Selenoprotein N is dynamically expressed during mouse development and detected early in muscle precursors
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A. Krol | S. Tajbakhsh | P. Guicheney | A. Lescure | S. Maugenre | P. Castets | M. Rederstorff | V. Allamand | C. Gartioux
[1] A. Krol,et al. Selenoprotein function and muscle disease. , 2009, Biochimica et biophysica acta.
[2] F. Muntoni,et al. Oxidative stress in SEPN1‐related myopathy: From pathophysiology to treatment , 2009, Annals of neurology.
[3] A. Holmgren,et al. Selenoproteins* , 2009, Journal of Biological Chemistry.
[4] T. Crawford,et al. Selenoprotein N is required for ryanodine receptor calcium release channel activity in human and zebrafish muscle , 2008, Proceedings of the National Academy of Sciences.
[5] F. Slack,et al. Small non-coding RNAs in animal development , 2008, Nature Reviews Molecular Cell Biology.
[6] W. Filipowicz,et al. Mechanisms of post-transcriptional regulation by microRNAs: are the answers in sight? , 2008, Nature Reviews Genetics.
[7] Heping Cheng,et al. Systemic ablation of RyR3 alters Ca2+ spark signaling in adult skeletal muscle. , 2007, Cell calcium.
[8] C. Tabin,et al. Regulation of tendon differentiation by scleraxis distinguishes force-transmitting tendons from muscle-anchoring tendons , 2007, Development.
[9] D. Rossi,et al. Expression and functional activity of ryanodine receptors (RyRs) during skeletal muscle development. , 2007, Cell calcium.
[10] Kum Kum Khanna,et al. From selenium to selenoproteins: synthesis, identity, and their role in human health. , 2007, Antioxidants & redox signaling.
[11] A. Krol,et al. Selenoprotein synthesis: UGA does not end the story. , 2006, Biochimie.
[12] Nathan I. Lopez,et al. Selenoprotein W during development and oxidative stress. , 2006, Journal of inorganic biochemistry.
[13] N. Petit,et al. A single homozygous point mutation in a 3′untranslated region motif of selenoprotein N mRNA causes SEPN1‐related myopathy , 2006, EMBO reports.
[14] N. Clarke,et al. SEPN1: Associated with congenital fiber‐type disproportion and insulin resistance , 2006, Annals of neurology.
[15] M. Berry. Insights into the hierarchy of selenium incorporation , 2005, Nature Genetics.
[16] Heping Cheng,et al. Ca2+ sparks and secretion in dorsal root ganglion neurons. , 2005, Proceedings of the National Academy of Sciences of the United States of America.
[17] Satoru Takahashi,et al. The Distal Sequence Element of the Selenocysteine tRNA Gene Is a Tissue-Dependent Enhancer Essential for Mouse Embryogenesis , 2005, Molecular and Cellular Biology.
[18] Gerhard K. H. Przemeck,et al. Cytoplasmic Thioredoxin Reductase Is Essential for Embryogenesis but Dispensable for Cardiac Development , 2005, Molecular and Cellular Biology.
[19] V. Gladyshev,et al. Selective Rescue of Selenoprotein Expression in Mice Lacking a Highly Specialized Methyl Group in Selenocysteine tRNA* , 2005, Journal of Biological Chemistry.
[20] F. Hanefeld,et al. Desmin‐related myopathy with mallory body–like inclusions is caused by mutations of the selenoprotein N gene , 2004, Annals of neurology.
[21] D. Driscoll,et al. Mechanism and regulation of selenoprotein synthesis. , 2003, Annual review of nutrition.
[22] Claus Jacob,et al. Sulfur and selenium: the role of oxidation state in protein structure and function. , 2003, Angewandte Chemie.
[23] G. Kryukov,et al. Spatial and temporal expression patterns of selenoprotein genes during embryogenesis in zebrafish. , 2003, Gene expression patterns : GEP.
[24] R. Guigó,et al. Characterization of Mammalian Selenoproteomes , 2003, Science.
[25] N. Petit,et al. Selenoprotein N: an endoplasmic reticulum glycoprotein with an early developmental expression pattern. , 2003, Human molecular genetics.
[26] F. Muntoni,et al. Mutations of the selenoprotein N gene, which is implicated in rigid spine muscular dystrophy, cause the classical phenotype of multiminicore disease: reassessing the nosology of early-onset myopathies. , 2002, American journal of human genetics.
[27] T. McDowell,et al. Functional properties of ryanodine receptors from rat dorsal root ganglia , 2002, FEBS letters.
[28] M. Bonnin,et al. Fgf8 transcripts are located in tendons during embryonic chick limb development , 2001, Mechanisms of Development.
[29] F. Muntoni,et al. Mutations in SEPN1 cause congenital muscular dystrophy with spinal rigidity and restrictive respiratory syndrome , 2001, Nature Genetics.
[30] Joseph L Goldstein,et al. Regulated Intramembrane Proteolysis A Control Mechanism Conserved from Bacteria to Humans , 2000, Cell.
[31] F. Muntoni,et al. Genetic heterogeneity of congenital muscular dystrophy with rigid spine syndrome , 1999, Neuromuscular Disorders.
[32] B. Flucher,et al. Type 3 and Type 1 Ryanodine Receptors Are Localized in Triads of the Same Mammalian Skeletal Muscle Fibers , 1999, The Journal of cell biology.
[33] N. Rosemblit,et al. Intracellular calcium release channel expression during embryogenesis. , 1999, Developmental biology.
[34] F Bertocchini,et al. Requirement for the ryanodine receptor type 3 for efficient contraction in neonatal skeletal muscles , 1997, The EMBO journal.
[35] D. Rossi,et al. Expression of the Ryanodine Receptor Type 3 Calcium Release Channel during Development and Differentiation of Mammalian Skeletal Muscle Cells* , 1997, The Journal of Biological Chemistry.
[36] M. Iino,et al. Functional and Morphological Features of Skeletal Muscle from Mutant Mice Lacking Both Type 1 and Type 3 Ryanodine Receptors , 1997, The Journal of physiology.
[37] M. Taketo,et al. Early embryonic lethality caused by targeted disruption of the mouse selenocysteine tRNA gene (Trsp). , 1997, Proceedings of the National Academy of Sciences of the United States of America.
[38] G. Cossu,et al. Redefining the Genetic Hierarchies Controlling Skeletal Myogenesis: Pax-3 and Myf-5 Act Upstream of MyoD , 1997, Cell.
[39] M. Barbacid,et al. Synchronous Onset of NGF and TrkA Survival Dependence in Developing Dorsal Root Ganglia , 1996, The Journal of Neuroscience.
[40] J. Leddy,et al. Temporal differences in the induction of dihydropyridine receptor subunits and ryanodine receptors during skeletal muscle development. , 1994, The Journal of biological chemistry.
[41] B. Thisse,et al. Loss of selenoprotein N function causes disruption of muscle architecture in the zebrafish embryo. , 2007, Experimental Cell Research.
[42] A. Krol,et al. Cellular and Molecular Life Sciences Review Understanding the importance of selenium and selenoproteins in muscle function , 2005 .
[43] S. Tajbakhsh,et al. The birth of muscle progenitor cells in the mouse: spatiotemporal considerations. , 2000, Current topics in developmental biology.