نتایج جستجو برای: smn2 protein

تعداد نتایج: 1234838  

Journal: :Arquivos De Neuro-psiquiatria 2023

Background: Spinal muscular atrophy (SMA) is a disorder caused by homozygous loss of function the SMN1 gene. This gene produces survival motor neuron (SMN) protein, which important in homeostasis. The SMN2 has homology with SMN1, but only expresses 10% functional full-length SMN protein. treatment available Brazilian public health system Nusinersen, an antisense oligonucleotide that increases p...

Journal: :Human molecular genetics 2010
Markus Riessland Bastian Ackermann Anja Förster Miriam Jakubik Jan Hauke Lutz Garbes Ina Fritzsche Ylva Mende Ingmar Blumcke Eric Hahnen Brunhilde Wirth

Proximal spinal muscular atrophy (SMA) is a common autosomal recessively inherited neuromuscular disorder determined by functional impairment of alpha-motor neurons within the spinal cord. SMA is caused by functional loss of the survival motor neuron gene 1 (SMN1), whereas disease severity is mainly influenced by the number of SMN2 copies. SMN2, which produces only low levels of full-length mRN...

2017
Cinsley Gentillon Andrew J Connell Ryan W Kirk Matthew E R Butchbach

C5-substituted 2,4-diaminoquinazolines (2,4-DAQs) ameliorate disease severity in SMA mice. It is uncertain, however, that these compounds increase SMN protein levels in vivo even though they were identified as activators of the SMN2 promoter. These compounds also regulate the expression of other transcripts in neuroblastoma cells. In this study, we investigate the mechanism by which the 2,4-DAQ...

Journal: :Human molecular genetics 2007
Tsuyoshi Kashima Nishta Rao Charles J David James L Manley

Homozygous deletion or mutation of the survival of motor neuron 1 gene (SMN1) causes spinal muscular atrophy. SMN1 has been duplicated in humans to create SMN2, which produces a low level of functional SMN protein. However, most SMN2 transcripts lack exon 7, resulting in a non-functional protein. A single nucleotide difference near the 5' end of exon 7 largely accounts for SMN2 exon 7 skipping,...

2012
Thomas O. Crawford Sergey V. Paushkin Dione T. Kobayashi Suzanne J. Forrest Cynthia L. Joyce Richard S. Finkel Petra Kaufmann Kathryn J. Swoboda Danilo Tiziano Rosa Lomastro Rebecca H. Li Felicia L. Trachtenberg Thomas Plasterer Karen S. Chen

BACKGROUND The universal presence of a gene (SMN2) nearly identical to the mutated SMN1 gene responsible for Spinal Muscular Atrophy (SMA) has proved an enticing incentive to therapeutics development. Early disappointments from putative SMN-enhancing agent clinical trials have increased interest in improving the assessment of SMN expression in blood as an early "biomarker" of treatment effect. ...

Journal: :Human Molecular Genetics 2009
Jan Hauke Markus Riessland Sebastian Lunke Ilker Y. Eyüpoglu Ingmar Blümcke Assam El-Osta Brunhilde Wirth Eric Hahnen

Spinal muscular atrophy (SMA), a common neuromuscular disorder, is caused by homozygous absence of the survival motor neuron gene 1 (SMN1), while the disease severity is mainly influenced by the number of SMN2 gene copies. This correlation is not absolute, suggesting the existence of yet unknown factors modulating disease progression. We demonstrate that the SMN2 gene is subject to gene silenci...

Journal: :Nature chemical biology 2015
James Palacino Susanne E Swalley Cheng Song Atwood K Cheung Lei Shu Xiaolu Zhang Mailin Van Hoosear Youngah Shin Donovan N Chin Caroline Gubser Keller Martin Beibel Nicole A Renaud Thomas M Smith Michael Salcius Xiaoying Shi Marc Hild Rebecca Servais Monish Jain Lin Deng Caroline Bullock Michael McLellan Sven Schuierer Leo Murphy Marcel J J Blommers Cecile Blaustein Frada Berenshteyn Arnaud Lacoste Jason R Thomas Guglielmo Roma Gregory A Michaud Brian S Tseng Jeffery A Porter Vic E Myer John A Tallarico Lawrence G Hamann Daniel Curtis Mark C Fishman William F Dietrich Natalie A Dales Rajeev Sivasankaran

Spinal muscular atrophy (SMA), which results from the loss of expression of the survival of motor neuron-1 (SMN1) gene, represents the most common genetic cause of pediatric mortality. A duplicate copy (SMN2) is inefficiently spliced, producing a truncated and unstable protein. We describe herein a potent, orally active, small-molecule enhancer of SMN2 splicing that elevates full-length SMN pro...

2014
Sean G. Mack Daniel J. Cook Prasad Dhurjati Matthew E. R. Butchbach

Spinal muscular atrophy (SMA), a leading genetic cause of infant death worldwide, is an autosomal recessive disorder caused by the loss of SMN1 (survival motor neuron 1), which encodes the protein SMN. The loss of SMN1 causes a deficiency in SMN protein levels leading to motor neuron cell death in the anterior horn of the spinal cord. SMN2, however, can also produce some functional SMN to parti...

2016
Matthew E. R. Butchbach

Proximal spinal muscular atrophy (SMA), a leading genetic cause of infant death worldwide, is an early-onset, autosomal recessive neurodegenerative disease characterized by the loss of spinal α-motor neurons. This loss of α-motor neurons is associated with muscle weakness and atrophy. SMA can be classified into five clinical grades based on age of onset and severity of the disease. Regardless o...

2013
C. Lebrero

Spinal muscular atrophy (SMA) is a recessive disorder involving the degradation and subsequent loss of motor neurons from the spinal cord. The main cause of SMA is related with the absence of the functional form of the survival motor neuron (SMN) gene (SMN1). This gene presents a telomeric (SMN1) and a centromeric (SMN2) copies that differ in 5 nucleotides. This mutation produces an alternative...

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