7q11.23 deletions in Williams syndrome arise as a consequence of unequal meiotic crossover.

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.

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.

Who cites it

39 citing papers in PubMed, 139 citations in OpenAlex.

1. DNA shape and epigenomics distinguish the mechanistic origin of human genomic structural variations.Nucleic acids research · 2025
   Article
2. RETRACTED: Retinoic Acid Induced 1 and Smith-Magenis Syndrome: From Genetics to Biology and Possible Therapeutic Strategies.International journal of molecular sciences · 2025
   Review
3. The contribution of GTF2I haploinsufficiency to Williams syndrome.Molecular and cellular probes · 2018
   Review
4. Pronounced maternal parent-of-origin bias for type-1 NF1 microdeletions.Human genetics · 2018
   Article
5. Modeling Williams syndrome with induced pluripotent stem cells.Neurogenesis (Austin, Tex.) · 2017
   Article
6. Children with 7q11.23 duplication syndrome: psychological characteristics.American journal of medical genetics. Part A · 2015
   Article
7. Williams-Beuren Syndrome: A Clinical Study of 55 Brazilian Patients and the Diagnostic Use of MLPA.BioMed research international · 2015
   Article
8. Prenatal phenotype of Williams-Beuren syndrome and of the reciprocal duplication syndrome.Clinical case reports · 2014
   Article
9. Williams syndrome as a model for elucidation of the pathway genes - the brain - cognitive functions: genetics and epigenetics.Acta naturae · 2014
   Article
10. Genetic contributions to visuospatial cognition in Williams syndrome: insights from two contrasting partial deletion patients.Journal of neurodevelopmental disorders · 2014
    Article
11. Enhanced maternal origin of the 22q11.2 deletion in velocardiofacial and DiGeorge syndromes.American journal of human genetics · 2013
    Article
12. Functional characterization of the human mariner transposon Hsmar2.PloS one · 2013
    Article
13. Detection of deletions at 7q11.23 in Williams-Beuren syndrome by polymorphic markers.Clinics (Sao Paulo, Brazil) · 2011
    Article
14. Copy number variants at Williams-Beuren syndrome 7q11.23 region.Human genetics · 2010
    Review
15. Inversion of the Williams syndrome region is a common polymorphism found more frequently in parents of children with Williams syndrome.American journal of medical genetics. Part C, Seminars in medical genetics · 2010
    Article
16. Introduction: Williams syndrome.American journal of medical genetics. Part C, Seminars in medical genetics · 2010
    Article
17. Genome destabilization by homologous recombination in the germ line.Nature reviews. Molecular cell biology · 2010
    Review
18. Pulmonary function and emphysema in Williams-Beuren syndrome.American journal of medical genetics. Part A · 2010
    Article
19. microRNAs and genetic diseases.PathoGenetics · 2009
    Article
20. More than the sum of its parts: new mouse models for dissecting the genetic complexities of Williams-Beuren syndrome.EMBO molecular medicine · 2009
    Article

Corrections and comments

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Authors and funding

8 authors.

Funding

Abstract

PubMed holds no abstract for this paper.

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