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Infinium coreexome arrays

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Infinium CoreExome arrays are high-density genotyping microarrays designed for comprehensive genome-wide coverage. They provide a cost-effective solution for genome-wide association studies and other large-scale genomic research projects.

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Lab products found in correlation

Genomestudio software, by Illumina (1 mentions)

Close spelling variants of this product

Infinium arrays (12 citations) CoreExome (7 citations) Infinium CoreExome-24 bead arrays (3 citations)

2 protocols using infinium coreexome arrays

1

Whole Genome Sequencing and Genotyping Reprocessing

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Previous to this study, 106 individuals from the cohort had their genomes sequenced to high coverage (TruSeq Nano libraries sequenced on HiSeqX) and 1293 individuals were genotyped using Illumina Infinium CoreExome arrays (v1.0–1.3) [34 (link)]. We reprocessed the 106 whole genomes to obtain joint variant calls as detailed below. For the array data, GRCh37 genotype calls were lifted over to GRCh38, resulting in 471,499 genotyped positions on autosomes which were then further imputed into the 1000 Genomes mapped onto GRCh38 reference panel [49 (link)] using Beagle v5.1 [30 (link)] (beagle.27Apr20.b81.jar).
Emde A.K., Phipps-Green A., Cadzow M., Gallagher C.S., Major T.J., Merriman M.E., Topless R.K., Takei R., Dalbeth N., Murphy R., Stamp L.K., de Zoysa J., Wilcox P.L., Fox K., Wasik K.A., Merriman T.R, & Castel S.E. (2021). Mid-pass whole genome sequencing enables biomedical genetic studies of diverse populations. BMC Genomics, 22, 666.
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2

Genotyping and Fine-Mapping Analysis of CANVAS Disorder

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Genotype calls were generated by the UCL Genomics genotyping facility using Infinium Core Exome arrays (Illumina). Raw data were processed and quality-checked using the GenomeStudio software (Illumina). All individuals passed the 99% call rate threshold and were included in the subsequent analysis using the PLINK 1.9 software48 (link). Uninformative markers or markers with missing genotypes > 10% were removed, and the resulting dataset was further pruned to remove markers in high linkage equilibrium. Finally, the dataset was thinned to include 1-cM-spaced markers covering all autosomes. In total, 3,476 markers were included. For fine-mapping analyses, all available informative markers were included.
Parametric linkage analysis was performed using Merlin49 (link) assuming a highly penetrant recessive model of inheritance and disease allele frequency < 1:10,000 The Merlin software was also used to obtain the most likely haplotypes in the candidate region. All genotyped individuals were included for haplotype analysis.
The rs11096992 and rs2066790 SNPs were genotyped in sporadic CANVAS patients and unaffected individuals using PCR followed by Sanger sequencing. Primers sequences, concentrations, and PCR thermocycling conditions are provided in Supplementary Table 3.
Cortese A., Simone R., Sullivan R., Vandrovcova J., Tariq H., Yau W.Y., Humphrey J., Jaunmuktane Z., Sivakumar P., Polke J., Ilyas M., Tribollet E., Tomaselli P.J., Devigili G., Callegari I., Versino M., Salpietro V., Efthymiou S., Kaski D., Wood N.W., Andrade N.S., Buglo E., Rebelo A., Rossor A.M., Bronstein A., Fratta P., Marques W.J., Züchner S., Reilly M.M, & Houlden H. (2019). Biallelic expansion of an intronic repeat in RFC1 is a common cause of late-onset ataxia. Nature genetics, 51(4), 649-658.
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