la pcr genome dna set (TaKaRa)


Name:
LA PCR Genome DNA Set
Description:
The LA PCR Genome DNA Set is designed for use as controls in long range PCR and enables the optimization of PCR conditions for a wide variety of templates The set includes templates that are highly purified high molecular weight genomic DNA from human and E coli and corresponding primers
Catalog Number:
9060
Price:
None
Category:
Long PCR controls Long range PCR PCR
Size:
20 Rxns
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Structured Review

The LA PCR Genome DNA Set is designed for use as controls in long range PCR and enables the optimization of PCR conditions for a wide variety of templates The set includes templates that are highly purified high molecular weight genomic DNA from human and E coli and corresponding primers
https://www.bioz.com/result/la pcr genome dna set/product/TaKaRa
Average 94 stars, based on 1 article reviews
Price from $9.99 to $1999.99
Images
1) Product Images from "Heteroplasmy variability in individuals with biparentally inherited mitochondrial DNA"
Article Title: Heteroplasmy variability in individuals with biparentally inherited mitochondrial DNA
Journal: bioRxiv
doi: 10.1101/2020.02.26.939405

Figure Legend Snippet: Tissue-related variation in heteroplasmy levels for maternal (H1a1) and paternal (R0a1) haplogroups in Patient II-4 of Family A. ( A ) Pedigree of Family A. The black-filled symbols indicate the four family members (II-1, II-3, II-4, and III-6) that show biparental mtDNA transmission. The diagonal-filled symbols indicate the three family members (IV-1, IV-2, and IV-3) who carry a high number and level of mtDNA heteroplasmies which underwent normal maternal transmission. ( B ) Variable heteroplasmy levels detected by PCR-NGS in blood, saliva, hair follicle (HF), urine, sperm, and fibroblast (FB) samples collected from Patient II-4. ( C ) Heteroplasmy drift over time increases the proportion of the paternal haplogroup in primary fibroblast cells derived from Patient II-4. ( D, E ) Single cell-derived DNA samples from Patient II-4 were sequenced to measure cell-to-cell variability in heteroplasmy levels. Sanger sequencing for single-sperm samples ( D ) and PCR-NGS for colonies derived from individual primary fibroblast cells ( E ) show marked differences in heteroplasmy levels, even for cells derived from the same tissue.
Techniques Used: Transmission Assay, Polymerase Chain Reaction, Next-Generation Sequencing, Derivative Assay, Sequencing
2) Product Images from "Spinal muscular atrophy caused by a novel Alu‐mediated deletion of exons 2a‐5 in SMN1 undetectable with routine genetic testing, et al. Spinal muscular atrophy caused by a novel Alu‐mediated deletion of exons 2a‐5 in SMN1 undetectable with routine genetic testing"
Article Title: Spinal muscular atrophy caused by a novel Alu‐mediated deletion of exons 2a‐5 in SMN1 undetectable with routine genetic testing, et al. Spinal muscular atrophy caused by a novel Alu‐mediated deletion of exons 2a‐5 in SMN1 undetectable with routine genetic testing
Journal: Molecular Genetics & Genomic Medicine
doi: 10.1002/mgg3.1238

Figure Legend Snippet: Identification of SMN1 variants. (a) qPCR analysis of four retrotransposon‐free SMN genomic regions in the intron 1 (I1), in the exon 3–intron 3 junction (E3I3), in the intron 5–exon 6 junction (I5E6), and ~1 kb downstream from exon 8 (+1 kb). Compared with four copies of SMN genes that are present in controls, we found that the patient has three copies at the I1, I5E6, and +1 kb loci and two copies at the E3I3 loci. The mother has three copies through the I1 to I5E6 loci and two copies at the +1 kb loci. The father has three copies only at the I5E6 loci. (b) Schematic representation of SMN1/2 exon (E)/intron (I) structure. Positions of sequence differences between SMN1 and SMN2 are represented by black vertical bars. The black triangles denote sequence‐specific variants in exons 7, 8 targeted by MLPA probes in routine testing. Locations of Alus in the breakpoint candidate regions in the intron 1 and 5, including the causal AluSp in the intron 1 and AluSq in the intron 5 indicated by vertical text, and primers binding sites for Alu PCR indicated by black arrowheads are shown below the scheme of the SMN structure. Position of the PCR4 spanning exons 5–8 that showed absence of SMN1 sequence‐specific variants indicating disruption of both SMN1 alleles in the patient is represented by yellow box. Range of the paternal deletion of exons 2a‐5 is represented by red box. (c) DNA sequence trace of the Alu PCR, Alu_259_4A, showing a double sequence caused by presence of AluSq wt in intron 5 together with a sequence originating from the intron 1 AluSp . Red arrows indicate the addition of AluSp ‐specific sequence in an Alu PCR product. (d) PCR genotyping of the SMN1Δ(2a‐5) variant showed presence of the deletion‐spanning amplification product in the patient (P) and father (F), but not in mother (M) and control (C). (e) DNA sequence trace of the breakpoint junction‐specific PCR and detail of the Δ2a‐5 breakpoint junction show the new Alu ‐ Alu chimeric element originating from the recombination between the AluSp in the intron 1 and AluSq in the intron 5. A breakpoint microhomology of the AluSp and AluSq is marked with a black box. (f) Schematic representation of SMN1 and SMN2 in the family members. Pink‐marked boxes represent maternal alleles (M) and blue boxes paternal alleles (F). The red crosses denote identified deletions and the dashed vertical lines denote loci of the qPCR (I1, E3I3, I5E6, and +1 kb) and MLPA (exon 7‐E7, exon 8‐E8) probes used for deletion mapping. The black junctions on the box terminals indicate a cis configuration of SMN1 and SMN2 alleles. The model shows (a) a whole deletion of one SMN1 allele in the patient (P) inherited from her mother and detected by the combination of the qPCR and MLPA; (b) a deletion of the second SMN1 allele in the patient inherited from her father and detected by the E3I3 qPCR and transcript analysis (Figure 1a ); and (c) deletion of one copy of one SMN2 allele in the mother detected by the MLPA and the + 1kb qPCR
Techniques Used: Real-time Polymerase Chain Reaction, Sequencing, Multiplex Ligation-dependent Probe Amplification, Binding Assay, Polymerase Chain Reaction, Variant Assay, Amplification
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