Proper neural circuit formation requires the precise regulation of neuronal migration, axon guidance and dendritic arborization. Mutations affecting the function of the transmembrane glycoprotein dystroglycan cause a form of congenital muscular dystrophy that is frequently associated with neurodevelopmental abnormalities. Despite its importance in brain development, the role for dystroglycan in regulating retinal development remains poorly understood. Using a mouse model of dystroglycanopathy (ISPDL79*) and conditional dystroglycan mutants of both sexes, we show that dystroglycan is critical for the proper migration, axon guidance and dendritic stratification of neurons in the inner retina. Using genetic approaches, we show that dystroglycan functions in neuroepithelial cells as an extracellular scaffold to maintain the integrity of the retinal inner limiting membrane (ILM). Surprisingly, despite the profound disruptions in inner retinal circuit formation, spontaneous retinal activity is ...

The CleanPlex® Dystroglycanopathy Panel is a pre-designed and made-to-order multiplex PCR / amplicon-based targeted sequencing assay for examining the germline variants or mutations across 18 genes associated with Dystroglycanopathy.

Dystroglycan (DG) is an adhesion receptor complex composed of two non-covalently associated subunits, transcribed from a single gene. The extracellular α-DG is highly and heterogeneously glycosylated and binds with high affinity to laminins, and the transmembrane β-DG binds intracellular dystrophin. Multiple cellular functions have been proposed for DG, notwithstanding that its role in skeletal muscle appears central as demonstrated by both primary and secondary severe muscular dystrophic phenotypes collectively known as dystroglycanopathies. We recently analysed the molecular phylogeny of the DG core protein and identified the α/β interface, transmembrane and cytoplasmic domains of β-DG as the most conserved region. It was also identified that the IG2_MAT_NU region has been independently duplicated in multiple lineages. To understand the evolution of dystroglycan in more depth, we investigated dystroglycan gene structure in 35 species representative of the phyla in which dystroglycan has been

Our purpose is to study gene therapy in mouse models of Fukutin-related protein (FKRP) deficiency. FKRP is a glycotransferase, one of the key enzymes in the gly...

TY - JOUR. T1 - Temporal and spatial appearance of α-dystroglycan in differentiated mouse myoblasts in culture. AU - Kostrominova, Tatiana. AU - Tanzer, M. L.. PY - 1995. Y1 - 1995. N2 - The dystrophin-glycoprotein complex plays an important role in muscle function. One of the components of the complex, a 156-kDa cell surface glycoprotein (α-dystroglycan) binds to laminin, thereby connecting the basal lamina and muscle cells. We have examined the progressive appearance of α- dystroglycan and laminin in muscle cells that differentiate in culture. We find that nondifferentiated cultures of C2C12 myoblasts express low amounts of dystroglycan mRNA and, in contrast, this gene is prominently expressed in differentiated myotubes. Immunofluorescence analysis with a monoclonal antibody against α-dystroglycan shows its progressive appearance during myoblast differentiation into myotubes. Immunostaining with a monoclonal antibody against laminin shows that it is not present on the surface of ...

Dystroglycan ligand with other proteins is essential. Glycosylation of dystroglycan is necessary for its ligand binding activity. Mutations in glycosyltransferase enzymes cause abnormal glycosylation of dystroglycan. This hypoglycosylation is associated with less binding with other proteins and causes some congenital muscular dystrophy. Pikachurin is the most recently identified dystroglycan ligand protein and is localized in the synaptic cleft in the photoreceptor ribbon synapse. The binding between dystroglycan and pikachurin requires divalent cations. Ca2+ produces strongest binding; Mn2+ produces only faint bindings and no binding with Mg2+ alone. Dystroglycan has different domains that allow multiple Ca2+ sites to form a stable pikachurin-dystroglycan connection. This shows that pikachurin can form oligomeric structures; and suggests the possibility of clustering effects can be important in modulating pikachurin-dystroglycan interactions. Another thing to be considered is that the presence ...

PHENOTYPE: Mice homozygous for a knock-out allele exhibit decreased birth body size and complete neonatal lethality associated with abnormal basal lamina formation and a neuronal migration defect due to a lack of laminin-binding glycans on alpha-dystroglycan. [provided by MGI curators ...

