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    BsmAI 5 000 units
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    Category:
    Restriction Enzymes
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    New England Biolabs bsmai
    BsmAI
    BsmAI 5 000 units
    https://www.bioz.com/result/bsmai/product/New England Biolabs
    Average 96 stars, based on 602 article reviews
    Price from $9.99 to $1999.99
    bsmai - by Bioz Stars, 2020-07
    96/100 stars

    Images

    1) Product Images from "Somatic Mosaicism in Menkes Disease Suggests Choroid Plexus-mediated Copper Transport to the Developing Brain"

    Article Title: Somatic Mosaicism in Menkes Disease Suggests Choroid Plexus-mediated Copper Transport to the Developing Brain

    Journal: American journal of medical genetics. Part A

    doi: 10.1002/ajmg.a.33632

    Analysis of mosaicism. A. Diagram of ATP7A exon 15 region that was amplified from genomic DNA from the mosaic Menkes disease patient and a normal control, showing position of a novel restriction site ( BsmAI ) created by the P1001L mutation. The 294 bp
    Figure Legend Snippet: Analysis of mosaicism. A. Diagram of ATP7A exon 15 region that was amplified from genomic DNA from the mosaic Menkes disease patient and a normal control, showing position of a novel restriction site ( BsmAI ) created by the P1001L mutation. The 294 bp

    Techniques Used: Amplification, Mutagenesis

    2) Product Images from "Pathogenicity of two COQ7 mutations and responses to 2,4‐dihydroxybenzoate bypass treatment"

    Article Title: Pathogenicity of two COQ7 mutations and responses to 2,4‐dihydroxybenzoate bypass treatment

    Journal: Journal of Cellular and Molecular Medicine

    doi: 10.1111/jcmm.13154

    COQ7 gene variants and a mitochondrial DNA mutation identified in the patient under study. ( A ) COQ7 gene variants. Sequencing chromatograms are shown for the c.308C > T and c.332T > C variants detected in COQ7 in the proband reported in this study, with the wild‐type sequence at the top. The chromatograms also show that the patient is homozygous for both the c.308C > T [p. Thr103Met] polymorphism and the c.332T > C [p.Leu111Pro] mutation. ( B ) Chromatograms showing a partial sequence of the mitochondria 12S rRNA gene in a normal control, the L111P patient reported in this study or the previously reported COQ7 patient carrying the V141E mutation. Both patients and the normal control used in this study carry the m.1438A > G polymorphism. The L111P patient, in addition, carries the m.1555A > G mutation. Black arrows denote altered nucleotides. ( C ) RFLP of mitochondrial DNA. Shown is an agarose gel electrophoresis of PCR products from the mitochondrial 12S rRNA gene digested by BsmAI. Wild‐type control: skin fibroblasts from a healthy unrelated individual; L111P: the proband reported in this study; V141E: COQ7 patient previously reported in 19 . The PCR product (643 bp) without the m.1555A > G mutation was cleaved in two fragments of 409 and 234 bp, which was the case for the wild‐type control and the V141E patient. The PCR product from the L111P patient's 12S rRNA gene was not cut by BsmAI, as the m.1555A > G mutation abolishes the BsmAI restriction site. Moreover, only a single band corresponding to the mutated fragment was seen in the sample from the L111P patient. This, together with the sequencing chromatogram, demonstrates homoplasmy for the m.1555A > G mutation.
    Figure Legend Snippet: COQ7 gene variants and a mitochondrial DNA mutation identified in the patient under study. ( A ) COQ7 gene variants. Sequencing chromatograms are shown for the c.308C > T and c.332T > C variants detected in COQ7 in the proband reported in this study, with the wild‐type sequence at the top. The chromatograms also show that the patient is homozygous for both the c.308C > T [p. Thr103Met] polymorphism and the c.332T > C [p.Leu111Pro] mutation. ( B ) Chromatograms showing a partial sequence of the mitochondria 12S rRNA gene in a normal control, the L111P patient reported in this study or the previously reported COQ7 patient carrying the V141E mutation. Both patients and the normal control used in this study carry the m.1438A > G polymorphism. The L111P patient, in addition, carries the m.1555A > G mutation. Black arrows denote altered nucleotides. ( C ) RFLP of mitochondrial DNA. Shown is an agarose gel electrophoresis of PCR products from the mitochondrial 12S rRNA gene digested by BsmAI. Wild‐type control: skin fibroblasts from a healthy unrelated individual; L111P: the proband reported in this study; V141E: COQ7 patient previously reported in 19 . The PCR product (643 bp) without the m.1555A > G mutation was cleaved in two fragments of 409 and 234 bp, which was the case for the wild‐type control and the V141E patient. The PCR product from the L111P patient's 12S rRNA gene was not cut by BsmAI, as the m.1555A > G mutation abolishes the BsmAI restriction site. Moreover, only a single band corresponding to the mutated fragment was seen in the sample from the L111P patient. This, together with the sequencing chromatogram, demonstrates homoplasmy for the m.1555A > G mutation.

