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About:hqqu

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Huiqi Qu’s research interest is the genetics and functional genomics of human complex diseases (e.g. tuberculosis, obesity, and diabetes). He is working on the genetics and functional genomics of tuberculosis and diabetes. By integrating proteomics, genomics, and GWAS study, they are trying to clarify the molecular mechanisms of tuberculosis susceptibility, and develop genetic markers for diabetes risk prediction.

Posts by hqqu :

  • Deletions of 5′ HOXC genes are associated with lower extremity malformations, including clubfoot and vertical talus, Posted on January 5, 2016 by hqqu in Uncategorized
  • CRISPR-Cas9 for medical genetic screens: applications and future perspectives, Posted on December 16, 2015 by hqqu in Uncategorized
  • Local genotype influences DNA methylation at two asthma-associated regions, 5q31 and 17q21, in a founder effect population, Posted on December 15, 2015 by hqqu in Uncategorized
  • Disruption of Golgi morphology and altered protein glycosylation in PLA2G6-associated neurodegeneration, Posted on December 14, 2015 by hqqu in Uncategorized
  • The Regulatory Element READ1 Epistatically Influences Reading and Language, with both Deleterious and Protective Alleles, Posted on December 12, 2015 by hqqu in Uncategorized
  • Low-level APC mutational mosaicism is the underlying cause in a substantial fraction of unexplained colorectal adenomatous polyposis cases, Posted on November 28, 2015 by hqqu in Uncategorized
  • Intellectual ability in tuberous sclerosis complex correlates with predicted effects of mutations on TSC1 and TSC2 proteins, Posted on November 26, 2015 by hqqu in Uncategorized
  • Homozygous missense mutation in the LMAN2L gene segregates with intellectual disability in a large consanguineous Pakistani family, Posted on November 14, 2015 by hqqu in Uncategorized
  • Congenital hyperinsulinism in children with paternal 11p uniparental isodisomy and Beckwith–Wiedemann syndrome, Posted on November 7, 2015 by hqqu in Uncategorized
  • UNC80 mutation causes a syndrome of hypotonia, severe intellectual disability, dyskinesia and dysmorphism, similar to that caused by mutations in its interacting cation channel NALCN, Posted on November 7, 2015 by hqqu in Uncategorized
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