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Novocastra β sarcoglycan
Restoration of dystrophin by scAAV9.U7.ACCA in adult Dup2 mice enhances sarcolemmal localization of dystrophin binding partners and ameliorates muscle pathology (A) Immunostaining of <t>β-sarcoglycan</t> (β-SG), β-dystroglycan (β-DG), and neuronal nitric oxidase synthase (nNOS) in tibialis anterior of Dup2 mice treated with scAAV9.U7.ACCA (ACCA), methylprednisolone (PDN), or both agents 3 months post injection compared with age-matched control mice. Scale bars, 200 μm. Images represent n = 5–6 per group. (B) Representative H E staining of tibialis anterior (TA) and diaphragm (Dia) from treated Dup2 and control mice. Scale bars, 100 μm. (C) Quantification of centronucleation (CN) in myofibers from TA and diaphragm H E images. (D) TA specific force measured during tetanic contraction. (E) Magnitude of TA force drop over ten cycles of eccentric contractions (ECC), reflecting the area under the curve (AUC) of the ECC force tracings. (F) ECC-induced force loss tracings for the TA reflecting ten eccentric contraction cycles. All bar graph data are presented as mean ± SD with individual points, and statistical comparisons were performed using one-way ANOVA with Sidak multiple comparisons test. ECC cycle tracings show mean ± SEM and were compared using two-way ANOVA with Bonferroni multiple comparisons test. ∗p
β Sarcoglycan, supplied by Novocastra, used in various techniques. Bioz Stars score: 90/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/β sarcoglycan/product/Novocastra
Average 90 stars, based on 10 article reviews
Price from $9.99 to $1999.99
β sarcoglycan - by Bioz Stars, 2022-12
90/100 stars

Images

1) Product Images from "Systemic delivery of an AAV9 exon-skipping vector significantly improves or prevents features of Duchenne muscular dystrophy in the Dup2 mouse"

Article Title: Systemic delivery of an AAV9 exon-skipping vector significantly improves or prevents features of Duchenne muscular dystrophy in the Dup2 mouse

Journal: Molecular Therapy. Methods & Clinical Development

doi: 10.1016/j.omtm.2022.07.005

Restoration of dystrophin by scAAV9.U7.ACCA in adult Dup2 mice enhances sarcolemmal localization of dystrophin binding partners and ameliorates muscle pathology (A) Immunostaining of β-sarcoglycan (β-SG), β-dystroglycan (β-DG), and neuronal nitric oxidase synthase (nNOS) in tibialis anterior of Dup2 mice treated with scAAV9.U7.ACCA (ACCA), methylprednisolone (PDN), or both agents 3 months post injection compared with age-matched control mice. Scale bars, 200 μm. Images represent n = 5–6 per group. (B) Representative H E staining of tibialis anterior (TA) and diaphragm (Dia) from treated Dup2 and control mice. Scale bars, 100 μm. (C) Quantification of centronucleation (CN) in myofibers from TA and diaphragm H E images. (D) TA specific force measured during tetanic contraction. (E) Magnitude of TA force drop over ten cycles of eccentric contractions (ECC), reflecting the area under the curve (AUC) of the ECC force tracings. (F) ECC-induced force loss tracings for the TA reflecting ten eccentric contraction cycles. All bar graph data are presented as mean ± SD with individual points, and statistical comparisons were performed using one-way ANOVA with Sidak multiple comparisons test. ECC cycle tracings show mean ± SEM and were compared using two-way ANOVA with Bonferroni multiple comparisons test. ∗p
Figure Legend Snippet: Restoration of dystrophin by scAAV9.U7.ACCA in adult Dup2 mice enhances sarcolemmal localization of dystrophin binding partners and ameliorates muscle pathology (A) Immunostaining of β-sarcoglycan (β-SG), β-dystroglycan (β-DG), and neuronal nitric oxidase synthase (nNOS) in tibialis anterior of Dup2 mice treated with scAAV9.U7.ACCA (ACCA), methylprednisolone (PDN), or both agents 3 months post injection compared with age-matched control mice. Scale bars, 200 μm. Images represent n = 5–6 per group. (B) Representative H E staining of tibialis anterior (TA) and diaphragm (Dia) from treated Dup2 and control mice. Scale bars, 100 μm. (C) Quantification of centronucleation (CN) in myofibers from TA and diaphragm H E images. (D) TA specific force measured during tetanic contraction. (E) Magnitude of TA force drop over ten cycles of eccentric contractions (ECC), reflecting the area under the curve (AUC) of the ECC force tracings. (F) ECC-induced force loss tracings for the TA reflecting ten eccentric contraction cycles. All bar graph data are presented as mean ± SD with individual points, and statistical comparisons were performed using one-way ANOVA with Sidak multiple comparisons test. ECC cycle tracings show mean ± SEM and were compared using two-way ANOVA with Bonferroni multiple comparisons test. ∗p