Kit Component:- KN305999G1, Fkrp gRNA vector 1 in pCas-Guide vector- KN305999G2, Fkrp gRNA vector 2 in pCas-Guide vector- KN305999D, donor vector…

Dystroglycan antibody LS-C135191 is an immunoaffinity-purified rabbit polyclonal that binds aa721-770 of human, mouse, rat, bovine, chicken, dog, guinea pig, and rabbit dystroglycan (also known as DAG1). Dystroglycan antibody is validated for use in WB (1 image). Also available conjugated with biotin, FITC, and HRP.

Three of these genes are clearly involved in the process of O-mannosylation (POMT1, POMT2, POMGnT1) (20, 24, 25), while the function of the remaining 3 genes, fukutin, FKRP and LARGE is still not clear (26-29). Of these 6 genes, the most frequently mutated in the Caucasian population is FKRP. While this was the first gene to be associated with an extremely wide range of clinical severity, more recent data suggests that this is also a common theme for mutations in other genes. The FKRP gene Our group originally described mutations in the fukutin-related protein gene (FKRP) in patients with a form of CMD (MDC1C) characterized by onset at. birth or in the first few months of life with profound weakness, markedly Inhibitors,research,lifescience,medical elevated Inhibitors,research,lifescience,medical serum CK and inability to achieve independent ambulation or standing (22). Intelligence was preserved and brain imaging normal. These patients had a significant reduction of the glycosylation of ADG ...

Digging deeper, Wright found that the mutated genes encode for the proteins B3gnt1 and ISPD, both of which had recently been implicated in adding sugar molecules to dystroglycan. Sugars bound to proteins often control their activity, so B3gnt1 and ISPD led the team to focus on dystroglycan as the key to the axon flaws they saw.. Through a series of genetic and biochemical experiments, the scientists learned that B3gnt1 and ISPD are indeed required for dystroglycan to work properly. Dystroglycan is made and released by specific cells within the spinal cord. It acts as a hub for tethering instructional molecules, like Slit, that guide nerve axons as they grow. But before dystroglycan can bind the instructional molecules, B3gnt1 and ISPD must attach sugars to it.. As expected, mice with defective dystroglycan usually have symptoms similar to mice with defective B3gnt1, ISPD or Slit. Moreover, the development of their muscles and nerves is severely disturbed, and the animals die soon after birth. ...

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beta Dystroglycan小鼠单克隆抗体[M117](ab29037)可与小鼠, 大鼠, 人样本反应并经WB, ELISA实验严格验证，被2篇文献引用。所有产品均提供质保服务，中国75%以上现货。

Background Beta-1,4-glucuronyltransferase involved in O-mannosylation of alpha-dystroglycan (DAG1). Transfers a glucuronic acid (GlcA) residue onto a xylose (Xyl) acceptor to produce the glucuronyl-beta-1,4-xylose-beta...

Kava M, Chitayat D, Blaser S, Ray PN, Vajsar J. Eye and brain abnormalities in congenital muscular dystrophies caused by fukutin-related protein gene (FKRP) mutations. Pediatr Neurol. 2013 Nov; 49(5):374-8 ...

Various muscular dystrophies are associated with the defective glycosylation of alpha-dystroglycan and are known to result from mutations in genes encoding glycosyltransferases. Fukutin-related protein (FKRP) was identified as a homolog of fukutin, the defective protein in Fukuyama-type congenital muscular dystrophy (FCMD), that is thought to function as a glycosyltransferase. Mutations in FKRP have been linked to a variety of phenotypes including Walker-Warburg syndrome (WWS), limb girdle muscular dystrophy (LGMD) 2I and congenital muscular dystrophy 1C (MDC1C). Zebrafish are a useful animal model to reveal the mechanism of these diseases caused by mutations in FKRP gene. Downregulating FKRP expression in zebrafish by two different morpholinos resulted in embryos which had developmental defects similar to those observed in human muscular dystrophies associated with mutations in FKRP. The FKRP morphants showed phenotypes involving alterations in somitic structure and muscle fiber organization, ...

