SureSelect Human All Exon

RUO

The SureSelect Human All Exon V8 provides comprehensive and most up-to-date coverage of protein coding regions from RefSeq, CCDS, and GENCODE. It also covers the TERT promoter and hard-to-capture exons that are omitted by other exomes on the market. Powered by machine learning-based probe design and a new production process, SureSelect Human All Exon V8 spans a 35.1 Mb target region of the human genome with an efficient end-to-end design size of only 41.6 Mb. The panel delivers excellent enrichment performance, as well as efficient, cost-effective exome sequencing. In addition, the panel is manufactured in large scale to provide consistent results for many years.

The SureSelect Human All Exon V8 is compatible with the streamlined SureSelectXT HS2, SureSelectXT HS, SureSelectXT Low Input, and SureSelectQXT library preparation and target enrichment systems, which feature a fast, 90-minute hybridization protocol, as well as the legacy SureSelectXT system. The V8 exome workflow is natively supported by the Bravo Automated Liquid Handling Platform for high-throughput sample preparation, and the Magnis NGS Prep System for complete, walkaway automation. The sequencing data can be analyzed using Alissa Interpret for automated variant interpretation and reporting, providing an efficient and scalable solution to derive insights.

For Research Use Only. Not for use in diagnostic procedures.

Exome

Features

Powered by machine-learning based probe design and manufactured using new production process to produce probes that will last years to provide consistent results.
Excellent coverage uniformity and efficient probe design enable variant calling with high confidence while reducing sequencing costs.
Targets the most up-to-date protein coding regions from RefSeq, GENCODE, and CCDS, including hard-to-capture exons that are omitted from other exomes, and the TERT promoter.
Natively supported by the Bravo Automated Liquiding Handling Platform for high-throughput sample preparation, and the Magnis NGS Prep System for complete, walkaway automation.
Streamlined and optimized variant analysis, interpretation, and reporting via Alissa Reporter and Alissa Interpret, providing an efficient, scalable, and highly secure cloud-based solution to trusted answers.

Specifications


Number of Reactions	16 - 96
Target Region	35.1 Mb

Featured References

Publications

Novel variant p.E269K confirms causative role of PLS1 mutations in autosomal dominant hearing loss. Diaz-Horta et al. Clinical Genetics 2019 Learn More
Dissecting molecular mechanisms of resistance to Notch1-targeted therapy in T-cell acute lymphoblastic leukemia xenografts. Agnusdei et al. Haematologica 2019 Learn More
Single-cell dissection of a rare human prostate basal cell carcinoma. Su et al. bioRxiv 2019 Learn More
Low Abundance of Circulating Tumor DNA in Localized Prostate Cancer. Hennigan et al. JCO Precision Oncology 2019 Learn More
A novel compound heterozygous variant of ECHS1 identified in a Japanese patient with Leigh syndrome. Uchino et al. Human Genome Variation 2019 Learn More
A novel nonsense mutation in ADAMTS17 caused autosomal recessive inheritance Weill–Marchesani syndrome from a Chinese family. Yi et al. Journal of Human Genetics 2019. Learn More
A novel mutation in VRK1 associated with distal spinal muscular atrophy. Li et al. Journal of Human Genetics 2019. Learn More
Novel compound heterozygous variants in the LARP7 gene in a patient with Alazami syndrome. Dateki et al. Human Genome Variation 2018 Learn More
Novel findings with reassessment of exome data: implications for validation testing and interpretation of genomic data. Gibson et al. Genetics in Medicine 2017 Learn More
Mutations in CDCA7 and HELLS cause immunodeficiency–centromeric instability–facial anomalies syndrome. Thijssen et al. Nature Communications 2015 Learn More
Compound heterozygous BRAT1 mutations cause familial Ohtahara syndrome with hypertonia and microcephaly. Saitsu et al. Journal of Human Genetics 2014 Learn More
Mutations in SWI-SNF chromatin remodeling complex gene ARID1B cause Coffin-Siris syndrome. Santen et al. Nature Genetics 2012 Learn More
Mutations affecting components of the SWI-SNF complex cause Coffin-Siris syndrome. Tsurusaki et al. Nature Genetics 2012 Learn More
Exome sequencing of gastric adenocarcinoma identifies recurrent somatic mutations in cell adhesion and chromatin remodeling genes. Zang et al. Nature Genetics 2012 Learn More
Exome sequencing identifies MAX mutations as a cause of hereditary pheochromocytoma.
Comino-Mendez et al. Nature Genetics 2011 Learn More
Exome sequencing identifies ATP4A gene as responsible of an atypical familial type I gastric neuroendocrine tumour. Calvete et al. Human Molecular Genetics 2015 Learn More
Whole-Exome Sequencing Identifies MDH2 as a New Familial Paraganglioma Gene. Carson et al. Journal of the National Cancer Institute 2015 Learn More
Germline mutations in ETV6 are associated with thrombocytopenia, red cell macrocytosis and predisposition to lymphoblastic leukemia. Noetzli et al. Nature Genetics 2015 Learn More
Rare and Coding Region Genetic Variants Associated With Risk of Ischemic Stroke. Auer et al. JAMA Neurology 2015 Learn More
Exome sequencing in amyotrophic lateral sclerosis identifies risk genes and pathways. Circulli et al. Science 2015 Learn More
Multiple rare alleles at LDLR and APOA5 confer risk for earlyonset myocardial infarction. Do et al. Nature 2015 Learn More
Diagnostic Exome Sequencing in Persons with Severe Intellectual Disability. de Ligt et al. New England Journal of Medicine 2012 Learn More
Enhanced utility of family-centered diagnostic exome sequencing with inheritance model–based analysis - results from 500 unselected families with undiagnosed genetic conditions. Farwell et al. Genetics in Medicine 2014 Learn More
Clinical Exome Sequencing for Genetic Identification of Rare Mendelian Disorders. Lee et al. JAMA 2014 Learn More
Genetic diagnosis of developmental disorders in the DDD study - a scalable analysis of genome-wide research data. Wright et al. The Lancet 2015 Learn More

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