    Techniques Used: Mutagenesis, Sequencing, Agarose Gel Electrophoresis, Polymerase Chain Reaction

    3) Product Images from "Slow-Channel Myasthenic Syndrome Caused By Enhanced Activation, Desensitization, and Agonist Binding Affinity Attributable to Mutation in the M2 Domain of the Acetylcholine Receptor α Subunit"

    Article Title: Slow-Channel Myasthenic Syndrome Caused By Enhanced Activation, Desensitization, and Agonist Binding Affinity Attributable to Mutation in the M2 Domain of the Acetylcholine Receptor α Subunit

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.17-15-05651.1997

    Identification and analysis of mutation in the AChR α subunit. A , Automated sequencing of α exon 7 around codon 249 in a control and the propositus. In the propositus, both G and T nucleotides are present at position 745 ( arrow ), indicating a heterozygous G→T transversion. This mutation changes codon 249 from a GTC for valine to a TTC for phenylalanine. B , Allele-specific PCR and mutagenic PCR plus Bsm AI analysis of genomic DNA in the propositus’ family. Both wild-type and mutant-allele-specific primers amplify an expected 168 bp fragment in propositus and his father, but only the wild-type primer amplifies the expected fragment in the other family members. On Bsm AI analysis after mutagenic PCR, the wild-type allele gives rise to a 134 bp fragment ( open arrowhead ) and a 23 bp fragment (not shown); the mutant allele yields an undigested 157 bp fragment ( closed arrowhead ). Both wild-type and mutant fragments appear in the propositus, but only the wild-type fragment appears in other family members. The incongruity between allele-specific PCR and restriction analysis in the father is attributable to the father being a mosaic for αV249F (see text). The arrow indicates propositus. C , Multiple alignment of AChR M2 membrane-spanning domains. The boxes enclose the conserved valine residues in human AChR subunits and in AChR α subunits of other species. The mutant phenylalanine is shown at the bottom.
    Figure Legend Snippet: Identification and analysis of mutation in the AChR α subunit. A , Automated sequencing of α exon 7 around codon 249 in a control and the propositus. In the propositus, both G and T nucleotides are present at position 745 ( arrow ), indicating a heterozygous G→T transversion. This mutation changes codon 249 from a GTC for valine to a TTC for phenylalanine. B , Allele-specific PCR and mutagenic PCR plus Bsm AI analysis of genomic DNA in the propositus’ family. Both wild-type and mutant-allele-specific primers amplify an expected 168 bp fragment in propositus and his father, but only the wild-type primer amplifies the expected fragment in the other family members. On Bsm AI analysis after mutagenic PCR, the wild-type allele gives rise to a 134 bp fragment ( open arrowhead ) and a 23 bp fragment (not shown); the mutant allele yields an undigested 157 bp fragment ( closed arrowhead ). Both wild-type and mutant fragments appear in the propositus, but only the wild-type fragment appears in other family members. The incongruity between allele-specific PCR and restriction analysis in the father is attributable to the father being a mosaic for αV249F (see text). The arrow indicates propositus. C , Multiple alignment of AChR M2 membrane-spanning domains. The boxes enclose the conserved valine residues in human AChR subunits and in AChR α subunits of other species. The mutant phenylalanine is shown at the bottom.