Techniques Used: Mouse Assay, Binding Assay, Immunostaining, Injection, Staining

2) Product Images from "Sarcoglycan A mutation in miniature dachshund dogs causes limb-girdle muscular dystrophy 2D"

Article Title: Sarcoglycan A mutation in miniature dachshund dogs causes limb-girdle muscular dystrophy 2D

Journal: Skeletal Muscle

doi: 10.1186/s13395-020-00257-y

Immunofluorescent staining and western blotting from a dystrophic miniature dachshund. A Immunofluorescent staining of muscle cryosections from a representative dystrophic miniature dachshund. Staining for the rod-domain of dystrophin and laminin α-2 was similar to control muscle while staining for the dystrophin C-terminus was patchy. Utrophin was not increased. Numerous regenerating myofibers were highlighted with the antibody against developmental myosin heavy chain (dMHC). Staining for α- and γ-sarcoglycans was absent and decreased for β-sarcoglycan. B Western blotting confirmed all three sarcoglycans were absent. β-actin was used as loading control
Figure Legend Snippet: Immunofluorescent staining and western blotting from a dystrophic miniature dachshund. A Immunofluorescent staining of muscle cryosections from a representative dystrophic miniature dachshund. Staining for the rod-domain of dystrophin and laminin α-2 was similar to control muscle while staining for the dystrophin C-terminus was patchy. Utrophin was not increased. Numerous regenerating myofibers were highlighted with the antibody against developmental myosin heavy chain (dMHC). Staining for α- and γ-sarcoglycans was absent and decreased for β-sarcoglycan. B Western blotting confirmed all three sarcoglycans were absent. β-actin was used as loading control

Techniques Used: Staining, Western Blot

3) Product Images from "Dystrophin R16/17-syntrophin PDZ fusion protein restores sarcolemmal nNOSμ"

Article Title: Dystrophin R16/17-syntrophin PDZ fusion protein restores sarcolemmal nNOSμ

Journal: Skeletal Muscle

doi: 10.1186/s13395-018-0182-x

Restoration of sarcolemmal nNOSμ by the R16/17-Syn PDZ fusion protein was independent of the DAPC. Representative photomicrographs of serial muscle sections visualized for GFP, syntrophin PDZ domain, nNOS expression, β-dystroglycan (β-DG), β-sarcoglycan (β-SG), and dystrobrevin (DB) in uninjected mdx mice and AAV.R16/17-Syn PDZ.GFP.Pal treated mdx mice. Asterisk, the same myofiber in serial sections. Scale bar = 50 μm
Figure Legend Snippet: Restoration of sarcolemmal nNOSμ by the R16/17-Syn PDZ fusion protein was independent of the DAPC. Representative photomicrographs of serial muscle sections visualized for GFP, syntrophin PDZ domain, nNOS expression, β-dystroglycan (β-DG), β-sarcoglycan (β-SG), and dystrobrevin (DB) in uninjected mdx mice and AAV.R16/17-Syn PDZ.GFP.Pal treated mdx mice. Asterisk, the same myofiber in serial sections. Scale bar = 50 μm

Techniques Used: Expressing, Mouse Assay

4) Product Images from "Whole exome sequencing identified a novel DAG1 mutation in a patient with rare, mild and late age of onset muscular dystrophy‐dystroglycanopathy, et al. Whole exome sequencing identified a novel DAG1 mutation in a patient with rare, mild and late age of onset muscular dystrophy‐dystroglycanopathy"

