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1. Full Text Caenorhabditis elegans Functional Orthologue of Human Protein h-Mucolipin-1 Is Required for Lysosome Biogenesis
by Sebastian Treusch and Sarah Knuth and Susan A. Slaugenhaupt and Ehud Goldin and Barth D. Grant and Hanna Fares and Roscoe O. Brady
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 3/2004, Volume 101, Issue 13, pp. 4483 - 4488
Mucolipidosis type IV (MLIV) is an autosomal recessive lysosomal storage disease characterized by severe psychomotor retardation, achlorhydria, and... 
Biological Sciences | Endocytosis | Phenotypes | Plasmids | Lysosomes | Kidney cells | Organelles | Budding | Vacuoles | Cells | Endosomes | Mucolipidosis type IV | CUP-5 | FUSION | ENDOCYTIC PATHWAY | MUCOLIPIDOSIS TYPE-IV | MULTIDISCIPLINARY SCIENCES | ABNORMAL TRANSPORT | IDENTIFICATION | CELL-DEATH | mucolipidosis type IV | ENDOSOMES | GENE | MUTATIONS | FLUORESCENT PROTEIN | Animals, Genetically Modified | Membrane Proteins - genetics | Humans | Molecular Sequence Data | Mucolipidoses - genetics | Lysosomes - physiology | Recombinant Fusion Proteins - metabolism | Caenorhabditis elegans - physiology | Animals | Mutagenesis | Membrane Proteins - physiology | Cell Death | Caenorhabditis elegans Proteins - physiology | Endocytosis - genetics | Caenorhabditis elegans Proteins - genetics | Caenorhabditis elegans | Research | Proteins | Tissue | Cellular biology | Disease | Worms | Index Medicus
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2. Full Text The GPR54 Gene as a Regulator of Puberty
by Seminara, Stephanie B and Messager, Sophie and Chatzidaki, Emmanouella E and Thresher, Rosemary R and Acierno, James S and Shagoury, Jenna K and Bo-Abbas, Yousef and Kuohung, Wendy and Schwinof, Kristine M and Hendrick, Alan G and Zahn, Dirk and Dixon, John and Kaiser, Ursula B and Slaugenhaupt, Susan A and Gusella, James F and O'Rahilly, Stephen and Carlton, Mark B.L and Crowley, William F and Aparicio, Samuel A.J.R and Colledge, William H
The New England Journal of Medicine, ISSN 0028-4793, 10/2003, Volume 349, Issue 17, pp. 1614 - 1627
Puberty does not occur in patients with idiopathic hypogonadotropic hypogonadism. This study investigated mutations in a candidate gene encoding a G... 
MENSTRUAL-CYCLE | MEDICINE, GENERAL & INTERNAL | PROTEIN-COUPLED RECEPTOR | KISS-1 | GONADOTROPIN-RELEASING-HORMONE | MEN | IDIOPATHIC HYPOGONADOTROPIC HYPOGONADISM | METASTASIS-SUPPRESSOR GENE | GNRH RECEPTOR | KALLMANNS-SYNDROME | LUTEINIZING-HORMONE | Receptors, Neuropeptide - deficiency | Gonadotropins - blood | Humans | Gonads - pathology | Male | Lod Score | Puberty - genetics | DNA Mutational Analysis | Female | Models, Animal | Gonadotropins - deficiency | Sexual Maturation - genetics | Receptors, G-Protein-Coupled | Receptors, Neuropeptide - genetics | Reverse Transcriptase Polymerase Chain Reaction | Genes, Recessive | Gonadotropin-Releasing Hormone - blood | Mice, Knockout | Hypogonadism - genetics | Phenotype | Animals | Pedigree | Mice | Mutation | Receptors, Kisspeptin-1 | Puberty | Genetic aspects | Studies | Pituitary gland | Hormones | Index Medicus | Abridged Index Medicus
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3. Full Text Zinc dyshomeostasis is linked with the loss of mucolipidosis IV-associated TRPML1 ion channel
by Eichelsdoerfer, Jonathan L and Evans, Jeffrey A and Slaugenhaupt, Susan A and Cuajungco, Math P
Journal of Biological Chemistry, ISSN 0021-9258, 11/2010, Volume 285, Issue 45, pp. 34304 - 34308
Chelatable zinc is important in brain function, and its homeostasis is maintained to prevent cytotoxic overload. However, certain pathologic events result in... 
