green colored fm1 43 dye  (Thermo Fisher)


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    Name:
    FM 1 43 Dye N 3 Triethylammoniumpropyl 4 4 Dibutylamino Styryl Pyridinium Dibromide
    Description:
    FM 1 43 membrane probe is an excellent reagent both for identifying actively firing neurons and for investigating the mechanisms of activity dependent vesicle cycling This water soluble dye which is nontoxic to cells and virtually nonfluorescent in aqueous medium is believed to insert into the outer leaflet of the cell membrane where it becomes intensely fluorescent In a neuron that is actively releasing neurotransmitters the dye becomes internalized within the recycled synaptic vesicles and the nerve terminals become brightly stained The nonspecific staining of cell surface membranes can simply be washed off prior to viewing FM 1 43 membrane probe is also available as 1 mg packaged into 10 vials each containing 100 µg T 35356 FM 1 43FX membrane probe F 35355 an analog of FM 1 43 membrane probe that can be fixed in place using aldehyde based fixatives is also available
    Catalog Number:
    T3163
    Price:
    None
    Category:
    Labeling Detection Products
    Applications:
    Cell Analysis|Endocytosis, Exocytosis & Phagocytosis|General Cell Tracing|Neuronal Tracing|Cell Tracing & Tracking|Cell Viability, Proliferation & Function
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    Structured Review

    Thermo Fisher green colored fm1 43 dye
    Defective membrane repair capacity in ML1 KO muscle (a) Immunofluorescence of dystrophin, β-dystroglycan (β-DG), integrin β1, laminin, caveolin-3 (Cav-3), and dysferlin in ML1-null Gastroc muscle. Scale bar = 10 µm. (b) Western blotting analysis of the DGC components, Cav-3, dysferlin, and MG53 in ML1 KO mice. Myosin served as a loading control. (c) A membrane repair assay performed on single FDB muscle fibers isolated from WT and ML1 KO mice. Membrane damage was induced with a two-photon laser at t = 0 s. Scale bar = 10 µm. The right panel shows the time-dependent changes (ΔF) in <t>FM1–43</t> fluorescence intensity normalized to the basal fluorescence (F 0 ) for WT (blue) and ML1 KO (red) fibers. (d) Representative images of in vitro differentiated myotubes in response to mechanical damage elicited by a microelectrode (arrows). The lower panel shows the percentage of “surviving” myotubes in response to microelectrode penetration. The experiments were performed in the presence of extracellular Ca 2+ , and defective membrane resealing led to excessive Ca 2+ influx that triggered prolonged muscle contraction. The “surviving” cells are those without prolonged contraction. Scale bar = 50 µm. (e) Responses of C2C12-derived myotubes to microelectrode penetration in Tyrode's solution (2 mM Ca 2+ ) in the presence of DMSO (0.1%; 1 st and 2 nd penetration), ML-SI3 (20 µM), BAPTA-AM (20 µM), and GPN (200 µM). The right panels show the time course of FM4–64 accumulation (ΔF/F 0 ) at injury sites following microelectrode penetration. Scale bar = 50 µm. Note that the same set of DMSO control data was compared with all groups of drug treatment. (f) The effect of ML-SI3, a TRPML-specific synthetic inhibitor, on EB dye uptake in WT Gastroc muscles injected with the cardiotoxin VII4 (CTX), a cytolytic toxin that disrupts cell membrane in living animals 24 . The lower panel shows that intramuscular coinjection of ML-SI3 with CTX on EB dye uptake in WT and ML1 KO muscle. Scale bar = 10 µm. Data are presented as the mean ± s.e.m, n = 3 animals for each condition.
    FM 1 43 membrane probe is an excellent reagent both for identifying actively firing neurons and for investigating the mechanisms of activity dependent vesicle cycling This water soluble dye which is nontoxic to cells and virtually nonfluorescent in aqueous medium is believed to insert into the outer leaflet of the cell membrane where it becomes intensely fluorescent In a neuron that is actively releasing neurotransmitters the dye becomes internalized within the recycled synaptic vesicles and the nerve terminals become brightly stained The nonspecific staining of cell surface membranes can simply be washed off prior to viewing FM 1 43 membrane probe is also available as 1 mg packaged into 10 vials each containing 100 µg T 35356 FM 1 43FX membrane probe F 35355 an analog of FM 1 43 membrane probe that can be fixed in place using aldehyde based fixatives is also available
    https://www.bioz.com/result/green colored fm1 43 dye/product/Thermo Fisher
    Average 99 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    green colored fm1 43 dye - by Bioz Stars, 2021-04
    99/100 stars

