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Humanomniexpress array

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The HumanOmniExpress array is a genome-wide genotyping platform designed for large-scale genetic studies. It interrogates over 700,000 genetic markers across the human genome, providing comprehensive coverage for genome-wide association studies and population genetics research.

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Lab products found in correlation

Abi 7500 real time pcr system, by Thermo Fisher Scientific (1 mentions) Taqman snp genotyping assay, by Thermo Fisher Scientific (1 mentions) Global screening array, by Illumina (1 mentions) Humancoreexome array, by Illumina (1 mentions) Infiniumcoreexome 24 v1 1 beadchip arrays, by Illumina (1 mentions) Genome wide human snp array 6, by Illumina (1 mentions) Infinium humanmethylation450 array, by Illumina (1 mentions) Beadstudio, by Illumina (1 mentions) Infinium global screening array, by Illumina (1 mentions) Human610 quad array, by Illumina (1 mentions) Humanomniexpressexome array, by Illumina (1 mentions) 370k array, by Illumina (1 mentions) Axiom array, by Thermo Fisher Scientific (1 mentions) 7900ht fast real time pcr system, by Thermo Fisher Scientific (1 mentions) Genomestudio, by Illumina (1 mentions) Cytoscan hd array, by Thermo Fisher Scientific (1 mentions) Cytoscan hd, by Thermo Fisher Scientific (1 mentions) Genomestudio software, by Illumina (1 mentions) Genomestudio v2011, by Illumina (1 mentions) Uk bileve axiom, by Thermo Fisher Scientific (1 mentions)

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HumanOmniExpress (97 citations) HumanOmniExpress Exome arrays v1.3 (6 citations) HumanOmniExpress BeadChip array (6 citations) HumanOmniExpress-12 v1_A genotyping arrays (2 citations) HumanOmniExpress-12 v1.1 BeadChip arrays (2 citations) HumanOmniExpress-24 v1.1 arrays (2 citations) HumanOmniExpress‐12v1.1 arrays (2 citations) HumanOmniExpress-12 array (2 citations)

32 protocols using humanomniexpress array

1

COPDGene Genotyping and Quality Control

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COPDGene subjects were of self-reported NHW or African-American ancestry, and genotyped using the HumanOmniExpress array (Illumina) [18 (link)]. Details on the processing of the COPDGene genotype data have been reported [18 (link)]. Briefly, genotyping was performed using the HumanOmniExpress array, and BeadStudio quality control, including reclustering on project samples was performed following Illumina guidelines. Subjects and markers with a call rate of < 95% were excluded. Population stratification exclusion and adjustment on self-reported white subjects was performed using EIGENSTRAT (EIGENSOFT Version 2.0).
Sun W., Kechris K., Jacobson S., Drummond M.B., Hawkins G.A., Yang J., Chen T.H., Quibrera P.M., Anderson W., Barr R.G., Basta P.V., Bleecker E.R., Beaty T., Casaburi R., Castaldi P., Cho M.H., Comellas A., Crapo J.D., Criner G., Demeo D., Christenson S.A., Couper D.J., Curtis J.L., Doerschuk C.M., Freeman C.M., Gouskova N.A., Han M.K., Hanania N.A., Hansel N.N., Hersh C.P., Hoffman E.A., Kaner R.J., Kanner R.E., Kleerup E.C., Lutz S., Martinez F.J., Meyers D.A., Peters S.P., Regan E.A., Rennard S.I., Scholand M.B., Silverman E.K., Woodruff P.G., O’Neal W.K, & Bowler R.P. (2016). Common Genetic Polymorphisms Influence Blood Biomarker Measurements in COPD. PLoS Genetics, 12(8), e1006011.
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2

Genotyping and ANCA Replication in IBD

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A total of 1853 patients with IBD from the Mount Sinai Hospital Cohort in Toronto were genotyped on Illumina HumanOmniExpress array. Average genotyping call rates for samples that passed QC were 99.88%. Thirty-two samples genotyped in replicate and yielded average 99.99% concordance for genotypes called. After similar QC procedures as the discovery cohort, 1834 subjects remain in the cleaned data set, of which 419 had ANCA status available measured in the same laboratory as the discovery cohort. The 419 individuals with consistent ANCA measurements were included in this study as replication cohort.
Li D., Silverberg M.S., Haritunians T., Dubinsky M.C., Landers C., Stempak J.M., Milgrom R., Guo X., Ida Chen Y.D., Rotter J.I., Taylor K.D., McGovern D.P, & Targan S.R. (2016). TNFRSF1B Is Associated with ANCA in IBD. Inflammatory bowel diseases, 22(6), 1346-1352.
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3