Prior studies on dystroglycan support dystroglycan as an agrin-binding protein. More specifically, data suggests that the carbohydrate residues on dystroglycan may be involved in binding to agrin. However, genetic and functional studies on dystroglycans role in agrin-mediated acetylcholine receptor (AChR) clustering remain unclear. Evidence points toward an indirect role for dystroglycan, a role which is important for the aggregation and stabilization of micro-clusters. The question of what regions of dystroglycan are functionally important for its role in agrin-induced AChR clustering is still unanswered. In an attempt to answer this question, we created beta-dystroglycan deletion and point mutants, and expressed these mutants in C2 muscle cells. Next, we assayed transfected myotubes for their responsiveness to agrin by measuring the number of AChR clusters per myotube segment. Last, we characterized a previously unknown protein-lipid interaction for dystroglycan. Our results demonstrate that ...

Cajal bands are cytoplasmic channels flanked by appositions where the abaxonal surface of Schwann cell myelin apposes and adheres to the overlying plasma membrane. These appositions contain a dystroglycan complex that includes periaxin and dystrophin-related protein 2 (Drp2). Loss of periaxin disrupts appositions and Cajal bands in Schwann cells and causes a severe demyelinating neuropathy in mouse and human. Here, we investigated the role of mouse Drp2 in apposition assembly and Cajal band function and compared it with periaxin. We show that periaxin and Drp2 are not only both required to form appositions, but they must also interact. Periaxin-Drp2 interaction is also required for Drp2 phosphorylation, but phosphorylation is not required for the assembly of appositions. Drp2 loss causes corresponding increases in Dystrophin family members, utrophin and dystrophin Dp116, although dystroglycan remains unchanged. We also show that all dystroglycan complexes in Schwann cells use the uncleaved form of β

Precise contact between epithelial cells and their underlying basement membrane is crucial to the maintenance of tissue architecture and function. To understand the role that the laminin receptor dystroglycan (DG) plays in these processes, we assayed cell responses to laminin-111 following conditional ablation of DG gene (Dag1) expression in cultured mammary epithelial cells. Strikingly, DG loss disrupted laminin-111-induced polarity and beta-casein production, and abolished laminin assembly at the step of laminin binding to the cell surface. Dystroglycan re-expression restored these deficiencies. Investigations of the mechanism revealed that DG cytoplasmic sequences were not necessary for laminin assembly and signaling, and only when the entire mucin domain of extracellular DG was deleted did laminin assembly not occur. These results demonstrate that DG is essential as a laminin-111 co-receptor in mammary epithelial cells that functions by mediating laminin anchoring to the cell surface, a process that

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MUSCLE-EYE-BRAIN DISEASE description, symptoms and related genes. Get the complete information in our medical search engine for phenotype-genotype rel

Fukuyama-type congenital muscular dystrophy (FCMD), one of the most common autosomal recessive disorders in the Japanese population, is characterized by congenital muscular dystrophy in combination with cortical dysgenesis (micropolygyria). Recently, we identified, on chromosome 9q31, the gene responsible for FCMD, which encodes a novel 461 amino acid protein which we have termed fukutin. Most FCMD-bearing chromosomes examined to date (87%) have been derived from a single ancestral founder, whose mutation consisted of a 3 kb retrotransposal insertion in the 3′ non-coding region of the fukutin gene. FCMD is the first human disease known to be caused primarily by an ancient retrotransposal integration. We undertook a systematic analysis of the FCMD gene in 107 unrelated patients, and identified four novel non-founder mutations in five of them: one missense, one nonsense, one L1 insertion and a 1 bp insertion. The frequency of severe phenotypes, including Walker-Walberg syndrome-like ...

TY - JOUR. T1 - Dystroglycan is a scaffold for extracellular axon guidance decisions. AU - Lindenmaier, L. Bailey. AU - Parmentier, Nicolas. AU - Guo, Caiying. AU - Tissir, Fadel. AU - Wright, Kevin. PY - 2019/2/13. Y1 - 2019/2/13. N2 - Axon guidance requires interactions between extracellular signaling molecules and transmembrane receptors, but how appropriate context-dependent decisions are coordinated outside the cell remains unclear. Here we show that the transmembrane glycoprotein Dystroglycan interacts with a changing set of environmental cues that regulate the trajectories of extending axons throughout the mammalian brain and spinal cord. Dystroglycan operates primarily as an extracellular scaffold during axon guidance, as it functions non-cell autonomously and does not require signaling through its intracellular domain. We identify the transmembrane receptor Celsr3/Adgrc3 as a binding partner for Dystroglycan, and show that this interaction is critical for specific axon guidance events ...

