: Transduction, Recombinant, Protease Inhibitor, Magnetic Beads, Plasmid Preparation, In Situ, Software, Imaging