LYSOSOMAL MEMBRANE PERMEABILIZATION | ENDOGENOUS ZINC | BIOCHEMISTRY & MOLECULAR BIOLOGY | MUTATION | ENHANCED ZINC | NEURONS | INJURY | CELL-CULTURE | AUTOPHAGY | RELEASE | BRAIN | Cell Line | Vacuoles - genetics | Humans | Homeostasis | Mucolipidoses - genetics | Mitochondria - metabolism | Chelating Agents - pharmacology | Mitochondria - pathology | Transient Receptor Potential Channels | Vacuoles - pathology | Zinc | Mice, Knockout | Brain - metabolism | Mucolipidoses - pathology | Animals | Lysosomes - metabolism | Mitochondria - genetics | Mucolipidoses - metabolism | Brain - pathology | TRPM Cation Channels - genetics | Vacuoles - metabolism | Fluorescent Dyes - pharmacology | Lysosomes - pathology | Mice | Index Medicus | Molecular Bases of Disease | Lysosomes | Reports | Ion channels | Iron | Lysosomal storage disease
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4. Full Text Neurologic, Gastric, and Opthalmologic Pathologies in a Murine Model of Mucolipidosis Type IV
by Venugopal, Bhuvarahamurthy and Browning, Marsha F and Curcio-Morelli, Cyntia and Varro, Andrea and Michaud, Norman and Nanthakumar, Nanda and Walkley, Steven U and Pickel, James and Slaugenhaupt, Susan A
The American Journal of Human Genetics, ISSN 0002-9297, 2007, Volume 81, Issue 5, pp. 1070 - 1083
Mucolipidosis type IV (MLIV) is an autosomal recessive lysosomal storage disorder caused by mutations in the gene, which encodes the 65-kDa protein... 
TARGETED DISRUPTION | GENE | CATION CHANNEL | ACID-SECRETION | MOUSE MODEL | DISEASE | GENETICS & HEREDITY | ABNORMAL TRANSPORT | LYSOSOMAL STORAGE | MEMBRANE-PROTEIN | CULTURED FIBROBLASTS | TRPM Cation Channels - deficiency | Body Weight | Eye Diseases - complications | Gastric Mucosa - pathology | Stomach Diseases - pathology | Paralysis - pathology | Transient Receptor Potential Channels | Stomach Diseases - complications | Eye Diseases - pathology | Pyramidal Cells - ultrastructure | Disease Models, Animal | Nervous System Diseases - pathology | Gastrins - blood | Gene Targeting | Inclusion Bodies - ultrastructure | Longevity | Nervous System Diseases - complications | Mice, Knockout | Gastric Mucosa - ultrastructure | Mucolipidoses - complications | Mucolipidoses - pathology | Animals | Hindlimb - pathology | Survival Analysis | Mice | Retinal Degeneration - pathology | Models | Research | Mucolipidoses | Mutation (Biology) | Gastrin | Neurology | Pathology | Ophthalmology | Digestive system | Rodents | Genes | Index Medicus
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5. Full Text Exon-specific U1 snRNAs improve ELP1 exon 20 definition and rescue ELP1 protein expression in a familial dysautonomia mouse model
by Donadon, Irving and Pinotti, Mirko and Rajkowska, Katarzyna and Pianigiani, Giulia and Barbon, Elena and Morini, Elisabetta and Motaln, Helena and Rogelj, Boris and Mingozzi, Federico and Slaugenhaupt, Susan A and Pagani, Franco
Human Molecular Genetics, ISSN 0964-6906, 07/2018, Volume 27, Issue 14, pp. 2466 - 2476
Abstract Familial dysautonomia (FD) is a rare genetic disease with no treatment, caused by an intronic point mutation (c.2204+6T>C) that negatively affects the... 