Article Title: Whole exome sequencing identified a novel DAG1 mutation in a patient with rare, mild and late age of onset muscular dystrophy‐dystroglycanopathy, et al. Whole exome sequencing identified a novel DAG1 mutation in a patient with rare, mild and late age of onset muscular dystrophy‐dystroglycanopathy

Journal: Journal of Cellular and Molecular Medicine

doi: 10.1111/jcmm.13979

Muscle Biopsy. A, haematoxylin‐eosin staining; B, IHC staining of dystrophin‐N; C, IHC staining of α‐sarcoglycan; D, IHC staining of β‐sarcoglycan
Figure Legend Snippet: Muscle Biopsy. A, haematoxylin‐eosin staining; B, IHC staining of dystrophin‐N; C, IHC staining of α‐sarcoglycan; D, IHC staining of β‐sarcoglycan

Techniques Used: Staining, Immunohistochemistry

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  • 90
    Novocastra sarcoglycans
    Splicing defect rescue by in vitro morpholino treatment: ( A ) Scheme of the pseudoexon and localization of the Morpholino sequence (MO, in red) used in this study. ( B ) Tape Station analysis of RT-PCR amplicons obtained in untreated (NT) and treated (MO) patient’s derived induced pluripotent stem cells documenting the amelioration of physiological splicing and the reduction in aberrant splicing products after MO delivery. Tape Station analysis allowed the identification of two additional bands corresponding to a predicted shorter form of Pseudoexon (PE-87) and a band with a molecular weight corresponding to the SGCB transcript containing the c.377_384dup duplication (dup). ( C ) qRT-PCR analysis of SGCB transcripts encompassing different exon junctions in untreated (NT) patient’s derived iPSCs and in Morpholino (MO)-treated cells displaying the increase in physiological splicing and the concomitant reduction in aberrant transcripts including Exon2-PE junction. ( D ) Immunocytochemical analysis <t>of</t> <t>beta-sarcoglycan</t> signal in untreated patient’s derived iPSCs (NT), in Morpholino (MO)-treated cells, and in iPSCs obtained from a control subject (CTRL). Magnification 40×. Scale bar 50 μm.
    Sarcoglycans, supplied by Novocastra, 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/result/sarcoglycans/product/Novocastra
    Average 90 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    sarcoglycans - by Bioz Stars, 2022-12
    90/100 stars
      Buy from Supplier

    90
    Novocastra β sarcoglycan
    Restoration of dystrophin by scAAV9.U7.ACCA in adult Dup2 mice enhances sarcolemmal localization of dystrophin binding partners and ameliorates muscle pathology (A) Immunostaining of <t>β-sarcoglycan</t> (β-SG), β-dystroglycan (β-DG), and neuronal nitric oxidase synthase (nNOS) in tibialis anterior of Dup2 mice treated with scAAV9.U7.ACCA (ACCA), methylprednisolone (PDN), or both agents 3 months post injection compared with age-matched control mice. Scale bars, 200 μm. Images represent n = 5–6 per group. (B) Representative H E staining of tibialis anterior (TA) and diaphragm (Dia) from treated Dup2 and control mice. Scale bars, 100 μm. (C) Quantification of centronucleation (CN) in myofibers from TA and diaphragm H E images. (D) TA specific force measured during tetanic contraction. (E) Magnitude of TA force drop over ten cycles of eccentric contractions (ECC), reflecting the area under the curve (AUC) of the ECC force tracings. (F) ECC-induced force loss tracings for the TA reflecting ten eccentric contraction cycles. All bar graph data are presented as mean ± SD with individual points, and statistical comparisons were performed using one-way ANOVA with Sidak multiple comparisons test. ECC cycle tracings show mean ± SEM and were compared using two-way ANOVA with Bonferroni multiple comparisons test. ∗p
    β Sarcoglycan, supplied by Novocastra, 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/result/β sarcoglycan/product/Novocastra
    Average 90 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    β sarcoglycan - by Bioz Stars, 2022-12
    90/100 stars
      Buy from Supplier