Identifying Shared Haplotype Regions

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In order to search for chromosomal segments sharing the same haplotype across affected individuals (within the same family or across different families), the non-parametric HH method18 (link) was used for the analysis of those affected individuals that were genotyped with the Illumina array. The HH is a type of haplotype described by the homozygous SNPs only (all heterozygous SNPs are removed) and, therefore, can be uniquely determined on each chromosome. Since affected family members who inherited the same mutation from a common ancestor share a chromosomal segment IBD around the disease gene, they should not have discordant homozygous calls in the IBD region and thus they should share the same HH. The HH approach predicts IBD regions through the identification of RCHHs defined as those regions with a shared HH among affected individuals and a genetic length longer than a certain cut-off value (recommended cut-off for Illumina HumanOmniExpress array is 2.5/3.0 cM for the analysis of one single family).
Cipriani V., Silva R.S., Arno G., Pontikos N., Kalhoro A., Valeina S., Inashkina I., Audere M., Rutka K., Puech B., Michaelides M., van Heyningen V., Lace B., Webster A.R, & Moore A.T. (2017). Duplication events downstream of IRX1 cause North Carolina macular dystrophy at the MCDR3 locus. Scientific Reports, 7, 7512.
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4

Genotyping and Imputation in Genetic Studies

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Subjects were genotyped using the HumanOmniExpress array (Illumina) employing BeadStudio quality control, which included reclustering on project samples following Illumina guidelines, as previously described for COPDGene. Genotype imputation was performed using the Michigan Imputation Server and the HRC 1.1 reference NHW and the 1000 Genome Phase 1 v3 for AAs.35 (link) Ancestry-based principal components (PCs) were calculated and used as previously described.36 (link),37 (link) Variants were filtered to include only single-nucleotide polymorphisms (SNPs) with minor allele frequencies >1% in the sample population.
Gillenwater L.A., Pratte K.A., Hobbs B.D., Cho M.H., Zhuang Y., Halper-Stromberg E., Cruickshank-Quinn C., Reisdorph N., Petrache I., Labaki W.W., O'Neal W.K., Ortega V.E., Jones D.P., Uppal K., Jacobson S., Michelotti G., Wendt C.H., Kechris K.J, & Bowler R.P. (2020). Plasma Metabolomic Signatures of Chronic Obstructive Pulmonary Disease and the Impact of Genetic Variants on Phenotype-Driven Modules. Network and Systems Medicine, 3(1), 159-181.
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5

Genome-wide genotyping and replication

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Genome-wide genotyping was performed on an Illumina HumanOmniExpress Array. Top associating markers in the discovery phase were genotyped in replication phase using TaqMan® SNP Genotyping Assays (Applied Biosystems, Foster City, CA, USA) and ABI 7500 Real-Time PCR System (Applied Biosystems) (for details, see Supplementary Material: Methods section on Sample processing: Discovery phase and Replication phase).
Hebbar P., Abu-Farha M., Alkayal F., Nizam R., Elkum N., Melhem M., John S.E., Channanath A., Abubaker J., Bennakhi A., Al-Ozairi E., Tuomilehto J., Pitkaniemi J., Alsmadi O., Al-Mulla F, & Thanaraj T.A. (2020). Genome-wide association study identifies novel risk variants from RPS6KA1, CADPS, VARS, and DHX58 for fasting plasma glucose in Arab population. Scientific Reports, 10, 152.
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6

Genetic Variants Associated with T2D and Glucose Homeostasis

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Single nucleotide polymorphisms (SNPs) were selected for analysis with a bias toward variants for T2D and glucose homeostasis traits (e.g., fasting glucose), which have exhibited relatively large effect sizes and which have been widely replicated. This resulted in the selection of 57 variants (23 (link)–27 (link)) for analysis. Based on the a priori evidence of association, this discovery set yields increased power as well as increased probability of detecting effects across ancestries. Genotyping and quality control have been described in detail (22 (link)). Briefly, samples were genotyped on the Illumina HumanOmniExpress array. Samples with call rates >0.98 and SNPs with call rates >0.99 and minor allele frequency >0.001 passed laboratory quality control following usual best practices (e.g., sufficient signal and cluster separation with no replicate errors) (28 (link)). For family-based studies, pedigree structures were confirmed using standard procedures (e.g., Kinship-based INference for Gwas [KING] [http://people.virginia.edu/∼wc9c/KING/index.html]), and SNPs were examined for Mendelian inconsistencies using PedCheck (http://watson.hgen.pitt.edu/register/docs/pedcheck.html).
Palmer N.D., Wagenknecht L.E., Langefeld C.D., Wang N., Buchanan T.A., Xiang A.H., Allayee H., Bergman R.N., Raffel L.J., Chen Y.D., Haritunians T., Fingerlin T., Goodarzi M.O., Taylor K.D., Rotter J.I., Watanabe R.M, & Bowden D.W. (2016). Improved Performance of Dynamic Measures of Insulin Response Over Surrogate Indices to Identify Genetic Contributors of Type 2 Diabetes: The GUARDIAN Consortium. Diabetes, 65(7), 2072-2080.
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7

