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610 quad beadchip

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The 610-Quad BeadChip is a high-throughput genotyping platform developed by Illumina. It is designed to analyze multiple samples simultaneously, enabling efficient and accurate genetic analysis. The device features a quadruple format, allowing for the processing of four samples on a single chip. This lab equipment is intended for researchers and scientists working in the field of genomics and genetic research.

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Lab products found in correlation

Paxgene tm tubes, by Qiagen (2 mentions) Ht12 v4.0 bead arrays, by Illumina (2 mentions) Ht 12 v4.0 chip, by Illumina (2 mentions) Humancoreexome 12 v1.0 beadchip, by Illumina (1 mentions) Humanomni5 quad, by Illumina (1 mentions) Humanomni1 quad, by Illumina (1 mentions) Snp 6.0 array, by Thermo Fisher Scientific (1 mentions) Human660w quad v1 a, by Illumina (1 mentions) Humanomni1 quad v1 0 b beadchip, by Illumina (1 mentions) Genome wide human snp array 6, by Thermo Fisher Scientific (1 mentions)

13 protocols using 610 quad beadchip

1

Robust Genetic Variant Imputation Pipeline

Cited 2 times
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Genotyping was performed with the Illumina 610-Quad BeadChip (n = 1457 individuals) and the HumanCoreExome-12 v1.0 BeadChip (n = 542 individuals), with approximately 700 thousand SNPs passing standard quality control filters, as outlined previously [12 (link)]. These SNPs were then phased using ShapeIT [46 (link)] and imputed using Minimac3 [47 (link)] to extend the genomic coverage to 7,035,128 SNPs using the Haplotype Reference Consortium of Caucasian European ancestry (Release 1) [48 (link)]. Individuals who were > 6 standard deviations from the principal components 1 and 2 (PC1/PC2) centroid were excluded, so our sample was of exclusively European ancestry. To ensure SNPs were imputed with high data quality, we performed post-imputation QC. SNPs with a call rate < 90%, MAF < 0.05, imputation score < 0.3, and Hardy–Weinberg equilibrium score of P < 1.0e-6 were excluded, with a total of 4,381,914 SNPs remaining.
Hwang L.D., Gharahkhani P., Breslin P.A., Gordon S.D., Zhu G., Martin N.G., Reed D.R, & Wright M.J. (2018). Bivariate genome-wide association analysis strengthens the role of bitter receptor clusters on chromosomes 7 and 12 in human bitter taste. BMC Genomics, 19, 678.
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2

Genetic Data Harmonization for Analyses

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ARIC: Genotype data were acquired on the Affymetrix 6.0 SNP array. Quality control steps for the ARIC data set followed the guidelines accompanying the dbGaP release and included removing SNPs with pre-identified chromosomal anomalies and with >5 discordant calls in replicate samples, and used a subset of unrelated subjects identified by the ARIC study. eMERGE: SNP genotype data were acquired on the Illumina Human660W-Quadv1_A. BioVU AF data set: Subjects were genotyped on the Illumina 610-quad Beadchip.14 (link)BioVU VESPA: Subjects were genotyped on the Illumina HumanOmni1-Quad and HumanOmni5-Quad platforms. Quality control steps for the eMERGE and BioVU data sets used established protocols18 (link) including filtering for a sample missingness rate<2.0%, a SNP missingness rate<2.0% and a SNP deviation from Hardy-Weinberg<0.001
All data sets were imputed to the October 2014 release of the 1000 Genomes cosmopolitan reference haplotypes. SNPs were pre-phased using SHAPEIT19 (link) and imputed using IMPUTE2.20 (link). The genetic correlation analyses used an intersection of the unimputed ARIC and imputed eMERGE data set and contained 503,404 SNPs with MAF>1.0%. The BSLMM analyses used an LD-reduced (r-square=0.9) set of SNPs with MAF>1.0% present on all platforms (n= 645,714 SNPs).
Mosley J.D., Shoemaker M.B., Wells Q.S., Darbar D., Shaffer C.M., Edwards T.L., Bastarache L., McCarty C.A., Thompson W., Chute C.G., Jarvik G.P., Crosslin D.R., Larson E.B., Kullo I.J., Pacheco J.A., Peissig P.L., Brilliant M.H., Linneman J.G., Witte J.S., Denny J.C, & Roden D.M. (2017). Investigating the Genetic Architecture of the PR Interval using Clinical Phenotypes. Circulation. Cardiovascular genetics, 10(2), e001482.
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3