    88
    Novocastra γ sarcoglycan
    Pathologic features of patients with beta-sarcoglycanopathy. (H,O) Hematoxylin-eosin staining showing a muscular dystrophic pattern in patients F1-II1 and F2-II1. (A–G) A normal control showing positive expression of sarcoglycans and dystrophin. (H–N) Patient F1-II1 showing a mild reduction of <t>α-sarcoglycan,</t> complete deficiency of β-sarcoglycan, a partial reduction of <t>γ-sarcoglycan,</t> a very slight reduction of dystrophin-N, and positive expression of dystrophin-C and dystrophin-R. (O–U) Patient F2-II1 showing a severe reduction of α-sarcoglycan, absent expression of β-sarcoglycan, a partial reduction of γ-sarcoglycan, a very slight reduction of dystrophin-N, positive expression of dystrophin-C, and a partial reduction of dystrophin-R. 200× magnification.
    γ Sarcoglycan, supplied by Novocastra, used in various techniques. Bioz Stars score: 88/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/γ sarcoglycan/product/Novocastra
    Average 88 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    γ sarcoglycan - by Bioz Stars, 2022-12
    88/100 stars
      Buy from Supplier

    Image Search Results


    Splicing defect rescue by in vitro morpholino treatment: ( A ) Scheme of the pseudoexon and localization of the Morpholino sequence (MO, in red) used in this study. ( B ) Tape Station analysis of RT-PCR amplicons obtained in untreated (NT) and treated (MO) patient’s derived induced pluripotent stem cells documenting the amelioration of physiological splicing and the reduction in aberrant splicing products after MO delivery. Tape Station analysis allowed the identification of two additional bands corresponding to a predicted shorter form of Pseudoexon (PE-87) and a band with a molecular weight corresponding to the SGCB transcript containing the c.377_384dup duplication (dup). ( C ) qRT-PCR analysis of SGCB transcripts encompassing different exon junctions in untreated (NT) patient’s derived iPSCs and in Morpholino (MO)-treated cells displaying the increase in physiological splicing and the concomitant reduction in aberrant transcripts including Exon2-PE junction. ( D ) Immunocytochemical analysis of beta-sarcoglycan signal in untreated patient’s derived iPSCs (NT), in Morpholino (MO)-treated cells, and in iPSCs obtained from a control subject (CTRL). Magnification 40×. Scale bar 50 μm.

    Journal: International Journal of Molecular Sciences

    Article Title: Antisense Morpholino-Based In Vitro Correction of a Pseudoexon-Generating Variant in the SGCB Gene

    doi: 10.3390/ijms23179817

    Figure Lengend Snippet: Splicing defect rescue by in vitro morpholino treatment: ( A ) Scheme of the pseudoexon and localization of the Morpholino sequence (MO, in red) used in this study. ( B ) Tape Station analysis of RT-PCR amplicons obtained in untreated (NT) and treated (MO) patient’s derived induced pluripotent stem cells documenting the amelioration of physiological splicing and the reduction in aberrant splicing products after MO delivery. Tape Station analysis allowed the identification of two additional bands corresponding to a predicted shorter form of Pseudoexon (PE-87) and a band with a molecular weight corresponding to the SGCB transcript containing the c.377_384dup duplication (dup). ( C ) qRT-PCR analysis of SGCB transcripts encompassing different exon junctions in untreated (NT) patient’s derived iPSCs and in Morpholino (MO)-treated cells displaying the increase in physiological splicing and the concomitant reduction in aberrant transcripts including Exon2-PE junction. ( D ) Immunocytochemical analysis of beta-sarcoglycan signal in untreated patient’s derived iPSCs (NT), in Morpholino (MO)-treated cells, and in iPSCs obtained from a control subject (CTRL). Magnification 40×. Scale bar 50 μm.

    Article Snippet: Immunohistochemical (IHC) analyses were performed using monoclonal antibodies directed against three different epitopes of dystrophin (rod-domain diluted 1:10, NH2-domain diluted 1:10, COOH-domain undiluted, all from Novocastra, Newcastle upon Tyne, UK), sarcoglycans (alpha-sarcoglycan 1:20, gamma-sarcoglycan 1:10, Novocastra, Newcastle upon Tyne, UK), and caveolin-3 (1:1000, BD Transduction Laboratories, Franklin Lakes, NJ, USA) as previously described [ ].

