Literature DB >> 35637341

From first report to clinical trials: a bibliometric overview and visualization of the development of Angelman syndrome research.

F Isabella Zampeta1,2, Ben Distel1,2,3, Ype Elgersma4,5, Rik Iping6.   

Abstract

Angelman syndrome is a rare neurodevelopmental disorder caused by mutations affecting the chromosomal 15q11-13 region, either by contiguous gene deletions, imprinting defects, uniparental disomy, or mutations in the UBE3A gene itself. Phenotypic abnormalities are driven primarily, but not exclusively (especially in 15q11-13 deletion cases) by loss of expression of the maternally inherited UBE3A gene expression. The disorder was first described in 1965 by the English pediatrician Harry Angelman. Since that first description of three children with Angelman syndrome, there has been extensive research into the genetic, molecular and phenotypic aspects of the disorder. In the last decade, this has resulted in over 100 publications per year. Collectively, this research has led the field to a pivotal point in which restoring UBE3A function by genetic therapies is currently explored in several clinical trials. In this study, we employed a bibliometric approach to review and visualize the development of Angelman syndrome research over the last 50 years. We look into different parameters shaping the progress of the Angelman syndrome research field, including source of funding, publishing journals and international collaborations between research groups. Using a network approach, we map the focus of the research field and how that shifted over time. This overview helps understand the shift of research focus in the field and can provide a comprehensive handbook of Angelman syndrome research development.
© 2022. The Author(s).

Entities:  

Year:  2022        PMID: 35637341     DOI: 10.1007/s00439-022-02460-x

Source DB:  PubMed          Journal:  Hum Genet        ISSN: 0340-6717            Impact factor:   4.132


  17 in total

1.  Induced pluripotent stem cell models of the genomic imprinting disorders Angelman and Prader-Willi syndromes.

Authors:  Stormy J Chamberlain; Pin-Fang Chen; Khong Y Ng; Fany Bourgois-Rocha; Fouad Lemtiri-Chlieh; Eric S Levine; Marc Lalande
Journal:  Proc Natl Acad Sci U S A       Date:  2010-09-27       Impact factor: 11.205

Review 2.  E6AP goes viral: the role of E6AP in viral- and non-viral-related cancers.

Authors:  Ivona Bandilovska; Simon P Keam; Cristina Gamell; Claudia Machicado; Sue Haupt; Ygal Haupt
Journal:  Carcinogenesis       Date:  2019-07-06       Impact factor: 4.944

3.  De novo truncating mutations in E6-AP ubiquitin-protein ligase gene (UBE3A) in Angelman syndrome.

Authors:  T Matsuura; J S Sutcliffe; P Fang; R J Galjaard; Y H Jiang; C S Benton; J M Rommens; A L Beaudet
Journal:  Nat Genet       Date:  1997-01       Impact factor: 38.330

4.  UBE3A/E6-AP mutations cause Angelman syndrome.

Authors:  T Kishino; M Lalande; J Wagstaff
Journal:  Nat Genet       Date:  1997-01       Impact factor: 38.330

Review 5.  A bibliometric overview of craniosynostosis research development.

Authors:  Rik Iping; Adrian M Cohen; Tareq Abdel Alim; Marie-Lise C van Veelen; Jeroen van de Peppel; Johannes P T M van Leeuwen; Koen F M Joosten; Irene M J Mathijssen
Journal:  Eur J Med Genet       Date:  2021-04-16       Impact factor: 2.708

6.  Ube3a-ATS is an atypical RNA polymerase II transcript that represses the paternal expression of Ube3a.

Authors:  Linyan Meng; Richard E Person; Arthur L Beaudet
Journal:  Hum Mol Genet       Date:  2012-04-05       Impact factor: 6.150

7.  Mutation of the Angelman ubiquitin ligase in mice causes increased cytoplasmic p53 and deficits of contextual learning and long-term potentiation.

Authors:  Y H Jiang; D Armstrong; U Albrecht; C M Atkins; J L Noebels; G Eichele; J D Sweatt; A L Beaudet
Journal:  Neuron       Date:  1998-10       Impact factor: 17.173

8.  Cloning and expression of the cDNA for E6-AP, a protein that mediates the interaction of the human papillomavirus E6 oncoprotein with p53.

Authors:  J M Huibregtse; M Scheffner; P M Howley
Journal:  Mol Cell Biol       Date:  1993-02       Impact factor: 4.272

9.  The Angelman syndrome ubiquitin ligase localizes to the synapse and nucleus, and maternal deficiency results in abnormal dendritic spine morphology.

Authors:  Scott V Dindot; Barbara A Antalffy; Meenakshi B Bhattacharjee; Arthur L Beaudet
Journal:  Hum Mol Genet       Date:  2007-10-16       Impact factor: 6.150

Review 10.  Epigenetic regulation of UBE3A and roles in human neurodevelopmental disorders.

Authors:  Janine M LaSalle; Lawrence T Reiter; Stormy J Chamberlain
Journal:  Epigenomics       Date:  2015-11-20       Impact factor: 4.778

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