DEFECTS | COMPLEX | SPINAL MUSCULAR-ATROPHY | MESSENGER-RNA | SMALL NUCLEAR-RNA | BIOCHEMISTRY & MOLECULAR BIOLOGY | GENETICS & HEREDITY | GENE-THERAPY | MUTATIONS | 5' SPLICE-SITE | IKBKAP GENE | ELONGATOR | Index Medicus
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6. Full Text Mutations in DCHS1 cause mitral valve prolapse
by Durst, Ronen and Sauls, Kimberly and Peal, David S and DeVlaming, Annemarieke and Toomer, Katelynn and Leyne, Maire and Salani, Monica and Talkowski, Michael E and Brand, Harrison and Perrocheau, Maëlle and Simpson, Charles and Jett, Christopher and Stone, Matthew R and Charles, Florie and Chiang, Colby and Lynch, Stacey N and Bouatia-Naji, Nabila and Delling, Francesca N and Freed, Lisa A and Tribouilloy, Christophe and Le Tourneau, Thierry and LeMarec, Hervé and Fernandez-Friera, Leticia and Solis, Jorge and Trujillano, Daniel and Ossowski, Stephan and Estivill, Xavier and Dina, Christian and Bruneval, Patrick and Chester, Adrian and Schott, Jean-Jacques and Irvine, Kenneth D and Mao, Yaopan and Wessels, Andy and Motiwala, Tahirali and Puceat, Michel and Tsukasaki, Yoshikazu and Menick, Donald R and Kasiganesan, Harinath and Nie, Xingju and Broome, Ann-Marie and Williams, Katherine and Johnson, Amanda and Markwald, Roger R and Jeunemaitre, Xavier and Hagege, Albert and Levine, Robert A and Milan, David J and Norris, Russell A and Slaugenhaupt, Susan A
Nature, ISSN 0028-0836, 09/2015, Volume 525, Issue 7567, pp. 109 - 113
Mitral valve prolapse (MVP) is a common cardiac valve disease that affects nearly 1 in 40 individuals(1-3). It can manifest as mitral regurgitation and is the... 
GENE | QUANTIFICATION | REGURGITATION | MULTIDISCIPLINARY SCIENCES | FAT | ECHOCARDIOGRAPHIC EVIDENCE | IDENTIFICATION | EXPRESSION | LOCUS | FILAMIN-A | Cadherins - metabolism | Humans | Male | Mitral Valve - surgery | Mitral Valve Prolapse - genetics | Cell Movement - genetics | Female | Protein Stability | Cadherins - genetics | Zebrafish Proteins - metabolism | RNA, Messenger - genetics | Mitral Valve Prolapse - pathology | Chromosomes, Human, Pair 11 - genetics | Mutation - genetics | Zebrafish - genetics | Phenotype | Animals | Pedigree | Mitral Valve - embryology | Mice | Mitral Valve - pathology | Zebrafish Proteins - genetics | Body Patterning - genetics | Mitral Valve - abnormalities | Cadherins - deficiency | Cadherins | Mitral valve prolapse | Genetic aspects | Health aspects | Mutation (Biology) | Proteins | Studies | Genotype & phenotype | Disease | Rodents | Zebrafish | Cardiovascular disease | Mutation | Gene expression | Chromosomes | Cell adhesion & migration | Index Medicus | Life Sciences
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7. Full Text Genetic association analyses highlight biological pathways underlying mitral valve prolapse
by Dina, C and Bouatia-Naji, N and Tucker, N and Delling, FN and Toomer, K and Durst, R and Perrocheau, M and Fernandez-Friera, L and Solis, J and Le Tourneau, T and Chen, MH and Probst, V and Bosse, Y and Pibarot, P and Zelenika, D and Lathrop, M and Hercberg, S and Roussel, R and Benjamin, EJ and Bonnet, F and Lo, SH and Dolmatova, E and Simonet, F and Lecointe, S and Kyndt, F and Redon, R and Le Marec, H and Froguel, P and Ellinor, PT and Vasan, RS and Bruneval, P and Markwald, RR and Norris, RA and Milan, DJ and Slaugenhaupt, SA and Levine, RA and Schott, JJ and Hagege, AA and Jeunemaitre, X and PROMESA Investigators and Leducq Transatlantic MITRAL Networ and MVP-France and Leducq Transatlantic MITRAL Network and PROMESA investigators
NATURE GENETICS, ISSN 1061-4036, 10/2015, Volume 47, Issue 10, pp. 1206 - 1206
Nonsyndromic mitral valve prolapse (MVP) is a common degenerative cardiac valvulopathy of unknown etiology that predisposes to mitral regurgitation, heart... 
