Evidence map›Paper›PMID 37327787›Full record

ArticleAmerican journal of human genetics2023

Haplotype-based analysis resolves missing heritability in oculocutaneous albinism type 1B.

Stacie K Loftus, Meredith F Gillis, Linnea Lundh, Laura L Baxter, Julia C Wedel, Dawn E Watkins-Chow, Frank X Donovan, NISC Comparative Sequencing Program, Yuri V Sergeev, William S Oetting and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in American journal of human genetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
4.2field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Human recombinant tyrosinase destabilization caused by the double mutation R217Q/R402Q.Protein science : a publication of the Protein Society · 2025
    Article
  7. Common Variants in theBiomedicines · 2024
    Article
  8. Article
  9. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 1 country.

Stacie K LoftusMedical Genetics Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA; Genetic Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: sloftus@mail.nih.gov.
Meredith F GillisMedical Genetics Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Linnea LundhMedical Genetics Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Laura L BaxterGenetic Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Julia C WedelGenetic Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Dawn E Watkins-ChowGenetic Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Frank X DonovanCancer Genomics Unit, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA.
NISC Comparative Sequencing ProgramNIH Intramural Sequencing Center, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Yuri V SergeevOphthalmic Genetics and Visual Function Branch, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA.
William S OettingDepartment of Experimental and Clinical Pharmacology, University of Minnesota, Minneapolis, MN 55455, USA.
William J PavanGenetic Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA.
David R AdamsOffice of the Clinical Director, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: dadams1@mail.nih.gov.
National Institutes of Health · USUniversity of Minnesota · US

Funding

Inter- and Intra-Species Comparative SequencingZIBHG000196 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI THOMAS, JAMES · 2009 to 2025
$177.6M
Human Biochemical GeneticsZIAHG000215 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI GAHL, WILLIAM · 2009 to 2025
$72.6M
Proteins From Hereditary Eye Diseases: In-silico and Experimental StudiesZIAEY000476 · NEI · NATIONAL EYE INSTITUTE · PI SERGEEV, YURI · 2009 to 2025
$16.8M
NHGRI/DIR Genomics CoreZICHG200346 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI CHANDRASEKHARAPPA, SETTARA · 2010 to 2025
$14.5M
Intramural NIH HHS ZIA EY000476
6 · The paper itself

Abstract

Oculocutaneous albinism (OCA) is a rare disorder of pigment production. Affected individuals have variably decreased global pigmentation and visual-developmental changes that lead to low vision. OCA is notable for significant missing heritability, particularly among individuals with residual pigmentation. Tyrosinase (TYR) is the rate-limiting enzyme in melanin pigment biosynthesis and mutations that decrease enzyme function are one of the most common causes of OCA. We present the analysis of high-depth short-read TYR sequencing data for a cohort of 352 OCA probands, ∼50% of whom were previously sequenced without yielding a definitive diagnostic result. Our analysis identified 66 TYR single-nucleotide variants (SNVs) and small insertion/deletions (indels), 3 structural variants, and a rare haplotype comprised of two common frequency variants (p.Ser192Tyr and p.Arg402Gln) in cis-orientation, present in 149/352 OCA probands. We further describe a detailed analysis of the disease-causing haplotype, p.[Ser192Tyr; Arg402Gln] ("cis-YQ"). Haplotype analysis suggests that the cis-YQ allele arose by recombination and that multiple cis-YQ haplotypes are segregating in OCA-affected individuals and control populations. The cis-YQ allele is the most common disease-causing allele in our cohort, representing 19.1% (57/298) of TYR pathogenic alleles in individuals with type 1 (TYR-associated) OCA. Finally, among the 66 TYR variants, we found several additional alleles defined by a cis-oriented combination of minor, potentially hypomorph-producing alleles at common variant sites plus a second, rare pathogenic variant. Together, these results suggest that identification of phased variants for the full TYR locus are required for an exhaustive assessment for potentially disease-causing alleles.

Indexed as

Albinism, OculocutaneousAllelesHaplotypesHumansMutationalbinismfoveal hypoplasiahaplotypehypopigmentationmissing genetic heritabilityoculocutaneous albinismpigmentationtyrosinase

Identifiers

PMID37327787
PMCPMC10357474
OpenAlexW4380742352

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.