Vitiligo and SLE Genetics Analysis

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Vitiligo patients and SLE patients were recruited according to the criteria of vitiligo European Task Force (20 (link)) and systemic lupus international collaborating clinics 2012 revision, respectively. Cases were diagnosed by at least two experts. The controls were recruited as individuals who did not have histories of autoimmune or systemic disorders. Cases and controls were age and geographic region matching. SNP genotyping data were obtained from our previously published paper, as performed using an Illumina 610-Quad Bead Chip (21 (link), 22 (link)). In the present study, which included 1117 vitiligo cases, 1046 SLE cases and 1693 healthy controls, written informed consent was obtained from all participants. Quality control of samples and sites was carried out according to a procedure detailed previously (7 (link)).
Cao L., Zhang R., Wang Y., Hu X., Yong L., Li B., Ge H., Chen W., Zhen Q., Yu Y., Mao Y., Li Z., Fan W, & Sun L. (2022). Fine Mapping Analysis of the MHC Region to Identify Variants Associated With Chinese Vitiligo and SLE and Association Across These Diseases. Frontiers in Immunology, 12, 758652.
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4

Brisbane Systems Genetics Study

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The Brisbane Systems Genetics Study (BSGS) comprises 846 individuals of European descent from 274 independent families23 (link). DNA samples from each individual were genotyped on the Illumina 610-Quad Beadchip by the Scientific Services Division at deCODE Genetics Iceland. Full details of genotyping procedures are given in Medland et al.31 (link) Standard quality control (QC) filters were applied and the remaining 528,509 autosomal SNPs were carried forward for further analysis.
Gene expression profiles were generated from peripheral blood collected with PAXgene TM tubes (QIAGEN, Valencia, CA) using Illumina HT12-v4.0 bead arrays. The Illumina HT-12 v4.0 chip contains 47,323 probes, although some probes are not assigned to RefSeq genes. We removed any probes that did not match the following criteria: contained a SNP within the probe sequence with MAF > 0.05 within 1000 genomes data; did not map to a listed RefSeq gene; were not significantly expressed (based on a detection p-value < 0.05) in at least 90% of samples. After this stringent QC 7339 probes remained for 2D-eQTL mapping. These data are accessible through GEO Series accession number GSE53195.
Hemani G., Shakhbazov K., Westra H.J., Esko T., Henders A.K., McRae A.F., Yang J., Gibson G., Martin N.G., Metspalu A., Franke L., Montgomery G.W., Visscher P.M, & Powell J.E. (2014). Detection and replication of epistasis influencing transcription in humans. Nature, 508(7495), 249-253.
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5

Genome-wide Association of T-cell Traits

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Using summary genome-wide association results of T-cell levels (CD3+, CD4+, and CD8+) and of derived CD4/CD8 ratio, as conducted in ref. 22 (link), polygenic scores were constructed. In brief: GWA analyses of T-lymphocyte subsets in peripheral blood were performed using a gene discovery set of 2,538 adolescent twins from 1,089 Australian families sampled from the general population, whose DNA was genotyped with Illumina 610-Quad BeadChip (529,721 SNPs). The genotype data set was then extended by imputation to 2.3 million SNPs using data from the CEU HapMap samples (phase I+II, release 22, build 36) and MACH software31 . Analyses of T-lymphocyte subsets were performed with AutoPrep (coulter) and direct fluorochromome-conjugated monoclonal antibodies to CD3, CD4, and CD8 antigens (Coulter). Subsequent analyses were performed on an Epics 753 cytofluorograph (Coulter) with the use of standardized control samples and machine settings. The CD4/CD8 ratio was calculated from the relative levels of CD4+ and CD8+ T-cells measured by flow-cytometry. GWA analyses were conducted on each T-lymphocyte subset and derived CD4/CD8 ratio, and were adjusted for age and sex and normalized with an inverse-normal transformation. Further details of the study are available elsewhere (22).
Rivera N.V., Hagemann-Jensen M., Ferreira M.A., Kullberg S., Eklund A., Martin N.G., Padyukov L, & Grunewald J. (2017). Common variants of T-cells contribute differently to phenotypic variation in sarcoidosis. Scientific Reports, 7, 5623.
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6

MTHFR C677T Variant Frequencies in ADNI

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The ADNI sample was genotyped using the Illumina 610-Quad BeadChip (San Diego, CA, USA). The only polymorphism examined in this study was the C677T functional variant in the methylene-tetrahydrofolate reductase (MTHFR) gene, at the rs1801133 locus. Allele frequency was computed from genotype frequency. The distributions of allele frequencies by diagnostic groups were evaluated by χ2 tests with a 0.05 significance level, using 3 × 2 and 2 × 2 contingency tables in SPSS 23.0.
Roussotte F.F., Hua X., Narr K.L., Small G.W, & Thompson P.M. (2017). The C677T variant in MTHFR modulates associations between brain integrity, mood, and cognitive functioning in old age. Biological psychiatry : cognitive neuroscience and neuroimaging, 2(3), 280-288.
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7

Genetic Imputation and Analysis of PD Risk

Cited 3 times
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The UDALL data set was genotyped using Illumina 610-quad BeadChip (Illumina, San Diego, CA).25 (link) The NGRC data set was genotyped using Illumina HumanOmni1-Quad_v1-0_B BeadChip (Illumina).26 (link) Final marker sets after quality control (described in detail in these previous publications) were used for the imputation of untyped SNPs separately in each of the 2 data sets. Imputation allowed us to obtain genetic information on additional variants through the genome for a more thorough investigation. Both data sets were imputed up to 38 million SNPs using IMPUTE2 and the 1000 Genomes reference panel (phase 1, March 2012).27 (link) During quality control, SNPs that had low imputation quality (info score <0.4) and low minor allele frequency (less than 1%) were removed from further analysis. SNPs within the 5-kb flanking regions of the start and end of CACNA1C and CACNA1D were examined for interaction with vitamin D status and association with PD.
Wang L., Maldonado L., Beecham G.W., Martin E.R., Evatt M.L., Ritchie J.C., Haines J.L., Zabetian C.P., Payami H., Pericak-Vance M.A., Vance J.M, & Scott W.K. (2016). DNA variants in CACNA1C modify Parkinson disease risk only when vitamin D level is deficient. Neurology: Genetics, 2(3), e72.
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8

Genome-wide Genotyping on Illumina 610-Quad

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All individuals were genotyped on an Illumina 610-Quad Beadchip (Illumina Inc, San Diego, CA) by the Scientific Services Division at deCODE Genetics, Iceland. Full details of the genotyping procedure are given in [37 (link)].
Goldinger A., Shakhbazov K., Henders A.K., McRae A.F., Montgomery G.W, & Powell J.E. (2015). Seasonal Effects on Gene Expression. PLoS ONE, 10(5), e0126995.
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9

Illumina Genotyping for Case-Control Study

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All genotyping for both cases and controls was performed on the Illumina 610-Quad BeadChip (Illumina, Inc., San Diego, CA, USA) by the Genomic Analysis Facility at Duke University. As described previously, cases and controls were genotyped separately. Thus, to allow detection of potential batch effects, 29 of the original CABG control samples were re-genotyped with the S. aureus case samples. These control sample replicates were randomly assigned across all genotyping plates. Additionally, each S. aureus plate included 2 case interplate replicate samples and 2 case intraplate replicate samples. All of the expected sample replicate pairs showed greater than 0.99 genotype concordance. One unique copy of each replicated sample was included in the analysis, preferentially retaining the sample with the higher genotyping call rate.
Nelson C.L., Pelak K., Podgoreanu M.V., Ahn S.H., Scott W.K., Allen A.S., Cowell L.G., Rude T.H., Zhang Y., Tong A., Ruffin F., Sharma-Kuinkel B.K, & Fowler, VG J.r. (2014). A genome-wide association study of variants associated with acquisition of Staphylococcus aureus bacteremia in a healthcare setting. BMC Infectious Diseases, 14, 83.
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10

Cognitive Assessments and Genotyping in Participants

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All subjects completed detailed cognitive assessments including the Mini-Mental State Examination (MMSE) [14 (link)]. Participants were genotyped using the Illumina 610-Quad BeadChip. ApoE genotyping was performed separately, using an ApoE genotyping kit, as described in http://www.adni-info.org/Scientists/Pdfs/adniproceduresmanual12.pdf.
Roussotte F.F., Gutman B.A., Hibar D.P., Madsen S.K., Narr K.L, & Thompson P.M. (2014). Carriers of a common variant in the dopamine transporter gene have greater dementia risk, cognitive decline, and faster ventricular expansion. Alzheimer's & dementia : the journal of the Alzheimer's Association, 11(10), 1153-1162.
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