PATHOGENESIS | METAANALYSIS | CARDIAC VALVULAR DYSTROPHY | CELL-MIGRATION | MARFAN-SYNDROME | GENETICS & HEREDITY | NATURAL-HISTORY | EXPRESSION | LOCUS | FILAMIN-A | GENOME-WIDE ASSOCIATION | Genome-Wide Association Study | Mice | Animals | Mitral Valve Prolapse - genetics | Humans | Case-Control Studies | Genome-wide association studies | Mitral valve prolapse | Genetic susceptibility | Genetic research | Development and progression | Genetic aspects | Research | Methods | Index Medicus | Life Sciences | Human health and pathology | Genetics | Human genetics | Cardiology and cardiovascular system
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8. Full Text Sensory and autonomic deficits in a new humanized mouse model of familial dysautonomia
by Morini, Elisabetta and Dietrich, Paula and Salani, Monica and Downs, Heather M and Wojtkiewicz, Gregory R and Alli, Shanta and Brenner, Anthony and Nilbratt, Mats and LeClair, John W and Oaklander, Anne Louise and Slaugenhaupt, Susan A and Dragatsis, Ioannis
Human Molecular Genetics, ISSN 0964-6906, 08/2015, Volume 25, Issue 6, pp. 1116 - 1128
Familial dysautonomia (FD) is an autosomal recessive neurodegenerative disease that affects the development and survival of sensory and autonomic neurons. FD... 
TRANSFER-RNA MODIFICATION | CELL-MIGRATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | TRANSCRIPTION | MUTATION | GENETICS & HEREDITY | SKIN BIOPSY | DORSAL-ROOT GANGLION | ELONGATOR COMPLEX | EXPRESSION | SPLICING DEFECT | IKBKAP GENE | Dysautonomia, Familial - pathology | Alternative Splicing | Exons | Introns | Humans | Male | Mice, Transgenic | RNA, Messenger - metabolism | Carrier Proteins - genetics | Animals | Carrier Proteins - metabolism | RNA Splicing - genetics | Autonomic Pathways - metabolism | Mice | Neurons - metabolism | Sensory Receptor Cells - metabolism | Mutation | Dysautonomia, Familial - metabolism | Disease Models, Animal | Dysautonomia, Familial - genetics | Index Medicus
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9. Full Text Loss of Mouse Ikbkap, a Subunit of Elongator, Leads to Transcriptional Deficits and Embryonic Lethality That Can Be Rescued by Human IKBKAP
by Yei-Tsung Chen and Matthew M. Hims and Ranjit S. Shetty and James Mull and Lijuan Liu and Maire Leyne and Susan A. Slaugenhaupt
Molecular and Cellular Biology, ISSN 0270-7306, 02/2009, Volume 29, Issue 3, pp. 736 - 744
Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley... 
FAMILIAL DYSAUTONOMIA | PROTEIN | IKAP | GENE | HEMATOPOIESIS | BIOCHEMISTRY & MOLECULAR BIOLOGY | MUTATION | B KINASE COMPLEX | HISTONE ACETYLATION | TIE2 RECEPTOR | CELL-DEATH | CELL BIOLOGY | Blood Vessels - abnormalities | Humans | Male | Embryo, Mammalian - metabolism | Protein Subunits - metabolism | Blood Vessels - embryology | Embryo Loss - pathology | Gene Expression Regulation, Developmental | Gene Deletion | Female | Transcription, Genetic | Extraembryonic Membranes - embryology | Embryo Loss - genetics | Transgenes | Extraembryonic Membranes - abnormalities | Gene Targeting | Embryonic Development | Embryo, Mammalian - abnormalities | Mice, Knockout | Animals | Carrier Proteins - metabolism | Protein Subunits - deficiency | Heterozygote | Mice | Crosses, Genetic | Index Medicus
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10. Full Text Macroautophagy is defective in mucolipin-1-deficient mouse neurons
by Curcio-Morelli, Cyntia and Charles, Florie A and Micsenyi, Matthew C and Cao, Yi and Venugopal, Bhuvarahamurthy and Browning, Marsha F and Dobrenis, Kostantin and Cotman, Susan L and Walkley, Steven U and Slaugenhaupt, Susan A
Neurobiology of Disease, ISSN 0969-9961, 2010, Volume 40, Issue 2, pp. 370 - 377
Abstract Mucolipidosis type IV is a neurodegenerative lysosomal disease clinically characterized by psychomotor retardation, visual impairment, and... 
