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LGC Genomics GmbH kasp chemistry
Kasp Chemistry, supplied by LGC Genomics GmbH, 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/product/kasp+chemistry/kasp+chemistry/us11884983-624-13-21
Average 90 stars, based on 1 article reviews
kasp chemistry - by Bioz Stars, 2026-09
90/100 stars

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Related Articles

DNA Extraction:

Article Title: Genetic diversity and population structure of fine aroma cacao (Theobroma cacao L.) from north Peru revealed by single nucleotide polymorphism (SNP) markers
Article Snippet: Six leaf discs (6 mm diameter) were prepared from each test plant using the BioArk leaf collection kit from LGC Biosearch Technologies. .. The plates were shipped to LGC Genomics, United Kingdom for DNA extraction and SNP genotyping using their proprietary KASP chemistry. ..

Article Title: Morphological and genetic diversity of cacao ( Theobroma cacao L.) in Uganda
Article Snippet: The discs were stored in a 96-well tube storage rack from LGC’s leaf sampling kit (LGC Genomics, UK) and shipped to LGC Genomics, UK. .. DNA extraction and SNP genotyping using KASP chemistry was performed by LGC Genomics at the 96 SNP sites previously described. .. Selected samples of the reference accessions were also genotyped with the Fluidigm Juno System to verify that both technologies produced comparable SNP calls.

other:

Article Title: Adaptation to milking agropastoralism in Chilean goat herders and nutritional benefit of lactase persistence
Article Snippet: Both sets of SNPs (30 AIMs and the 27 SNPs on chromosome 2) were typed by LGC Genomics (Hoddesdon, UK) using KASP chemistry.

Biomarker Discovery:

Article Title: Association of Single Nucleotide Polymorphisms in KCNA10 and SLC13A3 Genes with the Susceptibility to Chronic Kidney Disease of Unknown Etiology in Central Indian Patients.
Article Snippet: Global rise in the prevalence of endemic chronic kidney disease of unknown etiology (CKDu) possess major health issues.. The prevalence of CKDu is also rising in the Indian population.. Besides environmental factors, genetic factors play an important role in the predisposition to CKDu.

Polymerase Chain Reaction:

Article Title: Sox1a mediates the ability of the parapineal to impart habenular left-right asymmetry
Article Snippet: .. Mutants were genotyped for all further experiments by allelic discrimination via KASP chemistry using PCR primers designed by the manufacturer (LGC Genomics) and the CFX Connect Real-Time PCR Detection system (BIO-RAD) for detection and analysis. .. Whole-mount in situ hybridisation (ISH, FISH) Digoxygenin (Roche) labelled RNA probes were made using standard protocols and spanned a mini- mum of 800 bp.

Article Title: Individual Variance in Human Aggression: A Combined Effect of Polygenic Score and Social/Lifestyle Factors
Article Snippet: To date, the assessment of a simultaneous effect of SNPs on manifesting aggression via polygenic score (PGS) approach has been performed mainly in Western Europeans and is scarce in Russians.. In turn, genes belonging to monoaminergic systems, inflammatory response, hypothalamic-pituitary-adrenal axis, telomerase activity, and miRNA regulation have been previously associated with aggressive behavior or affective pathology.. Therefore, we aimed to estimate a combined effect of PGS based on 30 SNPs belonging to abovementioned systems and social/lifestyle factors on individual differences in BPAQ-measured aggression in young adults from the Volga-Ural region (VUR) of Russia.

Real-time Polymerase Chain Reaction:

Article Title: Sox1a mediates the ability of the parapineal to impart habenular left-right asymmetry
Article Snippet: .. Mutants were genotyped for all further experiments by allelic discrimination via KASP chemistry using PCR primers designed by the manufacturer (LGC Genomics) and the CFX Connect Real-Time PCR Detection system (BIO-RAD) for detection and analysis. .. Whole-mount in situ hybridisation (ISH, FISH) Digoxygenin (Roche) labelled RNA probes were made using standard protocols and spanned a mini- mum of 800 bp.



