A screen for regulators of survival of motor neuron protein levels.

[1]  J. Woodgett,et al.  Targeting GSK-3 family members in the heart: a very sharp double-edged sword. , 2011, Journal of molecular and cellular cardiology.

[2]  G. Dreyfuss,et al.  A degron created by SMN2 exon 7 skipping is a principal contributor to spinal muscular atrophy severity. , 2010, Genes & development.

[3]  Haruka Aoki,et al.  Chelation of Extracellular Calcium-Induced Cell Death was Prevented by Glycogen Synthase Kinase-3 Inhibitors in PC12 Cells , 2010, Cellular and Molecular Neurobiology.

[4]  Nam‐Gyun Kim,et al.  Regulation of protein stability by GSK3 mediated phosphorylation , 2009, Cell cycle.

[5]  S. Jablonka,et al.  Valproic acid blocks excitability in SMA type I mouse motor neurons , 2009, Neurobiology of Disease.

[6]  David R. Liu,et al.  A small-molecule inhibitor of tgf-Beta signaling replaces sox2 in reprogramming by inducing nanog. , 2009, Cell stem cell.

[7]  Faraz Farooq,et al.  p38 Mitogen-activated protein kinase stabilizes SMN mRNA through RNA binding protein HuR. , 2009, Human molecular genetics.

[8]  C. Beattie,et al.  Spinal muscular atrophy: why do low levels of survival motor neuron protein make motor neurons sick? , 2009, Nature Reviews Neuroscience.

[9]  S. Schreiber,et al.  A small molecule that directs differentiation of human ESCs into the pancreatic lineage. , 2009, Nature chemical biology.

[10]  K. Fischbeck,et al.  Regulation of SMN Protein Stability , 2008, Molecular and Cellular Biology.

[11]  A. MacKenzie,et al.  A two-site ELISA can quantify upregulation of SMN protein by drugs for spinal muscular atrophy , 2008, Neurology.

[12]  A. MacKenzie,et al.  Neurodevelopmental abnormalities in neurosphere‐derived neural stem cells from SMN‐depleted mice , 2008, Journal of neuroscience research.

[13]  S. Artavanis-Tsakonas,et al.  Modeling Spinal Muscular Atrophy in Drosophila , 2008, PloS one.

[14]  G. Dreyfuss,et al.  Inactivation of the SMN complex by oxidative stress. , 2008, Molecular cell.

[15]  J. Steitz,et al.  Where in the cell is the minor spliceosome? , 2008, Proceedings of the National Academy of Sciences.

[16]  C. Will,et al.  Minor spliceosome components are predominantly localized in the nucleus , 2008, Proceedings of the National Academy of Sciences.

[17]  Lili Wan,et al.  SMN Deficiency Causes Tissue-Specific Perturbations in the Repertoire of snRNAs and Widespread Defects in Splicing , 2008, Cell.

[18]  P. Cohen,et al.  The selectivity of protein kinase inhibitors: a further update. , 2007, The Biochemical journal.

[19]  F. Müller,et al.  Splicing Segregation: The Minor Spliceosome Acts outside the Nucleus and Controls Cell Proliferation , 2007, Cell.

[20]  M. Beck,et al.  Defective Ca2+ channel clustering in axon terminals disturbs excitability in motoneurons in spinal muscular atrophy , 2007, The Journal of cell biology.

[21]  D. Coen,et al.  Inhibitors of the sodium potassium ATPase that impair herpes simplex virus replication identified via a chemical screening approach. , 2007, Virology.

[22]  K. Fischbeck,et al.  Trichostatin A increases SMN expression and survival in a mouse model of spinal muscular atrophy. , 2007, The Journal of clinical investigation.

[23]  C. Lorson,et al.  Novel aminoglycosides increase SMN levels in spinal muscular atrophy fibroblasts , 2006, Human Genetics.

[24]  H. Wichterle,et al.  Multiprotein Complexes of the Survival of Motor Neuron Protein SMN with Gemins Traffic to Neuronal Processes and Growth Cones of Motor Neurons , 2006, The Journal of Neuroscience.

[25]  R. Kothary,et al.  Hypomorphic Smn knockdown C2C12 myoblasts reveal intrinsic defects in myoblast fusion and myotube morphology. , 2005, Experimental cell research.

[26]  G. Aistrup,et al.  Digitalis: new actions for an old drug. , 2005, American journal of physiology. Heart and circulatory physiology.

[27]  Xiaocun Chen,et al.  Diverse small-molecule modulators of SMN expression found by high-throughput compound screening: early leads towards a therapeutic for spinal muscular atrophy. , 2005, Human molecular genetics.

[28]  U. Monani,et al.  SMNDelta7, the major product of the centromeric survival motor neuron (SMN2) gene, extends survival in mice with spinal muscular atrophy and associates with full-length SMN. , 2005, Human molecular genetics.

[29]  Rick Gussio,et al.  Structure‐Aided Optimization of Kinase Inhibitors Derived from Alsterpaullone , 2005, Chembiochem : a European journal of chemical biology.

[30]  W. Hung,et al.  Degradation of survival motor neuron (SMN) protein is mediated via the ubiquitin/proteasome pathway , 2004, Neurochemistry International.

[31]  D. Brooks,et al.  Characterization of the Neutralizing Activity of Digoxin-Specific Fab toward Ouabain-Like Steroids , 2004, Journal of Pharmacology and Experimental Therapeutics.

[32]  Michel Goedert,et al.  GSK3 inhibitors: development and therapeutic potential , 2004, Nature Reviews Drug Discovery.

[33]  Michael Sendtner,et al.  Smn, the spinal muscular atrophy–determining gene product, modulates axon growth and localization of β-actin mRNA in growth cones of motoneurons , 2003, The Journal of cell biology.

[34]  U. Monani,et al.  Molecular, Cellular and Developmental Biology Program – Specialization 2018/2019 , 2017 .

[35]  Conrad Kunick,et al.  Alsterpaullone, a novel cyclin‐dependent kinase inhibitor, induces apoptosis by activation of caspase‐9 due to perturbation in mitochondrial membrane potential , 2003, Molecular carcinogenesis.

[36]  H. Wichterle,et al.  Directed Differentiation of Embryonic Stem Cells into Motor Neurons , 2002, Cell.

[37]  E. Androphy,et al.  Aclarubicin treatment restores SMN levels to cells derived from type I spinal muscular atrophy patients. , 2001, Human molecular genetics.

[38]  M. Cobb,et al.  Mitogen-activated protein (MAP) kinase pathways: regulation and physiological functions. , 2001, Endocrine reviews.

[39]  G. Mills,et al.  Phosphorylation and inactivation of glycogen synthase kinase 3 by protein kinase A. , 2000, Proceedings of the National Academy of Sciences of the United States of America.

[40]  C. Lorson,et al.  A single nucleotide in the SMN gene regulates splicing and is responsible for spinal muscular atrophy. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

[41]  G. Neri,et al.  SMN protein analysis in fibroblast, amniocyte and CVS cultures from spinal muscular atrophy patients and its relevance for diagnosis , 1999, European Journal of Human Genetics.

[42]  G. Dreyfuss,et al.  A Novel Function for SMN, the Spinal Muscular Atrophy Disease Gene Product, in Pre-mRNA Splicing , 1998, Cell.

[43]  A. Smith,et al.  Inactivation of the survival motor neuron gene, a candidate gene for human spinal muscular atrophy, leads to massive cell death in early mouse embryos. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[44]  Arnold Munnich,et al.  Correlation between severity and SMN protein level in spinal muscular atrophy , 1997, Nature Genetics.

[45]  G. Dreyfuss,et al.  A novel nuclear structure containing the survival of motor neurons protein. , 1996, The EMBO journal.

[46]  J. Weissenbach,et al.  Identification and characterization of a spinal muscular atrophy-determining gene , 1995, Cell.

[47]  W. Snider,et al.  Developmental expression of the platelet-derived growth factor alpha-receptor gene in mammalian central nervous system. , 1993, Proceedings of the National Academy of Sciences of the United States of America.

[48]  G. Langer,et al.  An Official Journal of the American Heart Association Ca Distribution after Na Pump Inhibition in Cultured Neonatal Rat Myocardial Cells , 2005 .

[49]  R. Pearson,et al.  Protein kinase phosphorylation site sequences and consensus specificity motifs: tabulations. , 1991, Methods in enzymology.

[50]  A. Zeiher,et al.  Glycogen Synthase Kinase 3 (cid:1) Inhibits Myocardin-Dependent Transcription and Hypertrophy Induction Through Site-Specific Phosphorylation , 2022 .