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Infinium humanhap550 genotyping chip

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The Infinium HumanHap550 genotyping chip is a lab equipment product developed by Illumina. It is a high-throughput DNA microarray platform designed for genome-wide association studies (GWAS). The chip can interrogate up to 550,000 single nucleotide polymorphisms (SNPs) across the human genome.

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HumanHap550 (58 citations) HumanHap550 chip (9 citations) Infinium HumanHap550 (3 citations) Infinium chips (3 citations) Infinium HumanHap550 chip (2 citations)

4 protocols using infinium humanhap550 genotyping chip

1

FTO Gene SNPs and Obesity Traits

Cited 2 times
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Several SNPs in the FTO gene have been reported to be associated with obesity traits 12 (link)–14 (link). These SNPs are in strong linkage disequilibrium (LD). Of the three SNPs in FTO that were first reported to be associated with obesity (rs1421085, rs17817449, rs9939609) and subsequently replicated in several studies, we focused on rs1421085, an obesity-related FTO SNP that has previously been associated with common mental disorders as well as with brain atrophy in non-demented older individuals 15 (link), 16 (link). In the BLSA, we confirmed that the rs1421085 SNP was in high LD with both rs17817449 LD=0.927) as well as with rs9939609 (LD=0.931). Genome-wide genotyping was performed using the Illumina Infinium HumanHap550 genotyping chip (Illumina, San Diego, California), assaying >555,000 unique SNPs per sample. Standard quality control of genotyping data was conducted including verification of data completeness, Hardy-Weinberg equilibrium, and Mendelian incompatibilities as described previously 17 , 18 (link). We entered the number of obesity-related risk C alleles of rs1421085 (0,1 or 2) assuming additive models. In 15O-water PET analyses where dominant models were used because of small sample size, participants with one or two obesity-related risk C alleles of rs1421085 were classified as FTO+ whereas those with T/T genotype were classified as FTO−.
Chuang Y.F., Tanaka T., Beason-Held L.L., An Y., Terracciano A., Sutin A.R., Kraut M., Singleton A.B., Resnick S.M, & Thambisetty M. (2014). FTO Genotype and Aging: Pleiotropic Longitudinal Effects on Adiposity, Brain function, Impulsivity and Diet. Molecular psychiatry, 20(1), 133-139.
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2

FTO Gene SNPs and Obesity Traits

Cited 2 times
Check if the same lab product or an alternative is used in the 5 most similar protocols
Several SNPs in the FTO gene have been reported to be associated with obesity traits 12 (link)–14 (link). These SNPs are in strong linkage disequilibrium (LD). Of the three SNPs in FTO that were first reported to be associated with obesity (rs1421085, rs17817449, rs9939609) and subsequently replicated in several studies, we focused on rs1421085, an obesity-related FTO SNP that has previously been associated with common mental disorders as well as with brain atrophy in non-demented older individuals 15 (link), 16 (link). In the BLSA, we confirmed that the rs1421085 SNP was in high LD with both rs17817449 LD=0.927) as well as with rs9939609 (LD=0.931). Genome-wide genotyping was performed using the Illumina Infinium HumanHap550 genotyping chip (Illumina, San Diego, California), assaying >555,000 unique SNPs per sample. Standard quality control of genotyping data was conducted including verification of data completeness, Hardy-Weinberg equilibrium, and Mendelian incompatibilities as described previously 17 , 18 (link). We entered the number of obesity-related risk C alleles of rs1421085 (0,1 or 2) assuming additive models. In 15O-water PET analyses where dominant models were used because of small sample size, participants with one or two obesity-related risk C alleles of rs1421085 were classified as FTO+ whereas those with T/T genotype were classified as FTO−.
Chuang Y.F., Tanaka T., Beason-Held L.L., An Y., Terracciano A., Sutin A.R., Kraut M., Singleton A.B., Resnick S.M, & Thambisetty M. (2014). FTO Genotype and Aging: Pleiotropic Longitudinal Effects on Adiposity, Brain function, Impulsivity and Diet. Molecular psychiatry, 20(1), 133-139.
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3

Genome-wide Genotyping and Imputation Protocol

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Genome-wide genotyping was performed using the Illumina Infinium HumanHap550 genotyping chip, which assays over 555,000 unique SNPs per sample. Standard quality control of genotyping data was conducted as described previously [29 (link)]. Briefly, individuals were excluded due to call rate < 95% genome-wide, cryptic relatedness due to proportional sharing (pi_hat) > 0.125 with another participant in the BLSA (effectively excluding first degree relatives), and non-European ancestry ascertained from multi-dimensional scaling analyses using HapMap reference populations. SNPs were excluded due to minor allele frequencies (MAF) < 1%, a missingness rate > 5%, Hardy-Weinberg equilibrium p-values < 1E-5, and non-random missingness by haplotype p-values < 1E-5. All quality control of genotype data was undertaken using PLINKv1.05 [PMID: 17701901]. Using 544892 SNPs that passed QC, imputation of 1000 genome SNPs was conducted using Minimac with integrated 1000G Phase I Integrated Release Version 3 Haplotypes as reference (PMID: 22820512).
Seddighi S., Varma V.R., An Y., Varma S., Beason-Held L.L., Tanaka T., Kitner-Triolo M.H., Kraut M.A., Davatzikos C, & Thambisetty M. (2018). SPARCL1 Accelerates Symptom Onset in Alzheimer’s Disease and Influences Brain Structure and Function During Aging. Journal of Alzheimer's disease : JAD, 61(1), 401-414.
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4

Genotyping APOE and BCHE Variants

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APOE genotypes were determined by two methods in the BLSA. Earlier assays were based on polymerase chain reaction (PCR) amplification of leukocyte DNA with HhaI restriction isotyping [32 (link)]. More recent assays used the TaqMan method, a PCR-based system using oligonucleotide probes specific for alleles that have been labeled using fluorogenic reporter dyes [33 (link)]. We defined two groups based on APOE genotype: APOE ε4 carriers (APOE ε4+) (carriers of 1 or 2 ε4 alleles) and non-carriers (APOE ε4−). On the other hand, the single nucleotide polymorphism of the BCHE gene (rs1803274) was assessed as a part of genome-wide genotyping in BLSA that used the Illumina Infinium HumanHap550 genotyping chip (Illumina, San Diego, CA), assaying > 555,000 unique SNPs per sample. Standard quality control of genotyping data was conducted including verification of data completeness, Hardy-Weinberg equilibrium, and Mendelian incompatibilities as described previously [34 , 35 (link)]. Similar to APOE genotype, we assumed dominant models and two groups of BCHE-K variants were defined: (BCHE-K+) (AA or AG) and non-carriers (BCHE-K-) (GG).
Balsinde J., Barbour S.E., Bianco I.D, & Dennis E.A. (1994). Arachidonic acid mobilization in P388D1 macrophages is controlled by two distinct Ca(2+)-dependent phospholipase A2 enzymes.. Proceedings of the National Academy of Sciences of the United States of America, 91(23), 11060-11064.
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