Connection

Co-Authors

This is a "connection" page, showing publications co-authored by JENNIFER POSEY and CHRISTINE ENG.
Connection Strength

0.859
  1. Resolution of Disease Phenotypes Resulting from Multilocus Genomic Variation. N Engl J Med. 2017 01 05; 376(1):21-31.
    View in: PubMed
    Score: 0.144
  2. Molecular diagnostic experience of whole-exome sequencing in adult patients. Genet Med. 2016 07; 18(7):678-85.
    View in: PubMed
    Score: 0.134
  3. Retrospective analysis of a clinical exome sequencing cohort reveals the mutational spectrum and identifies candidate disease-associated loci for BAFopathies. Genet Med. 2022 02; 24(2):364-373.
    View in: PubMed
    Score: 0.051
  4. Heterozygous variants in SPTBN1 cause intellectual disability and autism. Am J Med Genet A. 2021 07; 185(7):2037-2045.
    View in: PubMed
    Score: 0.049
  5. Low-level parental somatic mosaic SNVs in exomes from a large cohort of trios with diverse suspected Mendelian conditions. Genet Med. 2020 11; 22(11):1768-1776.
    View in: PubMed
    Score: 0.046
  6. A Genocentric Approach to Discovery of Mendelian Disorders. Am J Hum Genet. 2019 11 07; 105(5):974-986.
    View in: PubMed
    Score: 0.044
  7. Reanalysis of Clinical Exome Sequencing Data. N Engl J Med. 2019 06 20; 380(25):2478-2480.
    View in: PubMed
    Score: 0.043
  8. Copy number variant and runs of homozygosity detection by microarrays enabled more precise molecular diagnoses in 11,020 clinical exome cases. Genome Med. 2019 05 17; 11(1):30.
    View in: PubMed
    Score: 0.043
  9. Correction to: De novo and inherited TCF20 pathogenic variants are associated with intellectual disability, dysmorphic features, hypotonia, and neurological impairments with similarities to Smith-Magenis syndrome. Genome Med. 2019 03 25; 11(1):16.
    View in: PubMed
    Score: 0.042
  10. De novo and inherited TCF20 pathogenic variants are associated with intellectual disability, dysmorphic features, hypotonia, and neurological impairments with similarities to Smith-Magenis syndrome. Genome Med. 2019 02 28; 11(1):12.
    View in: PubMed
    Score: 0.042
  11. Phenotypic expansion in DDX3X - a common cause of intellectual disability in females. Ann Clin Transl Neurol. 2018 Oct; 5(10):1277-1285.
    View in: PubMed
    Score: 0.041
  12. Clinical exome sequencing reveals locus heterogeneity and phenotypic variability of cohesinopathies. Genet Med. 2019 03; 21(3):663-675.
    View in: PubMed
    Score: 0.041
  13. Lessons learned from additional research analyses of unsolved clinical exome cases. Genome Med. 2017 03 21; 9(1):26.
    View in: PubMed
    Score: 0.037
  14. Recurrent De Novo and Biallelic Variation of ATAD3A, Encoding a Mitochondrial Membrane Protein, Results in Distinct Neurological Syndromes. Am J Hum Genet. 2016 Oct 06; 99(4):831-845.
    View in: PubMed
    Score: 0.035
  15. A visual and curatorial approach to clinical variant prioritization and disease gene discovery in genome-wide diagnostics. Genome Med. 2016 Feb 02; 8(1):13.
    View in: PubMed
    Score: 0.034
  16. POGZ truncating alleles cause syndromic intellectual disability. Genome Med. 2016 Jan 06; 8(1):3.
    View in: PubMed
    Score: 0.034
Connection Strength

The connection strength for concepts is the sum of the scores for each matching publication.

Publication scores are based on many factors, including how long ago they were written and whether the person is a first or senior author.