Genome-Wide Genotyping and Imputation

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Genotyping was performed by Illumina (San Diego, CA) on the HumanOmniExpress Array. Eagle v. 2.3 was used for phasing and HRC reference panel version 1.1 was used for imputation. SNPs with minor allele frequency greater than 0.05 and imputation R2 greater than 0.5 were included in analysis. Details on genotyping QC and imputation have been previously published. [9 (link), 11 (link)].
Saferali A., Yun J.H., Parker M.M., Sakornsakolpat P., Chase R.P., Lamb A., Hobbs B.D., Boezen M.H., Dai X., de Jong K., Beaty T.H., Wei W., Zhou X., Silverman E.K., Cho M.H., Castaldi P.J, & Hersh C.P. (2019). Analysis of genetically driven alternative splicing identifies FBXO38 as a novel COPD susceptibility gene. PLoS Genetics, 15(7), e1008229.
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8

Replication of GWAS Findings in LOGOS

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The remainder ASPIS subsample (N = 738) served as an internal validation sample of GWAS results. The only difference between the discovery and replication subsamples is that the former was selected to have the fewest missing phenotypic data, which we found to correlate with superior performance in most tasks. Additional replication was attempted in the Learning on Genetics of Schizophrenia Spectrum (LOGOS) sample, an independent cohort of healthy young male army conscripts described in detail previously [Roussos P et al., 2011]. The LOGOS acquired the same recruitment procedures as the ASPIS, assessing healthy male conscripts (age range 18–29) at a Greek Army Training Camp (Heraklion, Crete) on several neurocognitive phenotypes that resemble the ones tested in the ASPIS. Available phenotypic scores on sustained attention (RVP; Rapid Visual Information Processing), spatial working memory (SWM) from the Cambridge Neuropsychological Test Automated Battery (CANTAB) and the N‐back task were analyzed. As equivalent to the ASPIS phenotypic assessments, we utilized RVP and N‐back data on the number of correct responses and reaction time. The total number of errors and a measure of strategy were assessed in the SWM test as outcomes. The LOGOS cohort was genotyped on the HumanOmniExpress array (Illumina, San Diego, CA) applying identical QC metrics.
Hatzimanolis A., Bhatnagar P., Moes A., Wang R., Roussos P., Bitsios P., Stefanis C.N., Pulver A.E., Arking D.E., Smyrnis N., Stefanis N.C, & Avramopoulos D. (2015). Common genetic variation and schizophrenia polygenic risk influence neurocognitive performance in young adulthood. American Journal of Medical Genetics, 168(5), 392-401.
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9

Genotyping and Genetic Risk Scores

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Human DNA from MPIP and MARS cohort subjects was extracted from EDTA blood samples and genotyped on Illumina Human610-Quad/Human660W-Quad arrays (MPIP cohort) and Illumina Sentix Human-1/HumanHap300/Human610-Quad/HumanOmniExpress arrays (MARS cohort). From the SNP data surviving QC, imputation of additional variants was performed using IMPUTE v2 (Howie et al., 2009 (link); see Supplemental Experimental Procedures for more detail on genotyping QC and imputation).
The MARS GRPSs included alleles from 20 of the 23 tag eSNPs (three SNPs diverged from HWE in the MARS sample, see Table S3). See also Supplemental Experimental Procedures.
Human DNA from participants of the DNS cohort was isolated from saliva and genotyped on the Illumina HumanOmniExpress array as well as a custom array containing an additional ∼300,000 SNPs. The DNS GRPSs included alleles from 19 of the 23 tag eSNPs (four SNPs not present on genotyping array; see Table S4 and Supplemental Experimental Procedures).
Arloth J., Bogdan R., Weber P., Frishman G., Menke A., Wagner K.V., Balsevich G., Schmidt M.V., Karbalai N., Czamara D., Altmann A., Trümbach D., Wurst W., Mehta D., Uhr M., Klengel T., Erhardt A., Carey C.E., Conley E.D., Ruepp A., Müller-Myhsok B., Hariri A.R, & Binder E.B. (2015). Genetic Differences in the Immediate Transcriptome Response to Stress Predict Risk-Related Brain Function and Psychiatric Disorders. Neuron, 86(5), 1189-1202.
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10

COPD and ECLIPSE Genotyping and Imputation

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In COPDGene, subjects were genotyped on the Illumina Human Omni Express array (San Diego, CA) and in ECLIPSE, the Illumina HumanHap 550 V3 array (San Diego, CA). Genotyping quality control (QC) was performed following previously described guidelines to remove low quality subjects and markers [14 (link)]. Unobserved genotypes were imputed using Michigan Imputation Server with the Haplotype Reference Consortium (HRC) panel [17 (link)].
Kim W., Cho M.H., Sakornsakolpat P., Lynch D.A., Coxson H.O., Tal-Singer R., Silverman E.K, & Beaty T.H. (2019). DSP variants may be associated with longitudinal change in quantitative emphysema. Respiratory Research, 20, 160.
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