    Images

    1) Product Images from "An Intracellular Ca2+ Channel is Required For Sarcolemma Repair to Prevent Muscular Dystrophy"

    Article Title: An Intracellular Ca2+ Channel is Required For Sarcolemma Repair to Prevent Muscular Dystrophy

    Journal: Nature medicine

    doi: 10.1038/nm.3611

    Defective membrane repair capacity in ML1 KO muscle (a) Immunofluorescence of dystrophin, β-dystroglycan (β-DG), integrin β1, laminin, caveolin-3 (Cav-3), and dysferlin in ML1-null Gastroc muscle. Scale bar = 10 µm. (b) Western blotting analysis of the DGC components, Cav-3, dysferlin, and MG53 in ML1 KO mice. Myosin served as a loading control. (c) A membrane repair assay performed on single FDB muscle fibers isolated from WT and ML1 KO mice. Membrane damage was induced with a two-photon laser at t = 0 s. Scale bar = 10 µm. The right panel shows the time-dependent changes (ΔF) in FM1–43 fluorescence intensity normalized to the basal fluorescence (F 0 ) for WT (blue) and ML1 KO (red) fibers. (d) Representative images of in vitro differentiated myotubes in response to mechanical damage elicited by a microelectrode (arrows). The lower panel shows the percentage of “surviving” myotubes in response to microelectrode penetration. The experiments were performed in the presence of extracellular Ca 2+ , and defective membrane resealing led to excessive Ca 2+ influx that triggered prolonged muscle contraction. The “surviving” cells are those without prolonged contraction. Scale bar = 50 µm. (e) Responses of C2C12-derived myotubes to microelectrode penetration in Tyrode's solution (2 mM Ca 2+ ) in the presence of DMSO (0.1%; 1 st and 2 nd penetration), ML-SI3 (20 µM), BAPTA-AM (20 µM), and GPN (200 µM). The right panels show the time course of FM4–64 accumulation (ΔF/F 0 ) at injury sites following microelectrode penetration. Scale bar = 50 µm. Note that the same set of DMSO control data was compared with all groups of drug treatment. (f) The effect of ML-SI3, a TRPML-specific synthetic inhibitor, on EB dye uptake in WT Gastroc muscles injected with the cardiotoxin VII4 (CTX), a cytolytic toxin that disrupts cell membrane in living animals 24 . The lower panel shows that intramuscular coinjection of ML-SI3 with CTX on EB dye uptake in WT and ML1 KO muscle. Scale bar = 10 µm. Data are presented as the mean ± s.e.m, n = 3 animals for each condition.
    Figure Legend Snippet: Defective membrane repair capacity in ML1 KO muscle (a) Immunofluorescence of dystrophin, β-dystroglycan (β-DG), integrin β1, laminin, caveolin-3 (Cav-3), and dysferlin in ML1-null Gastroc muscle. Scale bar = 10 µm. (b) Western blotting analysis of the DGC components, Cav-3, dysferlin, and MG53 in ML1 KO mice. Myosin served as a loading control. (c) A membrane repair assay performed on single FDB muscle fibers isolated from WT and ML1 KO mice. Membrane damage was induced with a two-photon laser at t = 0 s. Scale bar = 10 µm. The right panel shows the time-dependent changes (ΔF) in FM1–43 fluorescence intensity normalized to the basal fluorescence (F 0 ) for WT (blue) and ML1 KO (red) fibers. (d) Representative images of in vitro differentiated myotubes in response to mechanical damage elicited by a microelectrode (arrows). The lower panel shows the percentage of “surviving” myotubes in response to microelectrode penetration. The experiments were performed in the presence of extracellular Ca 2+ , and defective membrane resealing led to excessive Ca 2+ influx that triggered prolonged muscle contraction. The “surviving” cells are those without prolonged contraction. Scale bar = 50 µm. (e) Responses of C2C12-derived myotubes to microelectrode penetration in Tyrode's solution (2 mM Ca 2+ ) in the presence of DMSO (0.1%; 1 st and 2 nd penetration), ML-SI3 (20 µM), BAPTA-AM (20 µM), and GPN (200 µM). The right panels show the time course of FM4–64 accumulation (ΔF/F 0 ) at injury sites following microelectrode penetration. Scale bar = 50 µm. Note that the same set of DMSO control data was compared with all groups of drug treatment. (f) The effect of ML-SI3, a TRPML-specific synthetic inhibitor, on EB dye uptake in WT Gastroc muscles injected with the cardiotoxin VII4 (CTX), a cytolytic toxin that disrupts cell membrane in living animals 24 . The lower panel shows that intramuscular coinjection of ML-SI3 with CTX on EB dye uptake in WT and ML1 KO muscle. Scale bar = 10 µm. Data are presented as the mean ± s.e.m, n = 3 animals for each condition.

