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Nonsense Codon (Nonsense Mutation)

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An amino acid-specifying codon that has been converted to a stop codon (CODON, TERMINATOR) by mutation. Its occurance is abnormal causing premature termination of protein translation and results in production of truncated and non-functional proteins. A nonsense mutation is one that converts an amino acid-specific codon to a stop codon.

Also Known As:

Nonsense Mutation; Nonsense Mutations; Premature Stop Codon; Unassigned Codon; Codon, Nonsense; Amber Nonsense Codon; Amber Nonsense Mutation; Nonsense Codon, Amber; Ochre Nonsense Codon; Ochre Nonsense Mutation; Opal Nonsense Codon; Opal Nonsense Mutation; Premature Termination Codon; Amber Nonsense Codons; Amber Nonsense Mutations; Codon, Amber Nonsense; Codon, Ochre Nonsense; Codon, Opal Nonsense; Codon, Premature Stop; Codon, Premature Termination; Codons, Amber Nonsense; Codons, Nonsense; Codons, Ochre Nonsense; Codons, Opal Nonsense; Codons, Premature Stop; Codons, Premature Termination; Codons, Unassigned; Mutation, Amber Nonsense; Mutation, Ochre Nonsense; Mutation, Opal Nonsense; Mutations, Amber Nonsense; Mutations, Nonsense; Mutations, Ochre Nonsense; Mutations, Opal Nonsense; Nonsense Codon, Ochre; Nonsense Codon, Opal; Nonsense Codons; Nonsense Codons, Amber; Nonsense Codons, Ochre; Nonsense Codons, Opal; Nonsense Mutation, Amber; Nonsense Mutation, Ochre; Nonsense Mutation, Opal; Nonsense Mutations, Amber; Nonsense Mutations, Ochre; Nonsense Mutations, Opal; Ochre Nonsense Codons; Ochre Nonsense Mutations; Opal Nonsense Codons; Opal Nonsense Mutations; Premature Stop Codons; Premature Termination Codons; Stop Codon, Premature; Stop Codons, Premature; Termination Codon, Premature; Termination Codons, Premature; Unassigned Codons; Codon, Termination, Premature; Codon, Unassigned; Mutation, Nonsense

Networked: 1644 relevant articles (12 outcomes, 70 trials/studies)

Relationship Network

Bio-Agent Context: Research Results

Experts

1.	Nürnberg, Gudrun: 8 articles (02/2014 - 03/2008)
2.	Nürnberg, Peter: 8 articles (02/2014 - 03/2008)
3.	Matsuo, Masafumi: 8 articles (06/2012 - 03/2004)
4.	Takeshima, Yasuhiro: 7 articles (06/2012 - 03/2004)
5.	Najmabadi, Hossein: 6 articles (03/2015 - 02/2007)
6.	Rouleau, Guy A: 6 articles (01/2015 - 11/2010)
7.	Baasov, Timor: 6 articles (04/2014 - 05/2009)
8.	Zeviani, Massimo: 5 articles (07/2015 - 03/2007)
9.	Moore, Anthony T: 5 articles (04/2015 - 01/2009)
10.	Elfring, Gary L: 5 articles (10/2014 - 04/2007)

