Mammalian O-mannosylation: unsolved questions of structure/function.
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[1] K. Hoyte,et al. Overexpression of the cytotoxic T cell GalNAc transferase in skeletal muscle inhibits muscular dystrophy in mdx mice , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[2] R. U. Margolis,et al. Demonstration of mammalian protein O-mannosyltransferase activity: coexpression of POMT1 and POMT2 required for enzymatic activity. , 2004, Proceedings of the National Academy of Sciences of the United States of America.
[3] K. Campbell,et al. Glycomic Analyses of Mouse Models of Congenital Muscular Dystrophy* , 2011, The Journal of Biological Chemistry.
[4] P. M. Nienaber,et al. Fukutin-related Protein Associates with the Sarcolemmal Dystrophin-Glycoprotein Complex* , 2007, Journal of Biological Chemistry.
[5] Nicolle H. Packer,et al. Mucin‐type O‐glycosylation – putting the pieces together , 2010, The FEBS journal.
[6] S. Carbonetto,et al. Dystroglycan-α, a dystrophin-associated glycoprotein, is a functional agrin receptor , 1994, Cell.
[7] P. Stanley,et al. Mouse Large Can Modify Complex N- and Mucin O-Glycans on α-Dystroglycan to Induce Laminin Binding* , 2005, Journal of Biological Chemistry.
[8] C. Walsh,et al. Mutations in the O-mannosyltransferase gene POMT1 give rise to the severe neuronal migration disorder Walker-Warburg syndrome. , 2002, American journal of human genetics.
[9] I. Kanazawa,et al. Structures of Sialylated O-Linked Oligosaccharides of Bovine Peripheral Nerve α-Dystroglycan , 1997, The Journal of Biological Chemistry.
[10] Paul T Martin,et al. Genetic defects in muscular dystrophy. , 2010, Methods in enzymology.
[11] Susan C. Brown,et al. Mutations in the fukutin-related protein gene (FKRP) identify limb girdle muscular dystrophy 2I as a milder allelic variant of congenital muscular dystrophy MDC1C. , 2001, Human molecular genetics.
[12] N. Smalheiser,et al. Structural Analysis of Sequences O-Linked to Mannose Reveals a Novel Lewis X Structure in Cranin (Dystroglycan) Purified from Sheep Brain* , 1998, The Journal of Biological Chemistry.
[13] Kenji Nakamura,et al. Targeted disruption of exon 52 in the mouse dystrophin gene induced muscle degeneration similar to that observed in Duchenne muscular dystrophy. , 1997, Biochemical and biophysical research communications.
[14] Gerhard K. H. Przemeck,et al. Targeted disruption of the Walker-Warburg syndrome gene Pomt1 in mouse results in embryonic lethality. , 2004, Proceedings of the National Academy of Sciences of the United States of America.
[15] Susan C. Brown,et al. Mutations in the human LARGE gene cause MDC1D, a novel form of congenital muscular dystrophy with severe mental retardation and abnormal glycosylation of alpha-dystroglycan. , 2003, Human molecular genetics.
[16] Doron Betel,et al. Cloning and expression of a novel UDP-GlcNAc:alpha-D-mannoside beta1,2-N-acetylglucosaminyltransferase homologous to UDP-GlcNAc:alpha-3-D-mannoside beta1,2-N-acetylglucosaminyltransferase I. , 2002, The Biochemical journal.
[17] Martin Brockington,et al. Localization and functional analysis of the LARGE family of glycosyltransferases: significance for muscular dystrophy. , 2005, Human molecular genetics.
[18] T. Südhof,et al. A stoichiometric complex of neurexins and dystroglycan in brain , 2001, The Journal of cell biology.
[19] J. Hewitt,et al. Mutant glycosyltransferase and altered glycosylation of alpha-dystroglycan in the myodystrophy mouse. , 2001, Nature genetics.
[20] S. Carbonetto,et al. Dystroglycan-alpha, a dystrophin-associated glycoprotein, is a functional agrin receptor. , 1994, Cell.
