ArticlePloS one2011
Alternative splicing and nonsense-mediated RNA decay contribute to the regulation of SHOX expression.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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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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.
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Who cites it
24 citing papers in PubMed, 44 citations in OpenAlex.
- Langer mesomelic dysplasia as a rare manifestation ofFrontiers in genetics · 2026Review
- Linking shox/shox2 deficiency with fgfr3 gain-of-function and natriuretic peptides.Frontiers in endocrinology · 2026Article
- A gene desert required for regulatory control of pleiotropic Shox2 expression and embryonic survival.Nature communications · 2024Article
- Expression levels and DNA methylation profiles of the growth gene SHOX in cartilage tissues and chondrocytes.Scientific reports · 2024Article
- Article
- Functional Annotation of MicroRNAs Using Existing Resources.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Identification and Tissue-Specific Characterization of Novel SHOX-Regulated Genes in Zebrafish Highlights SOX Family Members Among Other Genes.Frontiers in genetics · 2021Article
- Short stature andPeerJ · 2020Article
- CFIm25 and alternative polyadenylation: Conflicting roles in cancer.Cancer letters · 2019Review
- Detection of SHOX gene aberrations in routine diagnostic practice and evaluation of phenotype scoring form effectiveness.Journal of human genetics · 2017Article
- The Short-Stature Homeobox-Containing Gene (Frontiers in endocrinology · 2017Article
- A Track Record on SHOX: From Basic Research to Complex Models and Therapy.Endocrine reviews · 2016Review
- SHOX Haploinsufficiency as a Cause of Syndromic and Nonsyndromic Short Stature.Molecular syndromology · 2016Review
- Copy number variants in patients with short stature.European journal of human genetics : EJHG · 2014Article
- Identification of novel SHOX target genes in the developing limb using a transgenic mouse model.PloS one · 2014Article
- Article
- There is a world beyond protein mutations: the role of non-coding RNAs in melanomagenesis.Experimental dermatology · 2013Article
- In-Silico Algorithms for the Screening of Possible microRNA Binding Sites and Their Interactions.Current genomics · 2013Article
- Prevalence of PALB2 mutations in Australasian multiple-case breast cancer families.Breast cancer research : BCR · 2013Article
- Mutually exclusive splicing regulates the Nav 1.6 sodium channel function through a combinatorial mechanism that involves three distinct splicing regulatory elements and their ligands.Nucleic acids research · 2012Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
The human SHOX gene is composed of seven exons and encodes a paired-related homeodomain transcription factor. SHOX mutations or deletions have been associated with different short stature syndromes implying a role in growth and bone formation. During development, SHOX is expressed in a highly specific spatiotemporal expression pattern, the underlying regulatory mechanisms of which remain largely unknown. We have analysed SHOX expression in diverse embryonic, fetal and adult human tissues and detected expression in many tissues that were not known to express SHOX before, e.g. distinct brain regions. By using RT-PCR and comparing the results with RNA-Seq data, we have identified four novel exons (exon 2a, 7-1, 7-2 and 7-3) contributing to different SHOX isoforms, and also established an expression profile for the emerging new SHOX isoforms. Interestingly, we found the exon 7 variants to be exclusively expressed in fetal neural tissues, which could argue for a specific role of these variants during brain development. A bioinformatical analysis of the three novel 3'UTR exons yielded insights into the putative role of the different 3'UTRs as targets for miRNA binding. Functional analysis revealed that inclusion of exon 2a leads to nonsense-mediated RNA decay altering SHOX expression in a tissue and time specific manner. In conclusion, SHOX expression is regulated by different mechanisms and alternative splicing coupled with nonsense-mediated RNA decay constitutes a further component that can be used to fine tune the SHOX expression level.
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Registered trials
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.