bsmai  (New England Biolabs)


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    Structured Review

    New England Biolabs bsmai
    The sequences of recognition and cleavage sites of <t>SspI</t> and <t>BsmAI.</t>
    Bsmai, supplied by New England Biolabs, used in various techniques. Bioz Stars score: 94/100, based on 31 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/bsmai/product/New England Biolabs
    Average 94 stars, based on 31 article reviews
    Price from $9.99 to $1999.99
    bsmai - by Bioz Stars, 2022-11
    94/100 stars

    Images

    1) Product Images from "The Influence of 5′R and 5′S cdA and cdG on the Activity of BsmAI and SspI Restriction Enzymes"

    Article Title: The Influence of 5′R and 5′S cdA and cdG on the Activity of BsmAI and SspI Restriction Enzymes

    Journal: Molecules

    doi: 10.3390/molecules26123750

    The sequences of recognition and cleavage sites of SspI and BsmAI.
    Figure Legend Snippet: The sequences of recognition and cleavage sites of SspI and BsmAI.

    Techniques Used:

    Cleavage of dsDNA containing ScdA and RcdA by 0.5 U BsmAI. ( A ) Quantity increase of cleaved strands 3–6. These strands are arranged in duplexes B and C, which contain cdA lesions located within the recognition site of SspI ( Figure 2 ). ( B ) Quantity increase of cleaved strands 7–18. These strands are arranged in duplexes D–E and H–I, which contain cdA lesions located within the cleavage site of BsmAI ( Figure 2 ).
    Figure Legend Snippet: Cleavage of dsDNA containing ScdA and RcdA by 0.5 U BsmAI. ( A ) Quantity increase of cleaved strands 3–6. These strands are arranged in duplexes B and C, which contain cdA lesions located within the recognition site of SspI ( Figure 2 ). ( B ) Quantity increase of cleaved strands 7–18. These strands are arranged in duplexes D–E and H–I, which contain cdA lesions located within the cleavage site of BsmAI ( Figure 2 ).

    Techniques Used:

    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 "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

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    • bsmai bstci  (New England Biolabs)
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    New England Biolabs bsmai bstci
    The sequences of recognition and cleavage sites of <t>SspI</t> and <t>BsmAI.</t>
    Bsmai Bstci, supplied by New England Biolabs, used in various techniques. Bioz Stars score: 94/100, based on 15 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/bsmai bstci/product/New England Biolabs
    Average 94 stars, based on 15 article reviews
    Price from $9.99 to $1999.99
    bsmai bstci - by Bioz Stars, 2022-11
    94/100 stars
    		  Buy from Supplier

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    The sequences of recognition and cleavage sites of SspI and BsmAI.

    Journal: Molecules

    Article Title: The Influence of 5′R and 5′S cdA and cdG on the Activity of BsmAI and SspI Restriction Enzymes

    doi: 10.3390/molecules26123750

    Figure Lengend Snippet: The sequences of recognition and cleavage sites of SspI and BsmAI.

    Article Snippet: BsmAI and SspI Cleavage AssayBsmAI and SspI were purchased from NEB (New England BioLabs, Ipswich, MA, USA).

    Techniques:

    Cleavage of dsDNA containing ScdA and RcdA by 0.5 U BsmAI. ( A ) Quantity increase of cleaved strands 3–6. These strands are arranged in duplexes B and C, which contain cdA lesions located within the recognition site of SspI ( Figure 2 ). ( B ) Quantity increase of cleaved strands 7–18. These strands are arranged in duplexes D–E and H–I, which contain cdA lesions located within the cleavage site of BsmAI ( Figure 2 ).

    Journal: Molecules

    Article Title: The Influence of 5′R and 5′S cdA and cdG on the Activity of BsmAI and SspI Restriction Enzymes

    doi: 10.3390/molecules26123750

    Figure Lengend Snippet: Cleavage of dsDNA containing ScdA and RcdA by 0.5 U BsmAI. ( A ) Quantity increase of cleaved strands 3–6. These strands are arranged in duplexes B and C, which contain cdA lesions located within the recognition site of SspI ( Figure 2 ). ( B ) Quantity increase of cleaved strands 7–18. These strands are arranged in duplexes D–E and H–I, which contain cdA lesions located within the cleavage site of BsmAI ( Figure 2 ).

    Article Snippet: BsmAI and SspI Cleavage AssayBsmAI and SspI were purchased from NEB (New England BioLabs, Ipswich, MA, USA).

    Techniques: