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NOP56 ribonucleoprotein homolog

Nop56
Nop56p is a yeast nucleolar protein that is part of a complex with the nucleolar proteins Nop58p and fibrillarin. Nop56p is required for assembly of the 60S ribosomal subunit and is involved in pre-rRNA processing. The protein encoded by this gene is similar in sequence to Nop56p and is also found in the nucleolus. Multiple transcript variants encoding several different isoforms have been found for this gene, but the full-length nature of most of them has not been determined. [provided by RefSeq, Jan 2009] (from NCBI)
Top mentioned proteins: Nop58p, CAN, AGE, 15.5K, HAD
Papers on Nop56
Genetic and clinical analysis of spinocerebellar ataxia type 36 in Mainland China.
New
Wang et al., Changsha, China. In Clin Genet, Jan 2016
To assess the frequency and clinical characteristics of SCA36 in patients from Mainland China, we combined the repeat-primed polymerase chain reaction method and Southern blot analysis to detect the GGCCTG hexanucleotide repeats of NOP56 in 364 probands with SCA, 126 probands with hereditary spastic paraplegia (HSP) and 99 probands with amyotrophic lateral sclerosis (ALS).
[Recent advances in clinical and genetic research of spinocerebellar ataxia type 36].
Review
New
Wang et al., Changsha, China. In Zhonghua Yi Xue Yi Chuan Xue Za Zhi, Jan 2016
Recently, the causative mutation for SCA36, namely intronic hexanucleotide GGCCTG expansion in NOP56 gene, has been identified in Japanese and Spanish pedigrees in succession.
NUFIP and the HSP90/R2TP chaperone bind the SMN complex and facilitate assembly of U4-specific proteins.
New
Bertrand et al., Montpellier, France. In Nucleic Acids Res, Nov 2015
They both contain the 15.5K and proteins with NOP domains (PRP31 for U4, NOP56/58 for snoRNPs).
Spinocerebellar ataxia type 36 exists in diverse populations and can be caused by a short hexanucleotide GGCCTG repeat expansion.
New
Dürr et al., Tokyo, Japan. In J Neurol Neurosurg Psychiatry, Sep 2015
OBJECTIVE: Spinocerebellar ataxia 36 (SCA36) is an autosomal-dominant neurodegenerative disorder caused by a large (>650) hexanucleotide GGCCTG repeat expansion in the first intron of the NOP56 gene.
Spinocerebellar ataxia 36 (SCA36): «Costa da Morte ataxia»
New
Sobrido et al., Santiago de Compostela, Spain. In Neurologia, Feb 2015
The condition is caused by a genetic mutation (intronic hexanucleotide repeat expansion) in the NOP56 gene on the short arm of chromosome 20 (20p13).
Characteristic RNA foci of the abnormal hexanucleotide GGCCUG repeat expansion in spinocerebellar ataxia type 36 (Asidan).
Abe et al., Okayama, Japan. In Eur J Neurol, 2014
BACKGROUND AND PURPOSE: Spinocerebellar ataxia type 36 (SCA36), also called Asidan, is an autosomal-dominant neurodegenerative disorder identified as a hexanucleotide GGCCTG repeat expansion in the first intron 1 of the NOP56 gene.
Spinocerebellar Ataxia Type 36
Review
Sobrido et al., Seattle, United States. In Unknown Journal, 2014
Confirmation of the diagnosis relies on detection of an abnormal hexanucleotide GGCCTG repeat expansion in NOP56.
Evaluating noncoding nucleotide repeat expansions in amyotrophic lateral sclerosis.
Gitler et al., Stanford, United States. In Neurobiol Aging, 2014
We analyzed the nucleotide repeat lengths of 6 genes (ATXN8, ATXN10, PPP2R2B, NOP56, DMPK, and JPH3) that have previously been associated with neurologic or neuromuscular disorders, in several hundred sporadic patients with ALS and healthy control subjects.
Protein Hit1, a novel box C/D snoRNP assembly factor, controls cellular concentration of the scaffolding protein Rsa1 by direct interaction.
Charpentier et al., Vandœuvre-lès-Nancy, France. In Nucleic Acids Res, 2013
Nop58p/NOP58, Nop56p/NOP56 and Nop1p/Fibrillarin on box C/D small nucleolar RNAs (C/D snoRNAs).