    Techniques Used: Mutagenesis, Sequencing, Polymerase Chain Reaction

    4) Product Images from "The lss Supernodulation Mutant of Medicago truncatula Reduces Expression of the SUNN Gene 1 Gene 1 [OA]"

    Article Title: The lss Supernodulation Mutant of Medicago truncatula Reduces Expression of the SUNN Gene 1 Gene 1 [OA]

    Journal: Plant Physiology

    doi: 10.1104/pp.110.164889

    Origin of expressed SUNN in sunn LSS/ lss SUNN plants. A, Diagram of mutation and PCR product locations and restriction sites used in B. H indicates a Hae III restriction site, while B indicates a Bsm AI site; within the PCR product, differential digestion
    Figure Legend Snippet: Origin of expressed SUNN in sunn LSS/ lss SUNN plants. A, Diagram of mutation and PCR product locations and restriction sites used in B. H indicates a Hae III restriction site, while B indicates a Bsm AI site; within the PCR product, differential digestion

    Techniques Used: Mutagenesis, Polymerase Chain Reaction

    5) Product Images from "Rapid Identification of Candida dubliniensis Using a Species-Specific Molecular Beacon"

    Article Title: Rapid Identification of Candida dubliniensis Using a Species-Specific Molecular Beacon

    Journal: Journal of Clinical Microbiology

    doi:

    The ITS2 region was PCR amplified with universal fungal primers ITS3 and ITS4, and the products were digested with restriction enzymes Bsm AI ( C. dubliniensis specific) (A) and Nsp BII ( C. albicans specific) (B). The restriction fragments were run on a 1.2% agarose gel and stained with GelStar (FMC Bioproducts). ∗, C. dubliniensis strains.
    Figure Legend Snippet: The ITS2 region was PCR amplified with universal fungal primers ITS3 and ITS4, and the products were digested with restriction enzymes Bsm AI ( C. dubliniensis specific) (A) and Nsp BII ( C. albicans specific) (B). The restriction fragments were run on a 1.2% agarose gel and stained with GelStar (FMC Bioproducts). ∗, C. dubliniensis strains.

    Techniques Used: Polymerase Chain Reaction, Amplification, Agarose Gel Electrophoresis, Staining

    Related Articles

    DNA Extraction:

    Article Title: Somatic Mosaicism in Menkes Disease Suggests Choroid Plexus-mediated Copper Transport to the Developing Brain
    Article Snippet: .. The 294 bp PCR products generated were purified using a DNA isolation kit (QIAGEN, Valencia, CA, USA), digested with BsmAI (NEB, Beverly, MA) and electrophoresed through 2% agarose. ..

    Nucleic Acid Electrophoresis:

    Article Title: Rapid Identification of Candida dubliniensis Using a Species-Specific Molecular Beacon
    Article Snippet: .. The PCR amplification products (∼500 ng) were digested with 1 μl of restriction enzymes Nsp BII ( C. albicans ITS2 specific) (AP Biotech, Piscataway, N.J.) and Bsm AI ( C. dubliniensis ITS2 specific) (New England Biolabs, Beverly, Mass.) for 1 h and were analyzed by gel electrophoresis in a 1.5% agarose gel. ..

    Amplification:

    Article Title: Genetic Analysis of EGLN1 C127S Variant in Taiwanese Parkinson's Disease
    Article Snippet: .. The amplified 401 bp PCR fragments, consisting of 75.3% CG content, were digested with the Bsm AI (New England Biolabs) and separated on a 2.0% agarose gel (allele G, 401-bp fragment; allele C, 233- and 168-bp fragments). ..

    Article Title: The lss Supernodulation Mutant of Medicago truncatula Reduces Expression of the SUNN Gene 1 Gene 1 [OA]
    Article Snippet: .. Following amplification, the PCR products were digested with Bsm AI (New England Biolabs) at 55°C for 4 h, which cuts only the sunn-2 allele, or Hae III (New England Biolabs) at 37°C for 4 h, which cuts only the sunn-1 allele. .. Following digestion, the samples were run on a 1% agarose gel and stained with ethidium bromide.

