Aaron M. Wenger, Ph.D.
Affiliations: | 2012 | Stanford University, Palo Alto, CA |
Area:
Computational BiologyGoogle:
"Aaron Wenger"Mean distance: 19.17 (cluster 17) | S | N | B | C | P |
Parents
Sign in to add mentorGil Bejerano | grad student | 2012 | Stanford | |
(Computational approaches to understanding the language of vertebrate cis-regulation.) |
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Publications
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Vollger MR, Korlach J, Eldred KC, et al. (2023) Synchronized long-read genome, methylome, epigenome, and transcriptome for resolving a Mendelian condition. Biorxiv : the Preprint Server For Biology |
Cheung WA, Johnson AF, Rowell WJ, et al. (2023) Direct haplotype-resolved 5-base HiFi sequencing for genome-wide profiling of hypermethylation outliers in a rare disease cohort. Nature Communications. 14: 3090 |
Wagner J, Olson ND, Harris L, et al. (2022) Benchmarking challenging small variants with linked and long reads. Cell Genomics. 2 |
Mehinovic E, Gray T, Campbell M, et al. (2022) Germline mosaicism of a missense variant in KCNC2 in a multiplex family with autism and epilepsy characterized by long-read sequencing. American Journal of Medical Genetics. Part A |
Wagner J, Olson ND, Harris L, et al. (2022) Curated variation benchmarks for challenging medically relevant autosomal genes. Nature Biotechnology |
Ebert P, Audano PA, Zhu Q, et al. (2021) Haplotype-resolved diverse human genomes and integrated analysis of structural variation. Science (New York, N.Y.) |
Pauper M, Kucuk E, Wenger AM, et al. (2020) Long-read trio sequencing of individuals with unsolved intellectual disability. European Journal of Human Genetics : Ejhg |
Birgmeier J, Haeussler M, Deisseroth CA, et al. (2020) AMELIE speeds Mendelian diagnosis by matching patient phenotype and genotype to primary literature. Science Translational Medicine. 12 |
Berger MJ, Wenger AM, Guturu H, et al. (2018) Independent erosion of conserved transcription factor binding sites points to shared hindlimb, vision and external testes loss in different mammals. Nucleic Acids Research |
Chen HI, Jagadeesh KA, Birgmeier J, et al. (2018) An MTF1 binding site disrupted by a homozygous variant in the promoter of ATP7B likely causes Wilson Disease. European Journal of Human Genetics : Ejhg |