Related Diseases

1.	Infection 01/01/2009 - "The G428A nonsense mutation in FUT2 provides strong but not absolute protection against symptomatic GII.4 Norovirus infection." 08/01/2007 - "A strong correlation (P = 0.003) was found between the secretor phenotype and symptomatic disease, extending previous knowledge and confirming that nonsense mutations in the FUT2 gene provide protection against symptomatic norovirus (GGII.4) infections." 07/01/2014 - "The present report is the first to describe norovirus GI.6 infection in patients with the G428A nonsense mutation in FUT2; this cluster of cases suggests that the G428A mutation in FUT2 may not confer resistance to norovirus GI.6. Direct-to-consumer genetic testing is empowering members of the public to identify novel associations with their genetic traits. " 07/01/2014 - "Immunodeficiency and disseminated mycobacterial infection associated with homozygous nonsense mutation of IKKβ." 11/01/2012 - "Resting CD4(+) T cells from healthy donors following SAMHD1 silencing or from a patient with Aicardi-Goutières syndrome homozygous for a nonsense mutation in SAMHD1 were permissive for HIV-1 infection. "
2.	Heart Failure 08/01/2004 - "Two new mutations leading to premature stop codons were identified in patients who evolved towards severe heart failure (< 25 years old): 657C>T and 173_179del. " 05/27/2004 - "We tested the hypothesis that possession of the C34T nonsense mutation in AMPD1 gene, which is known to improve survival in chronic heart failure, protects against cardiac dysfunction in donors. " 06/01/2014 - "One patient, heterozygous for a PKP2 nonsense mutation, developed severe heart failure and underwent cardiac transplantation. " 01/01/2005 - "Possession of the nonsense mutation in AMPD 1 C34T gene has been linked to improved survival in patients with heart failure, possibly by promoting the formation of adenosine. " 09/01/2003 - "Possession of the C34T (Glu12Stop) nonsense mutation in the AMP-deaminase 1 (AMPD1) gene has been shown to be associated with improved prognosis in heart failure and ischemic heart disease. "
3.	Cystic Fibrosis (Mucoviscidosis) 11/01/2010 - "This article summarizes our current knowledge of mutation-specific therapy, and focuses on orally bioavailable potentiators and correctors and suppressors of premature termination codons, including preclinical model systems and clinical trials in cystic fibrosis." 08/30/2008 - "This phase II prospective trial recruited adults with cystic fibrosis who had at least one nonsense mutation in the CFTR gene. " 03/03/2014 - "A well-known example of these diseases is cystic fibrosis (CF), where approximately 10% (worldwide) of patients have nonsense mutations in the CF transmembrane regulator (CFTR) gene. " 03/01/2014 - "We describe the presentation of a Hispanic adolescent with chronic respiratory symptoms and poor growth that led to a diagnosis of cystic fibrosis (CF) based on an indeterminate sweat chloride result and DNA sequence analysis that revealed a single new frameshift mutation, Nt3878insATCAG, which results in a premature stop codon in exon 20 of the CFTR gene. " 07/01/2007 - "Cystic fibrosis (CF) is an autosomal recessive disorder caused by many types of genetic defects, including premature stop codons. "
4.	Neoplasms (Cancer) 01/01/2006 - "The detection of Premature Stop Codons (PSCs) in human genes is very useful for the genetic diagnosis of different hereditary cancers, e.g. " 11/01/2015 - "Notably, SNVs causing intron retention were enriched in tumor suppressors, and 97% of these SNVs generated a premature termination codon, leading to loss of function through nonsense-mediated decay or truncated protein. " 09/01/2015 - "Of particular note, the infiltrative BCCs showed a nonsense mutation, c.943C>T, resulting in p.Q315X in the large tumor suppressor 1 (LATS1) gene, as well as the loss of the wild-type allele of LATS1 (6q25.1), thus indicating that the LATS1 gene was biallelically disrupted. " 03/01/2015 - "Importantly, a homozygous nonsense mutation of WWOX gene in humans leads to neural pathologies and early death, rather than spontaneous cancer development. " 01/01/2015 - "Targeted sequencing of the primary tumor revealed deletions of CDKN2A and CDKN2B, a nonsense mutation in ARID2, and single missense mutations of unknown significance in nine other genes. "
5.	Muscular Dystrophies (Muscular Dystrophy) 08/01/1999 - "Furthermore, these results raise the possibility of a novel treatment regimen for muscular dystrophy and other diseases caused by premature stop codon mutations. " 04/01/2014 - "A novel missense mutation in POMT1 modulates the severe congenital muscular dystrophy phenotype associated with POMT1 nonsense mutations." 01/01/2009 - "By-passing the nonsense mutation in the 4 CV mouse model of muscular dystrophy by induced exon skipping." 04/01/2001 - "Mild muscular dystrophy due to a nonsense mutation in the LAMA2 gene resulting in exon skipping." 11/01/2004 - "[Possible chemotherapy of muscular dystrophy caused by nonsense mutation]."

Related Drugs and Biologics

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2.	Messenger RNA (mRNA)
3.	RNA (Ribonucleic Acid)
4.	Protein Sorting Signals (Signal Peptide)
5.	Adenosine
6.	Incretins
7.	Tobramycin (Nebcin)
8.	Glyburide (Glibenclamide)
9.	AMP Deaminase (Myoadenylate Deaminase)
10.	sitagliptin (Januvia)

Related Therapies and Procedures

1.	Heterologous Transplantation (Xenotransplantation)
2.	Drug Therapy (Chemotherapy)
3.	Cord Blood Stem Cell Transplantation
4.	Heart Transplantation (Grafting, Heart)
5.	Transplantation (Transplant Recipients)