    Article Title: Rapid Identification of Candida dubliniensis Using a Species-Specific Molecular Beacon
    Article Snippet: .. The PCR amplification products (∼500 ng) were digested with 1 μl of restriction enzymes Nsp BII ( C. albicans ITS2 specific) (AP Biotech, Piscataway, N.J.) and Bsm AI ( C. dubliniensis ITS2 specific) (New England Biolabs, Beverly, Mass.) for 1 h and were analyzed by gel electrophoresis in a 1.5% agarose gel. ..

    Agarose Gel Electrophoresis:

    Article Title: Genetic Analysis of EGLN1 C127S Variant in Taiwanese Parkinson's Disease
    Article Snippet: .. The amplified 401 bp PCR fragments, consisting of 75.3% CG content, were digested with the Bsm AI (New England Biolabs) and separated on a 2.0% agarose gel (allele G, 401-bp fragment; allele C, 233- and 168-bp fragments). ..

    Article Title: Rapid Identification of Candida dubliniensis Using a Species-Specific Molecular Beacon
    Article Snippet: .. The PCR amplification products (∼500 ng) were digested with 1 μl of restriction enzymes Nsp BII ( C. albicans ITS2 specific) (AP Biotech, Piscataway, N.J.) and Bsm AI ( C. dubliniensis ITS2 specific) (New England Biolabs, Beverly, Mass.) for 1 h and were analyzed by gel electrophoresis in a 1.5% agarose gel. ..

    Purification:

    Article Title: Somatic Mosaicism in Menkes Disease Suggests Choroid Plexus-mediated Copper Transport to the Developing Brain
    Article Snippet: .. The 294 bp PCR products generated were purified using a DNA isolation kit (QIAGEN, Valencia, CA, USA), digested with BsmAI (NEB, Beverly, MA) and electrophoresed through 2% agarose. ..

    Polymerase Chain Reaction:

    Article Title: Association between a Functional Polymorphism (-1195T > C) in the IGFBP5 Promoter and Head and Neck Cancer Risk
    Article Snippet: .. When the PCR products were digested with Bsma I (New England Biolabs, Beverly, MA) at 55°C overnight, the 138-bp PCR products with the -1195T allele exhibited 118- and 20-bp bands, while the C allele remained uncut; and the 120-bp PCR products with the-709C allele exhibited 98- and 22-bp bands, while the G allele remained uncut. ..

    Article Title: Slow-Channel Myasthenic Syndrome Caused By Enhanced Activation, Desensitization, and Agonist Binding Affinity Attributable to Mutation in the M2 Domain of the Acetylcholine Receptor α Subunit
    Article Snippet: .. The PCR product was digested with Bsm AI (New England Biolabs, Beverly, MA). ..

    Article Title: Genetic Analysis of EGLN1 C127S Variant in Taiwanese Parkinson's Disease
    Article Snippet: .. The amplified 401 bp PCR fragments, consisting of 75.3% CG content, were digested with the Bsm AI (New England Biolabs) and separated on a 2.0% agarose gel (allele G, 401-bp fragment; allele C, 233- and 168-bp fragments). ..

    Article Title: Somatic Mosaicism in Menkes Disease Suggests Choroid Plexus-mediated Copper Transport to the Developing Brain
    Article Snippet: .. The 294 bp PCR products generated were purified using a DNA isolation kit (QIAGEN, Valencia, CA, USA), digested with BsmAI (NEB, Beverly, MA) and electrophoresed through 2% agarose. ..

    Article Title: The lss Supernodulation Mutant of Medicago truncatula Reduces Expression of the SUNN Gene 1 Gene 1 [OA]
    Article Snippet: .. Following amplification, the PCR products were digested with Bsm AI (New England Biolabs) at 55°C for 4 h, which cuts only the sunn-2 allele, or Hae III (New England Biolabs) at 37°C for 4 h, which cuts only the sunn-1 allele. .. Following digestion, the samples were run on a 1% agarose gel and stained with ethidium bromide.

    Article Title: Pathogenicity of two COQ7 mutations and responses to 2,4‐dihydroxybenzoate bypass treatment
    Article Snippet: .. The 643‐bp PCR product was subjected to sequencing using the same primers as well as restriction fragment length polymorphism (RFLP) analysis using BsmAI (New England Biolabs). .. The digestion of PCR products from samples without the 1555A > G mutation produces two fragments of 409 and 234 bp due to the recognition of the restriction site of BsmAI.