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(A) Schematic of the in vivo work to produce an F2 cross from Fh LivS1 (a clonal population of susceptible parasites) and Fh LivR1 (a clonal population of resistant parasites). The parental parasites Fh LivS1 and Fh LivR1 were produced separately and used to co-infect sheep (n = 2). Some of these parental parasites would cross-fertilise to produce an F1 cross of Fh LivS1 and Fh LivR1. Eggs were collected from the adult parasites within these sheep. A single miracidium (obtained from these eggs) was used to infect snails (n = 28) and produce clonal F1 populations. The metacercariae were genotyped to ensure they were from an F1 cross and then combined together and used to infect sheep (n = 4). Some of these F1 parasites would cross-fertilise to produce an F2 recombinant population. Eggs were collected from the adult parasites within these sheep. Snails (n = 41 and n = 44 for Experiment 1 and 2, respectively) were exposed to multiple miracidia obtained from these eggs and combined to produce a common pool of F2 metacercariae. For each experiment, two groups of animals were infected with metacercariae from this common pool. Once the infection had reached patency, one group of animals in each experiment was treated with triclabendazole (TCBZ) at a dose of 10mg/kg. At post mortem, those animals which received no treatment had a mixture of triclabendazole susceptible (TCBZ-S) and triclabendazole resistant (TCBZ-R) parasites, whilst those animals that were treated had only TCBZ-R parasites remaining. These parasites were then used for pooled <t>genotyping.</t> (B) A haplotype schematic to show the genetic principle behind the in vivo F2 cross. The F1 cross consists of one haplotype from the susceptible parent: Fh LivS1 ( Fh LivS1.Hap1 or Fh LivS1.Hap2) and one haplotype from the resistant parent: Fh LivR1 ( Fh LivR1.Hap1 or Fh LivR1.Hap2). In the subsequent F2 generation, recombination events take place and the resistant haplotype becomes introgressed amongst the susceptible haplotype producing an F2 recombinant population for study. (C) Plot to show the reduction in the number of F2 parasites recovered from treated animals compared to untreated animals in Experiments 1 and 2. Boxplot indicates the median number of parasites, upper and lower quartiles, and outliers; overlaid points indicate the number of parasites in each animal. In both experiments a significant difference (Mann-Whitney W = 25 p < 0.05) is seen in the number of F2 parasites from untreated and treated animals.
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(A) Schematic of the in vivo work to produce an F2 cross from Fh LivS1 (a clonal population of susceptible parasites) and Fh LivR1 (a clonal population of resistant parasites). The parental parasites Fh LivS1 and Fh LivR1 were produced separately and used to co-infect sheep (n = 2). Some of these parental parasites would cross-fertilise to produce an F1 cross of Fh LivS1 and Fh LivR1. Eggs were collected from the adult parasites within these sheep. A single miracidium (obtained from these eggs) was used to infect snails (n = 28) and produce clonal F1 populations. The metacercariae were genotyped to ensure they were from an F1 cross and then combined together and used to infect sheep (n = 4). Some of these F1 parasites would cross-fertilise to produce an F2 recombinant population. Eggs were collected from the adult parasites within these sheep. Snails (n = 41 and n = 44 for Experiment 1 and 2, respectively) were exposed to multiple miracidia obtained from these eggs and combined to produce a common pool of F2 metacercariae. For each experiment, two groups of animals were infected with metacercariae from this common pool. Once the infection had reached patency, one group of animals in each experiment was treated with triclabendazole (TCBZ) at a dose of 10mg/kg. At post mortem, those animals which received no treatment had a mixture of triclabendazole susceptible (TCBZ-S) and triclabendazole resistant (TCBZ-R) parasites, whilst those animals that were treated had only TCBZ-R parasites remaining. These parasites were then used for pooled <t>genotyping.</t> (B) A haplotype schematic to show the genetic principle behind the in vivo F2 cross. The F1 cross consists of one haplotype from the susceptible parent: Fh LivS1 ( Fh LivS1.Hap1 or Fh LivS1.Hap2) and one haplotype from the resistant parent: Fh LivR1 ( Fh LivR1.Hap1 or Fh LivR1.Hap2). In the subsequent F2 generation, recombination events take place and the resistant haplotype becomes introgressed amongst the susceptible haplotype producing an F2 recombinant population for study. (C) Plot to show the reduction in the number of F2 parasites recovered from treated animals compared to untreated animals in Experiments 1 and 2. Boxplot indicates the median number of parasites, upper and lower quartiles, and outliers; overlaid points indicate the number of parasites in each animal. In both experiments a significant difference (Mann-Whitney W = 25 p < 0.05) is seen in the number of F2 parasites from untreated and treated animals.