    Techniques Used: Immunofluorescence, Western Blot, Mouse Assay, Isolation, Fluorescence, In Vitro, Derivative Assay, Injection

    Related Articles

    other:

    Article Title: The Color of Lactotroph Secretory Granules Stained with FM1-43 Depends on Dye Concentration
    Article Snippet: FM1-43 was purchased from Molecular Probes/Invitrogen (Eugene, OR).

    Article Title: Annexin-A6 in Membrane Repair of Human Skeletal Muscle Cell: A Role in the Cap Subdomain
    Article Snippet: Sarcolemma repair assay was performed by laser ablation in the presence of Ca2+ and FM1-43, as previously described [ , ].

    Purification:

    Article Title: Membrane Recycling in the Neuronal Growth Cone Revealed by FM1–43 Labeling
    Article Snippet: For most experiments the cultures were loaded with FM1–43 and then fixed before fluorescence imaging to obtain large numbers of growth cones. .. FM1–43 stock solution was made up in purified water (Life Technologies, Grand Island, NY) to a concentration of 3 m m . .. Depolarizing loading medium consisted of MEM mixed with isotonic KCl to produce a final KCl concentration of 60 m m .

    Concentration Assay:

    Article Title: Membrane Recycling in the Neuronal Growth Cone Revealed by FM1–43 Labeling
    Article Snippet: For most experiments the cultures were loaded with FM1–43 and then fixed before fluorescence imaging to obtain large numbers of growth cones. .. FM1–43 stock solution was made up in purified water (Life Technologies, Grand Island, NY) to a concentration of 3 m m . .. Depolarizing loading medium consisted of MEM mixed with isotonic KCl to produce a final KCl concentration of 60 m m .

    Article Title: Nanoscale-Targeted Patch-Clamp Recordings of Functional Presynaptic Ion Channels
    Article Snippet: .. Active synapses were labeled with 20 μM (bath concentration) FM1-43 (Invitrogen) or 200 μM SynaptoRed C1 (SRC1, Biotium) by incubation in the extracellular solution, with 90 mM NaCl replaced by 90 mM KCl for 90 s followed by a 10–15 min wash in the original solution. ..

    Incubation:

    Article Title: Ca2+–Calmodulin Dependent Wound Repair in Dictyostelium Cell Membrane
    Article Snippet: Calreticulin is a Ca2+ –binding protein present in the endoplasmic reticulum [ ]. .. To visualize the recycling endosomes, 30 min after the cells were incubated with FM1-43, they were washed out by media exchange. .. Since the dye that stained the cell membrane was removed by washing, only stained internalized endosomes remained in the cells.

    Article Title: Nanoscale-Targeted Patch-Clamp Recordings of Functional Presynaptic Ion Channels
    Article Snippet: .. Active synapses were labeled with 20 μM (bath concentration) FM1-43 (Invitrogen) or 200 μM SynaptoRed C1 (SRC1, Biotium) by incubation in the extracellular solution, with 90 mM NaCl replaced by 90 mM KCl for 90 s followed by a 10–15 min wash in the original solution. ..

    Labeling:

    Article Title: Nanoscale-Targeted Patch-Clamp Recordings of Functional Presynaptic Ion Channels
    Article Snippet: .. Active synapses were labeled with 20 μM (bath concentration) FM1-43 (Invitrogen) or 200 μM SynaptoRed C1 (SRC1, Biotium) by incubation in the extracellular solution, with 90 mM NaCl replaced by 90 mM KCl for 90 s followed by a 10–15 min wash in the original solution. ..

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    • green colored fm1 43 dye  (Thermo Fisher)
    99
    Thermo Fisher green colored fm1 43 dye
    Defective membrane repair capacity in ML1 KO muscle (a) Immunofluorescence of dystrophin, β-dystroglycan (β-DG), integrin β1, laminin, caveolin-3 (Cav-3), and dysferlin in ML1-null Gastroc muscle. Scale bar = 10 µm. (b) Western blotting analysis of the DGC components, Cav-3, dysferlin, and MG53 in ML1 KO mice. Myosin served as a loading control. (c) A membrane repair assay performed on single FDB muscle fibers isolated from WT and ML1 KO mice. Membrane damage was induced with a two-photon laser at t = 0 s. Scale bar = 10 µm. The right panel shows the time-dependent changes (ΔF) in <t>FM1–43</t> fluorescence intensity normalized to the basal fluorescence (F 0 ) for WT (blue) and ML1 KO (red) fibers. (d) Representative images of in vitro differentiated myotubes in response to mechanical damage elicited by a microelectrode (arrows). The lower panel shows the percentage of “surviving” myotubes in response to microelectrode penetration. The experiments were performed in the presence of extracellular Ca 2+ , and defective membrane resealing led to excessive Ca 2+ influx that triggered prolonged muscle contraction. The “surviving” cells are those without prolonged contraction. Scale bar = 50 µm. (e) Responses of C2C12-derived myotubes to microelectrode penetration in Tyrode's solution (2 mM Ca 2+ ) in the presence of DMSO (0.1%; 1 st and 2 nd penetration), ML-SI3 (20 µM), BAPTA-AM (20 µM), and GPN (200 µM). The right panels show the time course of FM4–64 accumulation (ΔF/F 0 ) at injury sites following microelectrode penetration. Scale bar = 50 µm. Note that the same set of DMSO control data was compared with all groups of drug treatment. (f) The effect of ML-SI3, a TRPML-specific synthetic inhibitor, on EB dye uptake in WT Gastroc muscles injected with the cardiotoxin VII4 (CTX), a cytolytic toxin that disrupts cell membrane in living animals 24 . The lower panel shows that intramuscular coinjection of ML-SI3 with CTX on EB dye uptake in WT and ML1 KO muscle. Scale bar = 10 µm. Data are presented as the mean ± s.e.m, n = 3 animals for each condition.
    Green Colored Fm1 43 Dye, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/green colored fm1 43 dye/product/Thermo Fisher
    Average 99 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    green colored fm1 43 dye - by Bioz Stars, 2021-04
    99/100 stars
    		  Buy from Supplier