[21] R. U. Margolis,et al. Brain Contains HNK-1 Immunoreactive O-Glycans of the Sulfoglucuronyl Lactosamine Series that Terminate in 2-Linked or 2,6-Linked Hexose (Mannose)* , 1997, The Journal of Biological Chemistry.
[22] R. U. Margolis,et al. Novel mannitol-containing oligosaccharides obtained by mild alkaline borohydride treatment of a chondroitin sulfate proteoglycan from brain. , 1979, The Journal of biological chemistry.
[23] Takashi Fujikado,et al. Pikachurin, a dystroglycan ligand, is essential for photoreceptor ribbon synapse formation , 2008, Nature Neuroscience.
[24] K. Campbell,et al. LARGE can functionally bypass α-dystroglycan glycosylation defects in distinct congenital muscular dystrophies , 2004, Nature Medicine.
[25] S. Fujii,et al. N-Acetylglucosaminyltransferase IX Acts on the GlcNAcβ1,2-Manα1-Ser/Thr Moiety, Forming a 2,6-Branched Structure in Brain O-Mannosyl Glycan* , 2004, Journal of Biological Chemistry.
[26] N. Nakanishi,et al. LARGE2 facilitates the maturation of alpha-dystroglycan more effectively than LARGE. , 2005, Biochemical and biophysical research communications.
[27] J. Dennis,et al. Adaptive Regulation at the Cell Surface by N‐Glycosylation , 2009, Traffic.
[28] R. U. Margolis,et al. High prevalence of 2-mono- and 2,6-di-substituted manol-terminating sequences among O-glycans released from brain glycopeptides by reductive alkaline hydrolysis. , 1999, European journal of biochemistry.
[29] K. Campbell,et al. Muscular dystrophies involving the dystrophin-glycoprotein complex: an overview of current mouse models. , 2002, Current opinion in genetics & development.
[30] J. Lowe,et al. Role of glycosylation in development. , 2003, Annual review of biochemistry.
[31] J. Hewitt,et al. Glycosylation defects: a new mechanism for muscular dystrophy? , 2003, Human molecular genetics.
[32] N. Smalheiser,et al. The relationship between perlecan and dystroglycan and its implication in the formation of the neuromuscular junction. , 1998, Cell adhesion and communication.
[33] Liping Yu,et al. O-Mannosyl Phosphorylation of Alpha-Dystroglycan Is Required for Laminin Binding , 2010, Science.
[34] J. Ervasti,et al. Site Mapping and Characterization of O-Glycan Structures on α-Dystroglycan Isolated from Rabbit Skeletal Muscle* , 2010, The Journal of Biological Chemistry.
[35] I. Kanazawa,et al. An ancient retrotransposal insertion causes Fukuyama-type congenital muscular dystrophy , 1998, Nature.
[36] K. Campbell,et al. Dystroglycan: from biosynthesis to pathogenesis of human disease , 2006, Journal of Cell Science.
[37] K. Campbell,et al. Identification of alpha-dystroglycan as a receptor for lymphocytic choriomeningitis virus and Lassa fever virus. , 1998, Science.
[38] M. Mizuno,et al. Muscular dystrophy and neuronal migration disorder caused by mutations in a glycosyltransferase, POMGnT1. , 2001, Developmental cell.
[39] F. Muntoni,et al. Muscular dystrophies due to glycosylation defects , 2008, Neurotherapeutics.
[40] O. Ibraghimov-Beskrovnaya,et al. Primary structure of dystrophin-associated glycoproteins linking dystrophin to the extracellular matrix , 1992, Nature.
[41] K. Davies,et al. Muscular Dystrophy—Reason for Optimism? , 2002, Cell.
[42] Susan C. Brown,et al. Defective glycosylation in congenital muscular dystrophies , 2004, Current opinion in neurology.
[43] Eric P. Hoffman,et al. Dystrophin: The protein product of the duchenne muscular dystrophy locus , 1987, Cell.
[44] Susan C. Brown,et al. Mutations in the fukutin-related protein gene (FKRP) cause a form of congenital muscular dystrophy with secondary laminin alpha2 deficiency and abnormal glycosylation of alpha-dystroglycan. , 2001, American journal of human genetics.
