Evidence map›Paper›PMID 12587096›Full record

ArticleAmerican journal of human genetics2003

Reciprocal and nonreciprocal recombination at the glucocerebrosidase gene region: implications for complexity in Gaucher disease.

Nahid Tayebi, Barbara K Stubblefield, Joseph K Park, Eduard Orvisky, Jamie M Walker, Mary E LaMarca, Ellen Sidransky

Open access · bronzeAbstract read
In one paragraph

Article in American journal of human genetics, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 9% 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

57 citing papers in PubMed, 1 synthesis or guideline pooled it, 116 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Gene-Pseudogene Inversions as a Hidden Source of Missing Heritability.medRxiv : the preprint server for health sciences · 2025
    Article
  5. Article
  6. Obstacles to Early Diagnosis of Gaucher Disease.Therapeutics and clinical risk management · 2025
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Movement disorders clinical practice · 2022
    Article
  15. Article
  16. Newborn screening for Gaucher disease in Japan.Molecular genetics and metabolism reports · 2022
    Article
  17. Phenotypic Heterogeneity amongBiomedicines · 2022
    Article
  18. Article
  19. Article
  20. Review
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

7 authors at 3 institutions in 1 country.

Nahid TayebiClinical Neuroscience Branch, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892, USA.
Barbara K Stubblefield
Joseph K Park
Eduard Orvisky
Jamie M Walker
Mary E LaMarca
Ellen Sidransky
National Institutes of Health · USNational Human Genome Research Institute · USNational Institute of Mental Health · US

Funding

PHENOTYPIC &GENOTYPIC HETEROGENEITY IN GAUCHER DISEASE &NEUROGENETIC DISORDERSZ01MH002667 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI SIDRANSKY, ELLEN · 1993 to 2005
–
6 · The paper itself

Abstract

Gaucher disease results from an autosomal recessive deficiency of the lysosomal enzyme glucocerebrosidase. The glucocerebrosidase gene is located in a gene-rich region of 1q21 that contains six genes and two pseudogenes within 75 kb. The presence of contiguous, highly homologous pseudogenes for both glucocerebrosidase and metaxin at the locus increases the likelihood of DNA rearrangements in this region. These recombinations can complicate genotyping in patients with Gaucher disease and contribute to the difficulty in interpreting genotype-phenotype correlations in this disorder. In the present study, DNA samples from 240 patients with Gaucher disease were examined using several complementary approaches to identify and characterize recombinant alleles, including direct sequencing, long-template polymerase chain reaction, polymorphic microsatellite repeats, and Southern blots. Among the 480 alleles studied, 59 recombinant alleles were identified, including 34 gene conversions, 18 fusions, and 7 downstream duplications. Twenty-two percent of the patients evaluated had at least one recombinant allele. Twenty-six recombinant alleles were found among 310 alleles from patients with type 1 disease, 18 among 74 alleles from patients with type 2 disease, and 15 among 96 alleles from patients with type 3 disease. Several patients carried two recombinations or mutations on the same allele. Generally, alleles resulting from nonreciprocal recombination (gene conversion) could be distinguished from those arising by reciprocal recombination (crossover and exchange), and the length of the converted sequence was determined. Homozygosity for a recombinant allele was associated with early lethality. Ten different sites of crossover and a shared pentamer motif sequence (CACCA) that could be a hotspot for recombination were identified. These findings contribute to a better understanding of genotype-phenotype relationships in Gaucher disease and may provide insights into the mechanisms of DNA rearrangement in other disorders.

Indexed as

Point MutationRecombination, GeneticSequence DeletionAmino Acid SubstitutionBase SequenceCrossing Over, GeneticDNADNA PrimersFamilyGaucher DiseaseGenes, RecessiveGlucosylceramidaseHumansIntracellular MembranesLysosomesMolecular Sequence DataDNADNA PrimersGlucosylceramidase

Identifiers

PMID12587096
PMCPMC1180228
OpenAlexW2033394945

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.