mouse anti synaptic vesicle 2  (Developmental Studies Hybridoma Bank)

Journal: Cell Reports

Article Title: The insertion of an ATTTC repeat in an Alu element hyperactivates a neurodevelopmental enhancer in spinocerebellar ataxia type 37

doi: 10.1016/j.celrep.2026.117146

Figure Lengend Snippet: DAB1 overexpression induces axonal defects during development (A) Schematic representation of cerebellar and cerebellar-like structures in zebrafish. Granule cell (GC) axons, named parallel fibers (PFs), innervate Purkinje cells (PCs) in the molecular cell layer. Axons from GCs in eminentia granularis (EG) innervate a type of Purkinje-like neuron called crest cells (CrCs). (B) Representative confocal images of zebrafish larvae, from a GFP + cerebellar granule cell line, microinjected with control or human DAB1 mRNA at 5 dpf; axonal tracts of GCs from EG are indicated with orange (absent) or gray (present) arrows. (C) Percentage of present or absent GC axonal tracts that innervate PC-like neurons (graphic representation of data by mean ± SD of at least 20 embryos/condition/replicate; three independent experiments; ꭕ 2 test for the percentage of GC axonal tracts, present or absent; ∗∗∗ p < 0.001). (D) Schematics of muscle innervation by PMN axon tracts in zebrafish larvae at 24 hpf. (E) Representative confocal images (40× objective) of PMN axon tracts from the 6-somites-spanning region anterior to the cloaca from control or DAB1 mRNA-injected embryos; whole-mounted immunofluorescence with SV2 antibody, representative z-projection images (maximum intensity). (F) Length of zebrafish PMN axon tracts in control and DAB1 mRNA-microinjected embryos ( n = 23 embryos for control and n = 24 embryos in DAB1 mRNA condition; four independent experiments; independent t test, ∗ p < 0.05; data are represented by the mean ± SD). (G) Proposed mechanistic model showing disruption of DRL function by the (ATTTC) n , which hyperactivates the neurodevelopmental enhancer, leading to DAB1 upregulation and DAB1 protein accumulation in axons, likely contributing to SCA37. See also .

Article Snippet: Embryos were incubated with anti-synaptic vesicle 2 (SV2) antibody (1:200, #AB2315387, Developmental Studies Hybridoma Bank) diluted in blocking solution overnight, at 4°C.

Techniques: Over Expression, Control, Injection, Immunofluorescence, Disruption

Journal: Cell Reports

Article Title: The insertion of an ATTTC repeat in an Alu element hyperactivates a neurodevelopmental enhancer in spinocerebellar ataxia type 37

doi: 10.1016/j.celrep.2026.117146

Figure Lengend Snippet: DAB1 overexpression induces axonal defects during development (A) Schematic representation of cerebellar and cerebellar-like structures in zebrafish. Granule cell (GC) axons, named parallel fibers (PFs), innervate Purkinje cells (PCs) in the molecular cell layer. Axons from GCs in eminentia granularis (EG) innervate a type of Purkinje-like neuron called crest cells (CrCs). (B) Representative confocal images of zebrafish larvae, from a GFP + cerebellar granule cell line, microinjected with control or human DAB1 mRNA at 5 dpf; axonal tracts of GCs from EG are indicated with orange (absent) or gray (present) arrows. (C) Percentage of present or absent GC axonal tracts that innervate PC-like neurons (graphic representation of data by mean ± SD of at least 20 embryos/condition/replicate; three independent experiments; ꭕ 2 test for the percentage of GC axonal tracts, present or absent; ∗∗∗ p < 0.001). (D) Schematics of muscle innervation by PMN axon tracts in zebrafish larvae at 24 hpf. (E) Representative confocal images (40× objective) of PMN axon tracts from the 6-somites-spanning region anterior to the cloaca from control or DAB1 mRNA-injected embryos; whole-mounted immunofluorescence with SV2 antibody, representative z-projection images (maximum intensity). (F) Length of zebrafish PMN axon tracts in control and DAB1 mRNA-microinjected embryos ( n = 23 embryos for control and n = 24 embryos in DAB1 mRNA condition; four independent experiments; independent t test, ∗ p < 0.05; data are represented by the mean ± SD). (G) Proposed mechanistic model showing disruption of DRL function by the (ATTTC) n , which hyperactivates the neurodevelopmental enhancer, leading to DAB1 upregulation and DAB1 protein accumulation in axons, likely contributing to SCA37. See also .

Article Snippet: Anti-Synaptic Vesicle 2 (SV2) primary antibody , Developmental Studies Hybridoma Bank , Cat #SV2;RRID:AB_2315387.

Techniques: Over Expression, Control, Injection, Immunofluorescence, Disruption