    Article Title: Rapid Identification of Candida dubliniensis Using a Species-Specific Molecular Beacon
    Article Snippet: .. The PCR amplification products (∼500 ng) were digested with 1 μl of restriction enzymes Nsp BII ( C. albicans ITS2 specific) (AP Biotech, Piscataway, N.J.) and Bsm AI ( C. dubliniensis ITS2 specific) (New England Biolabs, Beverly, Mass.) for 1 h and were analyzed by gel electrophoresis in a 1.5% agarose gel. ..

    Article Title: CTLA-4 gene polymorphisms and their influence on predisposition to autoimmune thyroid diseases (Graves' disease and Hashimoto's thyroiditis)
    Article Snippet: .. Analysis of CTLA-4 polymorphism CTLA-4 polymorphisms (A49G, 1822 C/T and CT60 A/G) were assessed by PCR-RFLP (polymerase chain reaction-restriction fragment length polymorphism), using the following restriction enzymes: Fnu4HI , BsmAI , BsaAI (New England Biolabs, USA). .. First, genomic DNA sequences containing the polymorphic region, i.e., Fnu4HI or BsmAI or BsaAI restriction site, were amplified in a PCR reaction (Personal Thermocycler, Eppendorf, Germany), in a total volume of 25 µl, including: 3 µl 10x AmpliTaq Gold® 360 buffer (150 mM Tris-HCl, pH 8.3, 500 mM KCl), 0.12 µl (5 U/ µl) AmpliTaq Gold® 360 DNA Polymerase, 2 µl (25 mM) MgCl2 , 0.66 µl (10 mM) dNTPs (Applied Biosystems, USA), 1 µl (40 ng) DNA, 2.4 µl (1.2 µl 0.5 µM each primer: forward and reverse) and 15.82 µl nuclease-free water.

    Generated:

    Article Title: Somatic Mosaicism in Menkes Disease Suggests Choroid Plexus-mediated Copper Transport to the Developing Brain
    Article Snippet: .. The 294 bp PCR products generated were purified using a DNA isolation kit (QIAGEN, Valencia, CA, USA), digested with BsmAI (NEB, Beverly, MA) and electrophoresed through 2% agarose. ..

    Sequencing:

    Article Title: Pathogenicity of two COQ7 mutations and responses to 2,4‐dihydroxybenzoate bypass treatment
    Article Snippet: .. The 643‐bp PCR product was subjected to sequencing using the same primers as well as restriction fragment length polymorphism (RFLP) analysis using BsmAI (New England Biolabs). .. The digestion of PCR products from samples without the 1555A > G mutation produces two fragments of 409 and 234 bp due to the recognition of the restriction site of BsmAI.

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    New England Biolabs bsmai
    Analysis of mosaicism. A. Diagram of ATP7A exon 15 region that was amplified from genomic <t>DNA</t> from the mosaic Menkes disease patient and a normal control, showing position of a novel restriction site ( <t>BsmAI</t> ) created by the P1001L mutation. The 294 bp
    Bsmai, supplied by New England Biolabs, used in various techniques. Bioz Stars score: 96/100, based on 32 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/bsmai/product/New England Biolabs
    Average 96 stars, based on 32 article reviews
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    Analysis of mosaicism. A. Diagram of ATP7A exon 15 region that was amplified from genomic DNA from the mosaic Menkes disease patient and a normal control, showing position of a novel restriction site ( BsmAI ) created by the P1001L mutation. The 294 bp

    Journal: American journal of medical genetics. Part A

    Article Title: Somatic Mosaicism in Menkes Disease Suggests Choroid Plexus-mediated Copper Transport to the Developing Brain

    doi: 10.1002/ajmg.a.33632

    Figure Lengend Snippet: Analysis of mosaicism. A. Diagram of ATP7A exon 15 region that was amplified from genomic DNA from the mosaic Menkes disease patient and a normal control, showing position of a novel restriction site ( BsmAI ) created by the P1001L mutation. The 294 bp

    Article Snippet: The 294 bp PCR products generated were purified using a DNA isolation kit (QIAGEN, Valencia, CA, USA), digested with BsmAI (NEB, Beverly, MA) and electrophoresed through 2% agarose.