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(A) Schematic of the in vivo work to produce an F2 cross from Fh LivS1 (a clonal population of susceptible parasites) and Fh LivR1 (a clonal population of resistant parasites). The parental parasites Fh LivS1 and Fh LivR1 were produced separately and used to co-infect sheep (n = 2). Some of these parental parasites would cross-fertilise to produce an F1 cross of Fh LivS1 and Fh LivR1. Eggs were collected from the adult parasites within these sheep. A single miracidium (obtained from these eggs) was used to infect snails (n = 28) and produce clonal F1 populations. The metacercariae were genotyped to ensure they were from an F1 cross and then combined together and used to infect sheep (n = 4). Some of these F1 parasites would cross-fertilise to produce an F2 recombinant population. Eggs were collected from the adult parasites within these sheep. Snails (n = 41 and n = 44 for Experiment 1 and 2, respectively) were exposed to multiple miracidia obtained from these eggs and combined to produce a common pool of F2 metacercariae. For each experiment, two groups of animals were infected with metacercariae from this common pool. Once the infection had reached patency, one group of animals in each experiment was treated with triclabendazole (TCBZ) at a dose of 10mg/kg. At post mortem, those animals which received no treatment had a mixture of triclabendazole susceptible (TCBZ-S) and triclabendazole resistant (TCBZ-R) parasites, whilst those animals that were treated had only TCBZ-R parasites remaining. These parasites were then used for pooled <t>genotyping.</t> (B) A haplotype schematic to show the genetic principle behind the in vivo F2 cross. The F1 cross consists of one haplotype from the susceptible parent: Fh LivS1 ( Fh LivS1.Hap1 or Fh LivS1.Hap2) and one haplotype from the resistant parent: Fh LivR1 ( Fh LivR1.Hap1 or Fh LivR1.Hap2). In the subsequent F2 generation, recombination events take place and the resistant haplotype becomes introgressed amongst the susceptible haplotype producing an F2 recombinant population for study. (C) Plot to show the reduction in the number of F2 parasites recovered from treated animals compared to untreated animals in Experiments 1 and 2. Boxplot indicates the median number of parasites, upper and lower quartiles, and outliers; overlaid points indicate the number of parasites in each animal. In both experiments a significant difference (Mann-Whitney W = 25 p < 0.05) is seen in the number of F2 parasites from untreated and treated animals.
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(A) Schematic of the in vivo work to produce an F2 cross from Fh LivS1 (a clonal population of susceptible parasites) and Fh LivR1 (a clonal population of resistant parasites). The parental parasites Fh LivS1 and Fh LivR1 were produced separately and used to co-infect sheep (n = 2). Some of these parental parasites would cross-fertilise to produce an F1 cross of Fh LivS1 and Fh LivR1. Eggs were collected from the adult parasites within these sheep. A single miracidium (obtained from these eggs) was used to infect snails (n = 28) and produce clonal F1 populations. The metacercariae were genotyped to ensure they were from an F1 cross and then combined together and used to infect sheep (n = 4). Some of these F1 parasites would cross-fertilise to produce an F2 recombinant population. Eggs were collected from the adult parasites within these sheep. Snails (n = 41 and n = 44 for Experiment 1 and 2, respectively) were exposed to multiple miracidia obtained from these eggs and combined to produce a common pool of F2 metacercariae. For each experiment, two groups of animals were infected with metacercariae from this common pool. Once the infection had reached patency, one group of animals in each experiment was treated with triclabendazole (TCBZ) at a dose of 10mg/kg. At post mortem, those animals which received no treatment had a mixture of triclabendazole susceptible (TCBZ-S) and triclabendazole resistant (TCBZ-R) parasites, whilst those animals that were treated had only TCBZ-R parasites remaining. These parasites were then used for pooled genotyping. (B) A haplotype schematic to show the genetic principle behind the in vivo F2 cross. The F1 cross consists of one haplotype from the susceptible parent: Fh LivS1 ( Fh LivS1.Hap1 or Fh LivS1.Hap2) and one haplotype from the resistant parent: Fh LivR1 ( Fh LivR1.Hap1 or Fh LivR1.Hap2). In the subsequent F2 generation, recombination events take place and the resistant haplotype becomes introgressed amongst the susceptible haplotype producing an F2 recombinant population for study. (C) Plot to show the reduction in the number of F2 parasites recovered from treated animals compared to untreated animals in Experiments 1 and 2. Boxplot indicates the median number of parasites, upper and lower quartiles, and outliers; overlaid points indicate the number of parasites in each animal. In both experiments a significant difference (Mann-Whitney W = 25 p < 0.05) is seen in the number of F2 parasites from untreated and treated animals.