    Image Search Results


    Defective membrane repair capacity in ML1 KO muscle (a) Immunofluorescence of dystrophin, β-dystroglycan (β-DG), integrin β1, laminin, caveolin-3 (Cav-3), and dysferlin in ML1-null Gastroc muscle. Scale bar = 10 µm. (b) Western blotting analysis of the DGC components, Cav-3, dysferlin, and MG53 in ML1 KO mice. Myosin served as a loading control. (c) A membrane repair assay performed on single FDB muscle fibers isolated from WT and ML1 KO mice. Membrane damage was induced with a two-photon laser at t = 0 s. Scale bar = 10 µm. The right panel shows the time-dependent changes (ΔF) in FM1–43 fluorescence intensity normalized to the basal fluorescence (F 0 ) for WT (blue) and ML1 KO (red) fibers. (d) Representative images of in vitro differentiated myotubes in response to mechanical damage elicited by a microelectrode (arrows). The lower panel shows the percentage of “surviving” myotubes in response to microelectrode penetration. The experiments were performed in the presence of extracellular Ca 2+ , and defective membrane resealing led to excessive Ca 2+ influx that triggered prolonged muscle contraction. The “surviving” cells are those without prolonged contraction. Scale bar = 50 µm. (e) Responses of C2C12-derived myotubes to microelectrode penetration in Tyrode's solution (2 mM Ca 2+ ) in the presence of DMSO (0.1%; 1 st and 2 nd penetration), ML-SI3 (20 µM), BAPTA-AM (20 µM), and GPN (200 µM). The right panels show the time course of FM4–64 accumulation (ΔF/F 0 ) at injury sites following microelectrode penetration. Scale bar = 50 µm. Note that the same set of DMSO control data was compared with all groups of drug treatment. (f) The effect of ML-SI3, a TRPML-specific synthetic inhibitor, on EB dye uptake in WT Gastroc muscles injected with the cardiotoxin VII4 (CTX), a cytolytic toxin that disrupts cell membrane in living animals 24 . The lower panel shows that intramuscular coinjection of ML-SI3 with CTX on EB dye uptake in WT and ML1 KO muscle. Scale bar = 10 µm. Data are presented as the mean ± s.e.m, n = 3 animals for each condition.

    Journal: Nature medicine

    Article Title: An Intracellular Ca2+ Channel is Required For Sarcolemma Repair to Prevent Muscular Dystrophy

    doi: 10.1038/nm.3611

    Figure Lengend Snippet: Defective membrane repair capacity in ML1 KO muscle (a) Immunofluorescence of dystrophin, β-dystroglycan (β-DG), integrin β1, laminin, caveolin-3 (Cav-3), and dysferlin in ML1-null Gastroc muscle. Scale bar = 10 µm. (b) Western blotting analysis of the DGC components, Cav-3, dysferlin, and MG53 in ML1 KO mice. Myosin served as a loading control. (c) A membrane repair assay performed on single FDB muscle fibers isolated from WT and ML1 KO mice. Membrane damage was induced with a two-photon laser at t = 0 s. Scale bar = 10 µm. The right panel shows the time-dependent changes (ΔF) in FM1–43 fluorescence intensity normalized to the basal fluorescence (F 0 ) for WT (blue) and ML1 KO (red) fibers. (d) Representative images of in vitro differentiated myotubes in response to mechanical damage elicited by a microelectrode (arrows). The lower panel shows the percentage of “surviving” myotubes in response to microelectrode penetration. The experiments were performed in the presence of extracellular Ca 2+ , and defective membrane resealing led to excessive Ca 2+ influx that triggered prolonged muscle contraction. The “surviving” cells are those without prolonged contraction. Scale bar = 50 µm. (e) Responses of C2C12-derived myotubes to microelectrode penetration in Tyrode's solution (2 mM Ca 2+ ) in the presence of DMSO (0.1%; 1 st and 2 nd penetration), ML-SI3 (20 µM), BAPTA-AM (20 µM), and GPN (200 µM). The right panels show the time course of FM4–64 accumulation (ΔF/F 0 ) at injury sites following microelectrode penetration. Scale bar = 50 µm. Note that the same set of DMSO control data was compared with all groups of drug treatment. (f) The effect of ML-SI3, a TRPML-specific synthetic inhibitor, on EB dye uptake in WT Gastroc muscles injected with the cardiotoxin VII4 (CTX), a cytolytic toxin that disrupts cell membrane in living animals 24 . The lower panel shows that intramuscular coinjection of ML-SI3 with CTX on EB dye uptake in WT and ML1 KO muscle. Scale bar = 10 µm. Data are presented as the mean ± s.e.m, n = 3 animals for each condition.

    Article Snippet: Myofiber damage assay After mice were sacrificed by cervical dislocation, FDB muscles were surgically removed to be digested in a Tyrode's solution containing type I collagenase (2 mg/ml; Sigma) at 37 °C for 60 min. After re-suspension in the Tyrode's solution, single FDB fibers were mounted on a glass bottom chamber in Tyrode's or zero Ca2+ solution in the presence of 2.5 µM green-colored FM1–43 dye (Molecular Probes).

    Techniques: Immunofluorescence, Western Blot, Mouse Assay, Isolation, Fluorescence, In Vitro, Derivative Assay, Injection