    Techniques: In Vitro, Sequencing, Reverse Transcription Polymerase Chain Reaction, Derivative Assay, Molecular Weight, Quantitative RT-PCR

    Skeletal muscle involvement in our Patient: ( A ) Modified Gomori Trichrome on patient’s muscle section showing the presence of necrotic fibers. Immunofluorescent staining for alpha-sarcoglycan ( B ) and gamma-sarcoglycan ( C ) (insert: alpha- and gamma-sarcoglycan in control muscle sections). Magnification 20×. Scale bar 50 μm. ( D ) Western blot analysis of sarcoglycans proteins and muscle actinin used as a reference in patient’s (PT) and control (CTRL) muscle biopsies. Protein levels of sarcoglycans normalized to actinin are reported in the bar chart (error bars mean standard deviations among controls, n = 3).

    Journal: International Journal of Molecular Sciences

    Article Title: Antisense Morpholino-Based In Vitro Correction of a Pseudoexon-Generating Variant in the SGCB Gene

    doi: 10.3390/ijms23179817

    Figure Lengend Snippet: Skeletal muscle involvement in our Patient: ( A ) Modified Gomori Trichrome on patient’s muscle section showing the presence of necrotic fibers. Immunofluorescent staining for alpha-sarcoglycan ( B ) and gamma-sarcoglycan ( C ) (insert: alpha- and gamma-sarcoglycan in control muscle sections). Magnification 20×. Scale bar 50 μm. ( D ) Western blot analysis of sarcoglycans proteins and muscle actinin used as a reference in patient’s (PT) and control (CTRL) muscle biopsies. Protein levels of sarcoglycans normalized to actinin are reported in the bar chart (error bars mean standard deviations among controls, n = 3).

    Article Snippet: Immunohistochemical (IHC) analyses were performed using monoclonal antibodies directed against three different epitopes of dystrophin (rod-domain diluted 1:10, NH2-domain diluted 1:10, COOH-domain undiluted, all from Novocastra, Newcastle upon Tyne, UK), sarcoglycans (alpha-sarcoglycan 1:20, gamma-sarcoglycan 1:10, Novocastra, Newcastle upon Tyne, UK), and caveolin-3 (1:1000, BD Transduction Laboratories, Franklin Lakes, NJ, USA) as previously described [ ].

    Techniques: Modification, Staining, Western Blot

    Restoration of dystrophin by scAAV9.U7.ACCA in adult Dup2 mice enhances sarcolemmal localization of dystrophin binding partners and ameliorates muscle pathology (A) Immunostaining of β-sarcoglycan (β-SG), β-dystroglycan (β-DG), and neuronal nitric oxidase synthase (nNOS) in tibialis anterior of Dup2 mice treated with scAAV9.U7.ACCA (ACCA), methylprednisolone (PDN), or both agents 3 months post injection compared with age-matched control mice. Scale bars, 200 μm. Images represent n = 5–6 per group. (B) Representative H E staining of tibialis anterior (TA) and diaphragm (Dia) from treated Dup2 and control mice. Scale bars, 100 μm. (C) Quantification of centronucleation (CN) in myofibers from TA and diaphragm H E images. (D) TA specific force measured during tetanic contraction. (E) Magnitude of TA force drop over ten cycles of eccentric contractions (ECC), reflecting the area under the curve (AUC) of the ECC force tracings. (F) ECC-induced force loss tracings for the TA reflecting ten eccentric contraction cycles. All bar graph data are presented as mean ± SD with individual points, and statistical comparisons were performed using one-way ANOVA with Sidak multiple comparisons test. ECC cycle tracings show mean ± SEM and were compared using two-way ANOVA with Bonferroni multiple comparisons test. ∗p

