نتایج جستجو برای: smn gene

تعداد نتایج: 1142093  

Journal: :Human molecular genetics 2013
Gabriel Sanchez Alain Y Dury Lyndsay M Murray Olivier Biondi Helina Tadesse Rachid El Fatimy Rashmi Kothary Frédéric Charbonnier Edouard W Khandjian Jocelyn Côté

SMN1, the causative gene for spinal muscular atrophy (SMA), plays a housekeeping role in the biogenesis of small nuclear RNA ribonucleoproteins. SMN is also present in granular foci along axonal projections of motoneurons, which are the predominant cell type affected in the pathology. These so-called RNA granules mediate the transport of specific mRNAs along neurites and regulate mRNA localizat...

Journal: :Results and problems in cell differentiation 2009
Wilfried Rossoll Gary J Bassell

Spinal muscular atrophy (SMA) is a neurodegenerative disease that results from loss of function of the SMN1 gene, encoding the ubiquitously expressed survival of motor neuron (SMN) protein, a protein best known for its housekeeping role in the SMN-Gemin multiprotein complex involved in spliceosomal small nuclear ribonucleoprotein (snRNP) assembly. However, numerous studies reveal that SMN has m...

2016
W. David Arnold Sandra Duque Chitra C. Iyer Phillip Zaworski Vicki L. McGovern Shannon J. Taylor Katharine M. von Herrmann Dione T. Kobayashi Karen S. Chen Stephen J. Kolb Sergey V. Paushkin Arthur H. M. Burghes

INTRODUCTION AND OBJECTIVE Spinal muscular atrophy (SMA) is an autosomal recessive motor neuron disorder. SMA is caused by homozygous loss of the SMN1 gene and retention of the SMN2 gene resulting in reduced levels of full length SMN protein that are insufficient for motor neuron function. Various treatments that restore levels of SMN are currently in clinical trials and biomarkers are needed t...

Journal: :The Journal of neuroscience : the official journal of the Society for Neuroscience 2010
Olivier Biondi Julien Branchu Gabriel Sanchez Camille Lancelin Séverine Deforges Philippe Lopes Claude Pariset Sylvie Lécolle Jocelyn Côté Christophe Chanoine Frédéric Charbonnier

Spinal muscular atrophy (SMA), a lethal neurodegenerative disease that occurs in childhood, is caused by the misexpression of the survival of motor neuron (SMN) protein in motor neurons. It is still unclear whether activating motor units in SMA corrects the delay in the postnatal maturation of the motor unit resulting in an enhanced neuroprotection. In the present work, we demonstrate that an a...

Journal: :Molecular biology of the cell 2018
Kelsey M Gray Kevin A Kaifer David Baillat Ying Wen Thomas R Bonacci Allison D Ebert Amanda C Raimer Ashlyn M Spring Sara Ten Have Jacqueline J Glascock Kushol Gupta Gregory D Van Duyne Michael J Emanuele Angus I Lamond Eric J Wagner Christian L Lorson A Gregory Matera

Spinal muscular atrophy (SMA) is caused by homozygous mutations in human SMN1 Expression of a duplicate gene (SMN2) primarily results in skipping of exon 7 and production of an unstable protein isoform, SMNΔ7. Although SMN2 exon skipping is the principal contributor to SMA severity, mechanisms governing stability of survival motor neuron (SMN) isoforms are poorly understood. We used a Drosophil...

Journal: :The Journal of Molecular Diagnostics 2001

Journal: :Human molecular genetics 2013
James P Van Meerbeke Rebecca M Gibbs Heather L Plasterer Wenyan Miao Zhihua Feng Ming-Yi Lin Agnieszka A Rucki Claribel D Wee Bing Xia Shefali Sharma Vincent Jacques Darrick K Li Livio Pellizzoni James R Rusche Chien-Ping Ko Charlotte J Sumner

Spinal muscular atrophy (SMA) is caused by mutations of the survival motor neuron 1 (SMN1) gene, retention of the survival motor neuron 2 (SMN2) gene and insufficient expression of full-length survival motor neuron (SMN) protein. Quinazolines increase SMN2 promoter activity and inhibit the ribonucleic acid scavenger enzyme DcpS. The quinazoline derivative RG3039 has advanced to early phase clin...

Journal: :The Journal of Cell Biology 1999
Teresa Carvalho Fátima Almeida Alexandre Calapez Miguel Lafarga Maria T. Berciano Maria Carmo-Fonseca

The spliceosomal snRNAs U1, U2, U4, and U5 are synthesized in the nucleus, exported to the cytoplasm to assemble with Sm proteins, and reimported to the nucleus as ribonucleoprotein particles. Recently, two novel proteins involved in biogenesis of small nuclear ribonucleoproteins (snRNPs) were identified, the Spinal muscular atrophy disease gene product (SMN) and its associated protein SIP1. It...

Journal: :Human molecular genetics 2012
Thomas W Bebee Catherine E Dominguez Somayeh Samadzadeh-Tarighat Kristi L Akehurst Dawn S Chandler

Spinal muscular atrophy (SMA) is a progressive neurodegenerative disease associated with low levels of the essential survival motor neuron (SMN) protein. Reduced levels of SMN is due to the loss of the SMN1 gene and inefficient splicing of the SMN2 gene caused by a C>T mutation in exon 7. Global analysis of the severe SMNΔ7 SMA mouse model revealed altered splicing and increased levels of the h...

Journal: :Human molecular genetics 2010
Matthew E R Butchbach Jasbir Singh Margrét Thorsteinsdóttir Luciano Saieva Elzbieta Slominski John Thurmond Thorkell Andrésson Jun Zhang Jonathan D Edwards Louise R Simard Livio Pellizzoni Jill Jarecki Arthur H M Burghes Mark E Gurney

Proximal spinal muscular atrophy (SMA), one of the most common genetic causes of infant death, results from the selective loss of motor neurons in the spinal cord. SMA is a consequence of low levels of survival motor neuron (SMN) protein. In humans, the SMN gene is duplicated; SMA results from the loss of SMN1 but SMN2 remains intact. SMA severity is related to the copy number of SMN2. Compound...

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