Copy Number Variants Are Enriched in Individuals With Early-Onset Obesity and Highlight Novel Pathogenic Pathways
Author(s) -
Maria Pettersson,
Heli Viljakainen,
Petra Loid,
Taina Mustila,
Minna Pekkinen,
Miriam Armenio,
Johanna C. AnderssonAssarsson,
Outi Mäkitie,
Anna Lindstrand
Publication year - 2017
Publication title -
the journal of clinical endocrinology and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.206
H-Index - 353
eISSN - 1945-7197
pISSN - 0021-972X
DOI - 10.1210/jc.2017-00565
Subject(s) - copy number variation , genetics , biology , gene duplication , comparative genomic hybridization , candidate gene , obesity , gene , microarray , phenotype , allele , bioinformatics , gene expression , chromosome , endocrinology , genome
Only a few genetic causes for childhood obesity have been identified to date. Copy number variants (CNVs) are known to contribute to obesity, both syndromic (15q11.2 deletions, Prader-Willi syndrome) and nonsyndromic (16p11.2 deletions) obesity.
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