Neurology | Mucolipidosis type IV | Mucolipin 1 | Lysosomal disease | Neuronal storage | Macroautophagy | UBIQUITIN-PROTEASOME SYSTEM | CHAPERONE-MEDIATED AUTOPHAGY | MUCOLIPIDOSIS TYPE-IV | TRAFFICKING | MEMBRANE-PROTEIN | ALPHA-SYNUCLEIN | MODEL | LYSOSOMAL STORAGE DISORDERS | NEUROSCIENCES | MONITORING AUTOPHAGY | DISEASE | Neurons - pathology | TRPM Cation Channels - deficiency | Lysosome-Associated Membrane Glycoproteins - metabolism | Microtubule-Associated Proteins - metabolism | Sequestosome-1 Protein | Heat-Shock Proteins - metabolism | Cells, Cultured | Ubiquitin - metabolism | Mucolipidoses - genetics | Transient Receptor Potential Channels | Microscopy, Electron | Amines - metabolism | Autophagy | Mice, Knockout | Transcription Factors - metabolism | Microscopy, Confocal | Animals | Neurons - ultrastructure | Mucolipidoses - metabolism | TRPM Cation Channels - genetics | Mice | Neurons - metabolism | Adaptor Proteins, Signal Transducing - metabolism | Microscopy, Fluorescence | Ubiquitin | Cell research | Proteases | Neurons | Analysis | Index Medicus
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11. Full Text Robust lysosomal calcium signaling through channel TRPML1 is impaired by lysosomal lipid accumulation
by Gomez, Nestor Mas and Lu, Wennan and Lim, Jason C and Kiselyov, Kirill and Campagno, Keith E and Campagno, Yulia and Slaugenhaupt, Susan A and Pfeffer, Bruce A and Fliesler, Steven J and Mitchell, Claire H
FASEB Journal, ISSN 0892-6638, 02/2018, Volume 32, Issue 2, pp. 782 - 794
The transient receptor potential cation channelmucolipin 1 (TRPML1) channel is a conduit for lysosomal calcium efflux, and channel activity may be affected by... 
Calcium signaling | Mucolipin | Cellular aging | Lysosomal storage disease | RPE | STEM-CELLS | ACTIVATION | LIPOFUSCIN | lysosomal storage disease | mucolipin | MUCOLIPIDOSIS TYPE-IV | BIOCHEMISTRY & MOLECULAR BIOLOGY | calcium signaling | cellular aging | AUTOPHAGY | CELL BIOLOGY | GENE | DISEASE | BIOLOGY | ION CHANNELS | Cell Line | Retinal Pigment Epithelium - metabolism | Calcium - metabolism | Humans | Lipid Metabolism | Transient Receptor Potential Channels - agonists | Quinolines - pharmacology | Mice, Knockout | Macular Degeneration - metabolism | Phthalimides - pharmacology | Retinal Pigment Epithelium - pathology | Animals | Lysosomes - metabolism | Macular Degeneration - congenital | Macular Degeneration - genetics | Transient Receptor Potential Channels - genetics | Lysosomes - pathology | Mice | Transient Receptor Potential Channels - metabolism | Calcium Signaling | Disease Models, Animal | Macular Degeneration - pathology | Index Medicus | Research
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12. Full Text Genetic association analyses highlight biological pathways underlying mitral valve prolapsed
by Dina, Christian and Bouatia-Naji, Nabila and Tucker, Nathan and Delling, Francesca N and Toomer, Katelynn and Durst, Ronen and Perrocheau, Maelle and Fernandez-Friera, Leticia and Solis, Jorge and Le Tourneau, Thierry and Chen, Ming-Huei and Probst, Vincent and Bosse, Yohan and Pibarot, Philippe and Zelenika, Diana and Lathrop, Mark and Hercberg, Serge and Roussel, Ronan and Benjamin, Emelia J and Bonnet, Fabrice and Lo, Su Hao and Dolmatova, Elena and Simonet, Floriane and Lecointe, Simon and Kyndt, Florence and Redon, Richard and Le Marec, Hervé and Froguel, Philippe and Ellinor, Patrick T and Vasan, Ramachandran S and Bruneval, Patrick and Markwald, Roger R and Norris, Russell A and Milan, David J and Slaugenhaupt, Susan A and Levine, Robert A and Schott, Jean-Jacques and Hagege, Albert A and Jeunemaitre, Xavier
Nature Genetics, ISSN 1061-4036, 09/2015, Volume 47, Issue 10, pp. 1206 - 1211
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