    Journal: Molecular Therapy. Methods & Clinical Development

    Article Title: Systemic delivery of an AAV9 exon-skipping vector significantly improves or prevents features of Duchenne muscular dystrophy in the Dup2 mouse

    doi: 10.1016/j.omtm.2022.07.005

    Figure Lengend Snippet: Restoration of dystrophin by scAAV9.U7.ACCA in adult Dup2 mice enhances sarcolemmal localization of dystrophin binding partners and ameliorates muscle pathology (A) Immunostaining of β-sarcoglycan (β-SG), β-dystroglycan (β-DG), and neuronal nitric oxidase synthase (nNOS) in tibialis anterior of Dup2 mice treated with scAAV9.U7.ACCA (ACCA), methylprednisolone (PDN), or both agents 3 months post injection compared with age-matched control mice. Scale bars, 200 μm. Images represent n = 5–6 per group. (B) Representative H E staining of tibialis anterior (TA) and diaphragm (Dia) from treated Dup2 and control mice. Scale bars, 100 μm. (C) Quantification of centronucleation (CN) in myofibers from TA and diaphragm H E images. (D) TA specific force measured during tetanic contraction. (E) Magnitude of TA force drop over ten cycles of eccentric contractions (ECC), reflecting the area under the curve (AUC) of the ECC force tracings. (F) ECC-induced force loss tracings for the TA reflecting ten eccentric contraction cycles. All bar graph data are presented as mean ± SD with individual points, and statistical comparisons were performed using one-way ANOVA with Sidak multiple comparisons test. ECC cycle tracings show mean ± SEM and were compared using two-way ANOVA with Bonferroni multiple comparisons test. ∗p

    Article Snippet: The following primary antibodies were used: dystrophin (1:400; ab15277, Abcam); α1-laminin (1:400; MAB4656, R & D Systems); nNos (1:200; sc-648, SCBT); β-dystroglycan (1:500; MANDAG2, DSHB or gift from Dr. Glenn Morris and the MDA Monoclonal Antibody Resource, www.glennmorris.org.uk); β-sarcoglycan (1:50; B-SARC-L-CE, Novocastra).

    Techniques: Mouse Assay, Binding Assay, Immunostaining, Injection, Staining

    Pathologic features of patients with beta-sarcoglycanopathy. (H,O) Hematoxylin-eosin staining showing a muscular dystrophic pattern in patients F1-II1 and F2-II1. (A–G) A normal control showing positive expression of sarcoglycans and dystrophin. (H–N) Patient F1-II1 showing a mild reduction of α-sarcoglycan, complete deficiency of β-sarcoglycan, a partial reduction of γ-sarcoglycan, a very slight reduction of dystrophin-N, and positive expression of dystrophin-C and dystrophin-R. (O–U) Patient F2-II1 showing a severe reduction of α-sarcoglycan, absent expression of β-sarcoglycan, a partial reduction of γ-sarcoglycan, a very slight reduction of dystrophin-N, positive expression of dystrophin-C, and a partial reduction of dystrophin-R. 200× magnification.

    Journal: Frontiers in Pediatrics

    Article Title: First Identification of Rare Exonic and Deep Intronic Splice-Altering Variants in Patients With Beta-Sarcoglycanopathy

    doi: 10.3389/fped.2022.900280

    Figure Lengend Snippet: Pathologic features of patients with beta-sarcoglycanopathy. (H,O) Hematoxylin-eosin staining showing a muscular dystrophic pattern in patients F1-II1 and F2-II1. (A–G) A normal control showing positive expression of sarcoglycans and dystrophin. (H–N) Patient F1-II1 showing a mild reduction of α-sarcoglycan, complete deficiency of β-sarcoglycan, a partial reduction of γ-sarcoglycan, a very slight reduction of dystrophin-N, and positive expression of dystrophin-C and dystrophin-R. (O–U) Patient F2-II1 showing a severe reduction of α-sarcoglycan, absent expression of β-sarcoglycan, a partial reduction of γ-sarcoglycan, a very slight reduction of dystrophin-N, positive expression of dystrophin-C, and a partial reduction of dystrophin-R. 200× magnification.

    Article Snippet: Primary monoclonal antibodies against the dystrophin and sarcoglycan proteins were used, including dystrophin-N (amino-terminal), dystrophin-R (rod-domain), dystrophin-C (carboxyl-terminal), α-sarcoglycan, β-sarcoglycan, and γ-sarcoglycan (Novocastra Laboratories, Newcastle) ( , ).

    Techniques: Staining, Expressing