Evidence map›Paper›PMID 11590544›Full record

ArticleAmerican journal of human genetics2001

Hermansky-Pudlak syndrome type 3 in Ashkenazi Jews and other non-Puerto Rican patients with hypopigmentation and platelet storage-pool deficiency.

M Huizing, Y Anikster, D L Fitzpatrick, A B Jeong, M D'Souza, M Rausche, J R Toro, M I Kaiser-Kupfer, J G White, W A Gahl

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In one paragraph

Article in American journal of human genetics, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

33 citing papers in PubMed, 90 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Hermansky-Pudlak Syndrome: Identification ofFrontiers in pharmacology · 2021
    Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Hermansky-Pudlak Syndrome.Clinics in chest medicine · 2016
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Newborn screening for hermansky-pudlak syndrome type 3 in Puerto Rico.Journal of pediatric hematology/oncology · 2010
    Article
  17. Hermansky-Pudlak syndrome: the importance of molecular subtyping.Journal of thrombosis and haemostasis : JTH · 2010
    Article
  18. Article
  19. Article
  20. 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

10 authors at 4 institutions in 2 countries.

M HuizingSection on Human Biochemical Genetics, Heritable Disorders Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA.
Y Anikster
D L Fitzpatrick
A B Jeong
M D'Souza
M Rausche
J R Toro
M I Kaiser-Kupfer
J G White
W A Gahl
Health and Human Development (2HD) Research Network · CMNational Eye Institute · USNational Institutes of Health · USUniversity of Minnesota · US

Funding

HUMAN BIOCHEMICAL GENETICSZ01HD000131 · NICHD · CHILD HEALTH AND HUMAN DEVELOPMENT · PI GAHL, WILLIAM ALLEN · 1985 to 2002
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6 · The paper itself

Abstract

Hermansky-Pudlak syndrome (HPS), consisting of oculocutaneous albinism and a bleeding diathesis due to the absence of platelet dense granules, displays extensive locus heterogeneity. HPS1 mutations cause HPS-1 disease, and ADTB3A mutations cause HPS-2 disease, which is known to involve abnormal intracellular vesicle formation. A third HPS-causing gene, HPS3, was recently identified on the basis of homozygosity mapping of a genetic isolate of HPS in central Puerto Rico. We now describe the clinical and molecular characteristics of eight patients with HPS-3 who are of non-Puerto Rican heritage. Five are Ashkenazi Jews; three of these are homozygous for a 1303+1G-->A splice-site mutation that causes skipping of exon 5, deleting an RsaI restriction site and decreasing the amounts of mRNA found on northern blotting. The other two are heterozygous for the 1303+1G-->A mutation and for either an 1831+2T-->G or a 2621-2A-->G splicing mutation. Of 235 anonymous Ashkenazi Jewish DNA samples, one was heterozygous for the 1303+1G-->A mutation. One seven-year-old boy of German/Swiss extraction was compound heterozygous for a 2729+1G-->C mutation, causing skipping of exon 14, and resulting in a C1329T missense (R396W), with decreased mRNA production. A 15-year-old Irish/English boy was heterozygous for an 89-bp insertion between exons 16 and 17 resulting from abnormal splicing; his fibroblast HPS3 mRNA is normal in amount but is increased in size. A 12-year-old girl of Puerto Rican and Italian background has the 3,904-bp founder deletion from central Puerto Rico on one allele. All eight patients have mild symptoms of HPS; two Jewish patients had received the diagnosis of ocular, rather than oculocutaneous, albinism. These findings expand the molecular diagnosis of HPS, provide a screening method for a mutation common among Jews, and suggest that other patients with mild hypopigmentation and decreased vision should be examined for HPS.

Indexed as

Membrane Transport ProteinsAdaptor Protein Complex 3Adaptor Protein Complex beta SubunitsAlbinism, OculocutaneousAlternative SplicingBase SequenceCarrier ProteinsChildDNA Mutational AnalysisExonsFemaleFounder EffectHermanski-Pudlak SyndromeHumansHypopigmentationIntracellular Signaling Peptides and ProteinsAdaptor Protein Complex 3Adaptor Protein Complex beta SubunitsAP3B1 protein, humanCarrier ProteinsHPS1 protein, humanHPS3 protein, humanIntracellular Signaling Peptides and ProteinsMembrane ProteinsMembrane Transport ProteinsProteinsRNA, MessengerRNA Splice Sites

Identifiers

PMID11590544
PMCPMC1274349
OpenAlexW2026654715

What OpenQuestion holds

Textmetadata
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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.