ArticleBMC genetics2001
A necdin/MAGE-like gene in the chromosome 15 autism susceptibility region: expression, imprinting, and mapping of the human and mouse orthologues.
Article in BMC genetics, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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.
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Who cites it
19 citing papers in PubMed, 33 citations in OpenAlex.
- UBE3A: The Role in Autism Spectrum Disorders (ASDs) and a Potential Candidate for Biomarker Studies and Designing Therapeutic Strategies.Diseases (Basel, Switzerland) · 2023Review
- Tumor suppressor p53 modulates activity-dependent synapse strengthening, autism-like behavior and hippocampus-dependent learning.Molecular psychiatry · 2023Article
- Necdin: A purposive integrator of molecular interaction networks for mammalian neuron vitality.Genes to cells : devoted to molecular & cellular mechanisms · 2021Review
- Deubiquitylases in developmental ubiquitin signaling and congenital diseases.Cell death and differentiation · 2021Review
- Emerging roles of the MAGE protein family in stress response pathways.The Journal of biological chemistry · 2020Review
- Downregulation of Brain Enriched Type 2 MAGEs Is Associated With Immune Infiltration and Poor Prognosis in Glioma.Frontiers in oncology · 2020Article
- Cellular and disease functions of the Prader-Willi Syndrome geneThe Biochemical journal · 2017Review
- A Comprehensive Guide to the MAGE Family of Ubiquitin Ligases.Journal of molecular biology · 2017Review
- Identification of Novel MAGE-G1-Interacting Partners in Retinoic Acid-Induced P19 Neuronal Differentiation Using SILAC-Based Proteomics.Scientific reports · 2017Article
- Destabilized SMC5/6 complex leads to chromosome breakage syndrome with severe lung disease.The Journal of clinical investigation · 2016Article
- Article
- Absence of substantial copy number differences in a pair of monozygotic twins discordant for features of autism spectrum disorder.Case reports in genetics · 2014Article
- Relative expression of type II MAGE genes during retinoic acid-induced neural differentiation of mouse embryonic carcinoma P19 cells: a comparative real-time PCR analysis.Cellular and molecular neurobiology · 2012Article
- Necdin modulates proliferative cell survival of human cells in response to radiation-induced genotoxic stress.BMC cancer · 2012Article
- Deletions flanked by breakpoints 3 and 4 on 15q13 may contribute to abnormal phenotypes.European journal of human genetics : EJHG · 2011Article
- Describing the hexapeptide identity platform between the influenza A H5N1 and Homo sapiens proteomes.Biologics : targets & therapy · 2010Article
- The comorbidity of autism with the genomic disorders of chromosome 15q11.2-q13.Neurobiology of disease · 2010Review
- EBNA3C can modulate the activities of the transcription factor Necdin in association with metastasis suppressor protein Nm23-H1.Journal of virology · 2009Article
- Identification of the proteins, including MAGEG1, that make up the human SMC5-6 protein complex.Molecular and cellular biology · 2008Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundProximal chromosome 15q is implicated in neurodevelopmental disorders including Prader-Willi and Angelman syndromes, autistic disorder and developmental abnormalities resulting from chromosomal deletions or duplications. A subset of genes in this region are subject to genomic imprinting, the expression of the gene from only one parental allele.
resultsWe have now identified the NDNL2 (also known as MAGE-G) gene within the 15q autistic disorder susceptibility region and have mapped its murine homolog to the region of conserved synteny near necdin (Ndn) on mouse Chr 7. NDNL2/MAGE-G is a member of a large gene family that includes the X-linked MAGE cluster, MAGED1 (NRAGE), MAGEL2 and NDN, where the latter two genes are implicated in Prader-Willi syndrome. We have now determined that NDNL2/Ndnl2 is widely expressed in mouse and human fetal and adult tissues, and that it is apparently not subject to genomic imprinting by the PWS/AS Imprinting Center.
conclusionAlthough NDNL2/MAGE-G in the broadly defined chromosome 15 autistic disorder susceptibility region, it is not likely to be pathogenic based on its wide expression pattern and lack of imprinted expression.
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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.