    Techniques: Amplification, Mutagenesis

    COQ7 gene variants and a mitochondrial DNA mutation identified in the patient under study. ( A ) COQ7 gene variants. Sequencing chromatograms are shown for the c.308C > T and c.332T > C variants detected in COQ7 in the proband reported in this study, with the wild‐type sequence at the top. The chromatograms also show that the patient is homozygous for both the c.308C > T [p. Thr103Met] polymorphism and the c.332T > C [p.Leu111Pro] mutation. ( B ) Chromatograms showing a partial sequence of the mitochondria 12S rRNA gene in a normal control, the L111P patient reported in this study or the previously reported COQ7 patient carrying the V141E mutation. Both patients and the normal control used in this study carry the m.1438A > G polymorphism. The L111P patient, in addition, carries the m.1555A > G mutation. Black arrows denote altered nucleotides. ( C ) RFLP of mitochondrial DNA. Shown is an agarose gel electrophoresis of PCR products from the mitochondrial 12S rRNA gene digested by BsmAI. Wild‐type control: skin fibroblasts from a healthy unrelated individual; L111P: the proband reported in this study; V141E: COQ7 patient previously reported in 19 . The PCR product (643 bp) without the m.1555A > G mutation was cleaved in two fragments of 409 and 234 bp, which was the case for the wild‐type control and the V141E patient. The PCR product from the L111P patient's 12S rRNA gene was not cut by BsmAI, as the m.1555A > G mutation abolishes the BsmAI restriction site. Moreover, only a single band corresponding to the mutated fragment was seen in the sample from the L111P patient. This, together with the sequencing chromatogram, demonstrates homoplasmy for the m.1555A > G mutation.

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: Pathogenicity of two COQ7 mutations and responses to 2,4‐dihydroxybenzoate bypass treatment

    doi: 10.1111/jcmm.13154

    Figure Lengend Snippet: COQ7 gene variants and a mitochondrial DNA mutation identified in the patient under study. ( A ) COQ7 gene variants. Sequencing chromatograms are shown for the c.308C > T and c.332T > C variants detected in COQ7 in the proband reported in this study, with the wild‐type sequence at the top. The chromatograms also show that the patient is homozygous for both the c.308C > T [p. Thr103Met] polymorphism and the c.332T > C [p.Leu111Pro] mutation. ( B ) Chromatograms showing a partial sequence of the mitochondria 12S rRNA gene in a normal control, the L111P patient reported in this study or the previously reported COQ7 patient carrying the V141E mutation. Both patients and the normal control used in this study carry the m.1438A > G polymorphism. The L111P patient, in addition, carries the m.1555A > G mutation. Black arrows denote altered nucleotides. ( C ) RFLP of mitochondrial DNA. Shown is an agarose gel electrophoresis of PCR products from the mitochondrial 12S rRNA gene digested by BsmAI. Wild‐type control: skin fibroblasts from a healthy unrelated individual; L111P: the proband reported in this study; V141E: COQ7 patient previously reported in 19 . The PCR product (643 bp) without the m.1555A > G mutation was cleaved in two fragments of 409 and 234 bp, which was the case for the wild‐type control and the V141E patient. The PCR product from the L111P patient's 12S rRNA gene was not cut by BsmAI, as the m.1555A > G mutation abolishes the BsmAI restriction site. Moreover, only a single band corresponding to the mutated fragment was seen in the sample from the L111P patient. This, together with the sequencing chromatogram, demonstrates homoplasmy for the m.1555A > G mutation.

    Article Snippet: The 643‐bp PCR product was subjected to sequencing using the same primers as well as restriction fragment length polymorphism (RFLP) analysis using BsmAI (New England Biolabs).