Journal: PLOS Pathogens

Article Title: A major locus confers triclabendazole resistance in Fasciola hepatica and shows dominant inheritance

doi: 10.1371/journal.ppat.1011081

Figure Lengend Snippet: (A) Schematic of the in vivo work to produce an F2 cross from Fh LivS1 (a clonal population of susceptible parasites) and Fh LivR1 (a clonal population of resistant parasites). The parental parasites Fh LivS1 and Fh LivR1 were produced separately and used to co-infect sheep (n = 2). Some of these parental parasites would cross-fertilise to produce an F1 cross of Fh LivS1 and Fh LivR1. Eggs were collected from the adult parasites within these sheep. A single miracidium (obtained from these eggs) was used to infect snails (n = 28) and produce clonal F1 populations. The metacercariae were genotyped to ensure they were from an F1 cross and then combined together and used to infect sheep (n = 4). Some of these F1 parasites would cross-fertilise to produce an F2 recombinant population. Eggs were collected from the adult parasites within these sheep. Snails (n = 41 and n = 44 for Experiment 1 and 2, respectively) were exposed to multiple miracidia obtained from these eggs and combined to produce a common pool of F2 metacercariae. For each experiment, two groups of animals were infected with metacercariae from this common pool. Once the infection had reached patency, one group of animals in each experiment was treated with triclabendazole (TCBZ) at a dose of 10mg/kg. At post mortem, those animals which received no treatment had a mixture of triclabendazole susceptible (TCBZ-S) and triclabendazole resistant (TCBZ-R) parasites, whilst those animals that were treated had only TCBZ-R parasites remaining. These parasites were then used for pooled genotyping. (B) A haplotype schematic to show the genetic principle behind the in vivo F2 cross. The F1 cross consists of one haplotype from the susceptible parent: Fh LivS1 ( Fh LivS1.Hap1 or Fh LivS1.Hap2) and one haplotype from the resistant parent: Fh LivR1 ( Fh LivR1.Hap1 or Fh LivR1.Hap2). In the subsequent F2 generation, recombination events take place and the resistant haplotype becomes introgressed amongst the susceptible haplotype producing an F2 recombinant population for study. (C) Plot to show the reduction in the number of F2 parasites recovered from treated animals compared to untreated animals in Experiments 1 and 2. Boxplot indicates the median number of parasites, upper and lower quartiles, and outliers; overlaid points indicate the number of parasites in each animal. In both experiments a significant difference (Mann-Whitney W = 25 p < 0.05) is seen in the number of F2 parasites from untreated and treated animals.

Article Snippet: Assay design and genotyping was conducted by LGC Genomics (Hertfordshire, UK) using KASP genotyping chemistry.

Techniques: In Vivo, Produced, Recombinant, Infection, MANN-WHITNEY

 Genotyping  of individual F2 parasites to determine inheritance of parental SNP haplotypes.

Journal: PLOS Pathogens

Article Title: A major locus confers triclabendazole resistance in Fasciola hepatica and shows dominant inheritance

doi: 10.1371/journal.ppat.1011081

Figure Lengend Snippet: Genotyping of individual F2 parasites to determine inheritance of parental SNP haplotypes.

Article Snippet: Assay design and genotyping was conducted by LGC Genomics (Hertfordshire, UK) using KASP genotyping chemistry.

Techniques: