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@ARTICLE{Heilmann:136914,
      author       = {Heilmann, Stefanie and Kiefer, Amy K and Fricker, Nadine
                      and Drichel, Dmitriy and Hillmer, Axel M and Herold,
                      Christine and Tung, Joyce Y and Eriksson, Nicholas and
                      Redler, Silke and Betz, Regina C and Li, Rui and Kárason,
                      Ari and Nyholt, Dale R and Song, Kijoung and Vermeulen, Sita
                      H and Kanoni, Stavroula and Dedoussis, George and Martin,
                      Nicholas G and Kiemeney, Lambertus A and Mooser, Vincent and
                      Stefansson, Kari and Richards, J Brent and Becker, Tim and
                      Brockschmidt, Felix F and Hinds, David A and Nöthen, Markus
                      M},
      title        = {{A}ndrogenetic alopecia: identification of four genetic
                      risk loci and evidence for the contribution of {WNT}
                      signaling to its etiology.},
      journal      = {The journal of investigative dermatology},
      volume       = {133},
      number       = {6},
      issn         = {0022-202X},
      address      = {Amsterdam},
      publisher    = {Elsevier},
      reportid     = {DZNE-2020-03236},
      pages        = {1489-1496},
      year         = {2013},
      abstract     = {The pathogenesis of androgenetic alopecia (AGA,
                      male-pattern baldness) is driven by androgens, and genetic
                      predisposition is the major prerequisite. Candidate gene and
                      genome-wide association studies have reported that
                      single-nucleotide polymorphisms (SNPs) at eight different
                      genomic loci are associated with AGA development. However, a
                      significant fraction of the overall heritable risk still
                      awaits identification. Furthermore, the understanding of the
                      pathophysiology of AGA is incomplete, and each newly
                      associated locus may provide novel insights into
                      contributing biological pathways. The aim of this study was
                      to identify unknown AGA risk loci by replicating SNPs at the
                      12 genomic loci that showed suggestive association (5 ×
                      10−8<P<10−5) with AGA in a recent meta-analysis. We
                      analyzed a replication set comprising 2,759 cases and 2,661
                      controls of European descent to confirm the association with
                      AGA at these loci. Combined analysis of the replication and
                      the meta-analysis data identified four genome-wide
                      significant risk loci for AGA on chromosomes 2q35, 3q25.1,
                      5q33.3, and 12p12.1. The strongest association signal was
                      obtained for rs7349332 (P=3.55 × 10−15) on chr2q35, which
                      is located intronically in WNT10A. Expression studies in
                      human hair follicle tissue suggest that WNT10A has a
                      functional role in AGA etiology. Thus, our study provides
                      genetic evidence supporting an involvement of WNT signaling
                      in AGA development.},
      keywords     = {Adult / Alopecia: epidemiology / Alopecia: etiology /
                      Alopecia: genetics / Alopecia: metabolism / Cholestanetriol
                      26-Monooxygenase: genetics / Chromosomes, Human, Pair 12 /
                      Chromosomes, Human, Pair 2 / Chromosomes, Human, Pair 3 /
                      Chromosomes, Human, Pair 5 / European Continental Ancestry
                      Group: genetics / European Continental Ancestry Group:
                      statistics $\&$ numerical data / Frizzled Receptors:
                      genetics / Genetic Predisposition to Disease: epidemiology /
                      Genetic Predisposition to Disease: genetics / Genome-Wide
                      Association Study / Humans / Male / Middle Aged /
                      Polymorphism, Single Nucleotide: genetics / Risk Factors /
                      Wnt Proteins: genetics / Wnt Signaling Pathway: physiology /
                      Wnt3 Protein: genetics / FZD10 protein, human (NLM
                      Chemicals) / Frizzled Receptors (NLM Chemicals) / WNT10A
                      protein, human (NLM Chemicals) / WNT3 protein, human (NLM
                      Chemicals) / WNT6 protein, human (NLM Chemicals) / Wnt
                      Proteins (NLM Chemicals) / Wnt3 Protein (NLM Chemicals) /
                      CYP27A1 protein, human (NLM Chemicals) / Cholestanetriol
                      26-Monooxygenase (NLM Chemicals)},
      cin          = {AG Roes / GenomMathematik},
      ddc          = {610},
      cid          = {I:(DE-2719)1610003 / I:(DE-2719)1013007},
      pnm          = {345 - Population Studies and Genetics (POF3-345)},
      pid          = {G:(DE-HGF)POF3-345},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:23358095},
      doi          = {10.1038/jid.2013.43},
      url          = {https://pub.dzne.de/record/136914},
}