    Techniques: Mutagenesis, Sequencing, Agarose Gel Electrophoresis, Polymerase Chain Reaction

    Identification and analysis of mutation in the AChR α subunit. A , Automated sequencing of α exon 7 around codon 249 in a control and the propositus. In the propositus, both G and T nucleotides are present at position 745 ( arrow ), indicating a heterozygous G→T transversion. This mutation changes codon 249 from a GTC for valine to a TTC for phenylalanine. B , Allele-specific PCR and mutagenic PCR plus Bsm AI analysis of genomic DNA in the propositus’ family. Both wild-type and mutant-allele-specific primers amplify an expected 168 bp fragment in propositus and his father, but only the wild-type primer amplifies the expected fragment in the other family members. On Bsm AI analysis after mutagenic PCR, the wild-type allele gives rise to a 134 bp fragment ( open arrowhead ) and a 23 bp fragment (not shown); the mutant allele yields an undigested 157 bp fragment ( closed arrowhead ). Both wild-type and mutant fragments appear in the propositus, but only the wild-type fragment appears in other family members. The incongruity between allele-specific PCR and restriction analysis in the father is attributable to the father being a mosaic for αV249F (see text). The arrow indicates propositus. C , Multiple alignment of AChR M2 membrane-spanning domains. The boxes enclose the conserved valine residues in human AChR subunits and in AChR α subunits of other species. The mutant phenylalanine is shown at the bottom.

    Journal: The Journal of Neuroscience

    Article Title: Slow-Channel Myasthenic Syndrome Caused By Enhanced Activation, Desensitization, and Agonist Binding Affinity Attributable to Mutation in the M2 Domain of the Acetylcholine Receptor α Subunit

    doi: 10.1523/JNEUROSCI.17-15-05651.1997

    Figure Lengend Snippet: Identification and analysis of mutation in the AChR α subunit. A , Automated sequencing of α exon 7 around codon 249 in a control and the propositus. In the propositus, both G and T nucleotides are present at position 745 ( arrow ), indicating a heterozygous G→T transversion. This mutation changes codon 249 from a GTC for valine to a TTC for phenylalanine. B , Allele-specific PCR and mutagenic PCR plus Bsm AI analysis of genomic DNA in the propositus’ family. Both wild-type and mutant-allele-specific primers amplify an expected 168 bp fragment in propositus and his father, but only the wild-type primer amplifies the expected fragment in the other family members. On Bsm AI analysis after mutagenic PCR, the wild-type allele gives rise to a 134 bp fragment ( open arrowhead ) and a 23 bp fragment (not shown); the mutant allele yields an undigested 157 bp fragment ( closed arrowhead ). Both wild-type and mutant fragments appear in the propositus, but only the wild-type fragment appears in other family members. The incongruity between allele-specific PCR and restriction analysis in the father is attributable to the father being a mosaic for αV249F (see text). The arrow indicates propositus. C , Multiple alignment of AChR M2 membrane-spanning domains. The boxes enclose the conserved valine residues in human AChR subunits and in AChR α subunits of other species. The mutant phenylalanine is shown at the bottom.

    Article Snippet: The PCR product was digested with Bsm AI (New England Biolabs, Beverly, MA).

    Techniques: Mutagenesis, Sequencing, Polymerase Chain Reaction

    Origin of expressed SUNN in sunn LSS/ lss SUNN plants. A, Diagram of mutation and PCR product locations and restriction sites used in B. H indicates a Hae III restriction site, while B indicates a Bsm AI site; within the PCR product, differential digestion

    Journal: Plant Physiology

    Article Title: The lss Supernodulation Mutant of Medicago truncatula Reduces Expression of the SUNN Gene 1 Gene 1 [OA]

    doi: 10.1104/pp.110.164889

    Figure Lengend Snippet: Origin of expressed SUNN in sunn LSS/ lss SUNN plants. A, Diagram of mutation and PCR product locations and restriction sites used in B. H indicates a Hae III restriction site, while B indicates a Bsm AI site; within the PCR product, differential digestion

    Article Snippet: Following amplification, the PCR products were digested with Bsm AI (New England Biolabs) at 55°C for 4 h, which cuts only the sunn-2 allele, or Hae III (New England Biolabs) at 37°C for 4 h, which cuts only the sunn-1 allele.

    Techniques: Mutagenesis, Polymerase Chain Reaction