نتایج جستجو برای: smn2 protein

تعداد نتایج: 1234838  

Journal: :Neuron 2017
Constantin d’Ydewalle Daniel M. Ramos Noah J. Pyles Shi-Yan Ng Mariusz Gorz Celeste M. Pilato Karen Ling Lingling Kong Amanda J. Ward Lee L. Rubin Frank Rigo C. Frank Bennett Charlotte J. Sumner

The neuromuscular disorder spinal muscular atrophy (SMA), the most common inherited killer of infants, is caused by insufficient expression of survival motor neuron (SMN) protein. SMA therapeutics development efforts have focused on identifying strategies to increase SMN expression. We identified a long non-coding RNA (lncRNA) that arises from the antisense strand of SMN, SMN-AS1, which is enri...

2017
Xiang Lin Jin-Jing Li Wen-Jing Qian Qi-Jie Zhang Zhong-Feng Wang Ying-Qian Lu En-Lin Dong Jin He Ning Wang Li-Xiang Ma Wan-Jin Chen

Spinal muscular atrophy (SMA) is a devastating motor neuron disease caused by mutations of the survival motor neuron 1 (SMN1) gene. SMN2, a paralogous gene to SMN1, can partially compensate for the loss of SMN1. On the basis of age at onset, highest motor function and SMN2 copy numbers, childhood-onset SMA can be divided into three types (SMA I-III). An inverse correlation was observed between ...

Journal: :Human molecular genetics 2007
Chen-Hung Ting Chiao-Wei Lin Shin-Lan Wen Hsiu-Mei Hsieh-Li Hung Li

Proximal spinal muscular atrophy (SMA) is a motor neuron degeneration disorder for which there is currently no effective treatment. Here, we report three compounds (sodium vanadate, trichostatin A and aclarubicin) that effectively enhance SMN2 expression by inducing Stat5 activation in SMA-like mouse embryonic fibroblasts and human SMN2-transfected NSC34 cells. We found that Stat5 activation en...

بهرامی منجمی, غلامرضا, تنکابنی, سید حسن, نوروزی نیا, مهرداد,

Background and Objective: The severity of the spinal muscular atrophy phenotype is inversely associated with the expression levels of the SMN2 gene; this correlation is not absolute, for this reason there is currently no effective treatment. The interference of other severity modifying factors, apart from SMN2 gene expression has been suggested. Here we investigate the effects of valproic acid ...

2017
Jonathan J Cherry Christine J DiDonato Elliot J Androphy Alessandro Calo Kyle Potter Sara K Custer Sarah Du Timothy L Foley Ariamala Gopalsamy Emily J Reedich Susana M Gordo William Gordon Natalie Hosea Lyn H Jones Daniel K Krizay Gregory LaRosa Hongxia Li Sachin Mathur Carol A Menard Paraj Patel Rebeca Ramos-Zayas Anne Rietz Haojing Rong Baohong Zhang Michael A Tones

C5-substituted 2,4-diaminoquinazoline inhibitors of the decapping scavenger enzyme DcpS (DAQ-DcpSi) have been developed for the treatment of spinal muscular atrophy (SMA), which is caused by genetic deficiency in the Survival Motor Neuron (SMN) protein. These compounds are claimed to act as SMN2 transcriptional activators but data underlying that claim are equivocal. In addition it is unclear w...

Journal: :Human molecular genetics 1999
T Vitali V Sossi F Tiziano S Zappata A Giuli M Paravatou-Petsotas G Neri C Brahe

Spinal muscular atrophy (SMA) is a common autosomal recessive neuromuscular disorder which presents with various clinical phenotypes ranging from severe to very mild. All forms are caused by the homozygous absence of the survival motor neuron ( SMN1 ) gene. SMN1 and a nearly identical copy ( SMN2 ) are located in a duplicated region at 5q13 and encode identical proteins. The genetic basis for t...

2016
Joonbae Seo Natalia N. Singh Eric W. Ottesen Brian M. Lee Ravindra N. Singh

Spinal muscular atrophy (SMA), a leading genetic disease of children and infants, is caused by mutations or deletions of Survival Motor Neuron 1 (SMN1) gene. SMN2, a nearly identical copy of SMN1, fails to compensate for the loss of SMN1 due to skipping of exon 7. SMN2 predominantly produces SMNΔ7, an unstable protein. Here we report exon 6B, a novel exon, generated by exonization of an introni...

2018
Loren L. Flynn Chalermchai Mitrpant Ianthe L. Pitout Sue Fletcher Steve D. Wilton

The severe childhood disease spinal muscular atrophy (SMA) arises from the homozygous loss of the survival motor neuron 1 gene (SMN1). A homologous gene potentially encoding an identical protein, SMN2 can partially compensate for the loss of SMN1; however, the exclusion of a critical exon in the coding region during mRNA maturation results in insufficient levels of functional protein. The rate ...

2014
Jeremiah Hadwen Duncan MacKenzie Fahad Shamim Kevin Mongeon Martin Holcik Alex MacKenzie Faraz Farooq

BACKGROUND Spinal Muscular Atrophy (SMA) is one of the most common inherited causes of infant death and is caused by the loss of functional survival motor neuron (SMN) protein due to mutations or deletion in the SMN1 gene. One of the treatment strategies for SMA is to induce the expression of the protein from the homologous SMN2 gene, a rescuing paralog for SMA. METHODS AND RESULTS Here we de...

Journal: :genetics in the 3rd millennium 0
seyedeh sedigheh abedini maryam azad mandana hassanzad kimia kahrizi hossein najmabadi

spinal muscular atrophy (sma) is an autosomal recessive neuromuscular disorder caused by homozygous deletion of the survival motor neuron gene 1 (smn1) in more than 90% of patients. according to the age of onset and severity of the disease, sma is classified into three groups: type i (severe), type ii (intermediate) and type iii (mild). as reported, the smn2 gene, centromeric copy gene, showed ...

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