[45] K. Campbell,et al. Posttranslational Modification of α-Dystroglycan, the Cellular Receptor for Arenaviruses, by the Glycosyltransferase LARGE Is Critical for Virus Binding , 2005, Journal of Virology.
[46] Munhyang Lee,et al. Worldwide distribution and broader clinical spectrum of muscle-eye-brain disease. , 2003, Human molecular genetics.
[47] Takehiro Suzuki,et al. Regulation of Mammalian Protein O-Mannosylation , 2007, Journal of Biological Chemistry.
[48] I. Dunham,et al. The human LARGE gene from 22q12.3-q13.1 is a new, distinct member of the glycosyltransferase gene family. , 1999, Proceedings of the National Academy of Sciences of the United States of America.
[49] Leszek Rychlewski,et al. Comprehensive classification of nucleotidyltransferase fold proteins: identification of novel families and their representatives in human , 2009, Nucleic acids research.
[50] I. Kanazawa,et al. Structures of sialylated O-linked oligosaccharides of bovine peripheral nerve alpha-dystroglycan. The role of a novel O-mannosyl-type oligosaccharide in the binding of alpha-dystroglycan with laminin. , 1997, The Journal of biological chemistry.
[51] F. Muntoni,et al. Mutations in the FKRP gene can cause muscle-eye-brain disease and Walker–Warburg syndrome , 2004, Journal of Medical Genetics.
[52] T. Willer,et al. Characterization of POMT2, a novel member of the PMT protein O-mannosyltransferase family specifically localized to the acrosome of mammalian spermatids. , 2002, Glycobiology.
[53] Jonas Nilsson,et al. Characterization of site-specific O-glycan structures within the mucin-like domain of alpha-dystroglycan from human skeletal muscle. , 2010, Glycobiology.
[54] T. Endo. O-mannosyl glycans in mammals. , 1999, Biochimica et biophysica acta.
[55] P. Stanley,et al. Mutational and functional analysis of Large in a novel CHO glycosylation mutant. , 2009, Glycobiology.
[56] A. Coloma,et al. Identification of a human homolog of the Drosophila rotated abdomen gene (POMT1) encoding a putative protein O-mannosyl-transferase, and assignment to human chromosome 9q34.1. , 1999, Genomics.
[57] N. Nakanishi,et al. LARGE2 facilitates the maturation of α-dystroglycan more effectively than LARGE , 2005 .
[58] J. Ervasti,et al. Membrane organization of the dystrophin-glycoprotein complex , 1991, Cell.
[59] Michael D. Henry,et al. Loss of α-Dystroglycan Laminin Binding in Epithelium-derived Cancers Is Caused by Silencing of LARGE*S⃞♦ , 2009, Journal of Biological Chemistry.
[60] K. Matsumura,et al. Detection of O-mannosyl glycans in rabbit skeletal muscle α-dystroglycan , 1998 .
[61] P. Stanley,et al. Mouse large can modify complex N- and mucin O-glycans on alpha-dystroglycan to induce laminin binding. , 2005, The Journal of biological chemistry.
[62] J. Hewitt,et al. Mutant glycosyltransferase and altered glycosylation of α-dystroglycan in the myodystrophy mouse , 2001, Nature Genetics.
[63] S. Fujii,et al. N-Acetylglucosaminyltransferase IX acts on the GlcNAc beta 1,2-Man alpha 1-Ser/Thr moiety, forming a 2,6-branched structure in brain O-mannosyl glycan. , 2004, The Journal of biological chemistry.
[64] L. Kunkel,et al. Diagnosis and cell-based therapy for Duchenne muscular dystrophy in humans, mice, and zebrafish , 2006, Journal of Human Genetics.
[65] Doron Betel,et al. Cloning and expression of a novel UDP-GlcNAc:α-d-mannoside β1,2-N-acetylglucosaminyltransferase homologous to UDP-GlcNAc:α-3-d-mannoside β1,2-N-acetylglucosaminyltransferase I , 2002 .
[66] Paul T Martin,et al. Congenital muscular dystrophies involving the O-mannose pathway. , 2007, Current molecular medicine.
[67] Shun–ichi Kobayashi. Tokyo campus rising , 1998, Nature.