Early and selective reduction of NOP56 (Asidan) and RNA processing proteins in the motor neuron of ALS model mice.
Abe et al., Okayama, Japan. In Neurol Res, 2013
RESULTS: Compared to age-matched wild type (WT) mice, Tg mice showed progressive reduction of NOP56 levels in the large motor neurons of lumbar and cervical cords from the early-symptomatic stage (14 weeks of age) to the end stage of the disease (18 weeks).
Cognitive and affective impairments of a novel SCA/MND crossroad mutation Asidan.
GeneRIF
Koizumi et al., Okayama, Japan. In Eur J Neurol, 2012
We newly found intronic hexanucleotide GGCCTG gene expansion in NOP56 gene as the causative mutation in nine unrelated Japanese familial hereditary spinocerebellar ataxia patients
[Spinocerebellar ataxia type 36 (nicknamed Asidan)].
Review
Ikeda et al., Okayama, Japan. In Brain Nerve, 2012
We report the phenotype of spinocerebellar ataxia type 36 (SCA36), which is a novel type of dominant cerebellar ataxia nicknamed as "Asidan," caused by the expansion of a hexanucleotide GGCCTG repeat in intron 1 of the nucleolar protein 56 (NOP56) gene.
The clinical characteristics of spinocerebellar ataxia 36: a study of 2121 Japanese ataxia patients.
Kawakami et al., Hiroshima, Japan. In Mov Disord, 2012
Spinocerebellar ataxia 36 is caused by the expansion of the intronic GGCCTG hexanucleotide repeat in NOP56.
Clinical features of SCA36: a novel spinocerebellar ataxia with motor neuron involvement (Asidan).
Abe et al., Okayama, Japan. In Neurology, 2012
OBJECTIVE: To characterize the phenotype of spinocerebellar ataxia type 36 (SCA36), a novel dominant disorder (nicknamed "Asidan") caused by a hexanucleotide GGCCTG repeat expansion in intron 1 of the NOP56 gene.
Proteomic characterization of the human FTSJ3 preribosomal complexes.
Zanchin et al., Campinas, Brazil. In J Proteome Res, 2012
Approximately 50% of the components of FTSJ3 complexes are shared by complexes described for RPS19, Par14, nucleolin, and NOP56.
'Costa da Morte' ataxia is spinocerebellar ataxia 36: clinical and genetic characterization.
GeneRIF
Sobrido et al., Santiago de Compostela, Spain. In Brain, 2012
This study demonistrated that NOP56 mutation is response spinocerebellar ataxia 36 in Spainish family.
Expansion of intronic GGCCTG hexanucleotide repeat in NOP56 causes SCA36, a type of spinocerebellar ataxia accompanied by motor neuron involvement.
GeneRIF
Koizumi et al., Kyoto, Japan. In Am J Hum Genet, 2011
Expansion of the intronic GGCCTG hexanucleotide repeat in NOP56 causes a unique form of spinocerebellar ataxias, SCA36, which shows not only ataxia but also motor neuron dysfunction.
Evidence that the AAA+ proteins TIP48 and TIP49 bridge interactions between 15.5K and the related NOP56 and NOP58 proteins during box C/D snoRNP biogenesis.
GeneRIF
Watkins et al., Newcastle upon Tyne, United Kingdom. In Mol Cell Biol, 2009
snoRNP assembly factor NUFIP can regulate the interactions between TIP48 and TIP49 and the core box C/D proteins.
Fibrillarin and Nop56 interact before being co-assembled in box C/D snoRNPs.
GeneRIF
Roussel et al., Paris, France. In Exp Cell Res, 2009
Data demonstrate that fibrillarin and Nop56 directly interact in vivo, and that this interaction is indispensable for the association of both proteins with the box C/D snoRNPs.
Homologs of small nucleolar RNAs in Archaea.
Impact
Dennis et al., Vancouver, Canada. In Science, 2000
Eighteen small sno-like RNAs (sRNAs) were cloned from the archaeon Sulfolobus acidocaldarius by coimmunoprecipitation with archaeal fibrillarin and NOP56, the homologs of eukaryotic snoRNA-associated proteins.
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