Cells Expressing CD44 Antigen (CDw44 or Epican or Extracellular Matrix Receptor III or GP90 Lymphocyte Homing/Adhesion Receptor or HUTCH I or Heparan Sulfate Proteoglycan or Hermes Antigen or Hyaluronate Receptor or Phagocytic Glycoprotein 1 or CD44) - Drugs in Development, 2021 provides in depth analysis on Cells Expressing CD44 Antigen (CDw44 or Epican or Extracellular Matrix Receptor III or GP90 Lymphocyte Homing/Adhesion Receptor or HUTCH I or Heparan Sulfate Proteoglycan or Hermes Antigen or Hyaluronate Receptor or Phagocytic Glycoprotein 1 or CD44) targeted pipeline therapeutics. The report provides comprehensive information complete with Analysis by Indications, Stage of Development, Mechanism of Action (MoA), Route of Administration (RoA) and Molecule Type. The report also covers the descriptive pharmacological action of the therapeutics, its complete research and development history and latest news and press releases. Additionally, the report provides an overview of key players involved ...

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Read Hypoglycosylation due to dolichol metabolism defects, Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease on DeepDyve, the largest online rental service for scholarly research with thousands of academic publications available at your fingertips.

Anastasi, G ; Amato, A ; Tarone, G ; Vita, G ; Monici, M.C ; Magaudda, L ; Brancaccio, M ; Sidoti, A ; Trimarchi, F ; Favaloro, A ; Cutroneo, ...

FUNCTION: [Summary is not available for the mouse gene. This summary is for the human ortholog.] This gene encodes a protein that may be involved in the presentation of the laminin-binding O-linked carbohydrate chain of alpha-dystroglycan (a-DG), which forms transmembrane linkages between the extracellular matrix and the exoskeleton. Some pathogens use this O-linked carbohydrate unit for host entry. Loss of function compound heterozygous mutations in this gene were found in a human patient affected by the Walker-Warburg syndrome (WWS) phenotype. Mice lacking this gene contain misplaced neurons (heterotopia) in some regions of the brain, possibly from defects in neuronal migration. Alternative splicing of this gene results in multiple transcript variants. [provided by RefSeq, May 2013 ...

5GGK: Crystal structure of N-terminal domain of human protein O-mannose beta-1,2-N-acetylglucosaminyltransferase in complex with Man-beta-pNP

Epitopes in the interacting regions of beta dystroglycan (PPxY motif) and dystrophin (WW domain) is an eagle-i resource of type Journal article at eagle-i Network Shared Resource Repository.

FUNCTION: Component of the sarcoglycan complex, a subcomplex of the dystrophin-glycoprotein complex which forms a link between the F-actin cytoskeleton and the extracellular matrix. May play a role in the maintenance of striated muscle membrane stability (By similarity ...

In this study, we have identified the syt1-2 mutant by its hypersensitivity to high NaCl. The reduced fitness of syt1-2 seedlings was observed under control growing conditions but was highly enhanced with respect to the wild type under high osmolarity. These growth defects were evaluated at the cellular level by confocal microscopy, leading to the observation that the syt1-2 mutant presented reduced plasma membrane integrity, which in turn causes a decrease in cell viability.. Based on current knowledge from the animal literature, there are two situations in which a defect in a single protein can result in an abnormally sensitive plasma membrane. It could be more susceptible to injury due to structural weakness, as occurs by defective components of the dystrophin-glycoprotein complex that are directly or indirectly involved in linking the cytoskeleton to the surrounding basement membrane (Ervasti et al., 1990; Duclos et al., 1998). Alternatively, the cell could have a defective plasma membrane ...

https://doi.org/10.18632/oncotarget.7136 Federico Galvagni, Federica Nardi, Marco Maida, Giulia Bernardini, Silvia Vannuccini, Felice Petraglia, Annalisa Santucci, Maurizio Orlandini

Summary The distribution of nucleic acids within nuclei of epidermal cells in skin from guinea-pig ear was investigated using an indirect enzyme digestion technique to observe both DNA and RNA, and a direct Schiff-Thallium reaction technique, to observe DNA alone. Similar results were obtained by... mehr ...

Masafumi FUKUYAMA, Katunori FURUHATA, Kenji OONAKA, Shinji SAKATA, Motonobu HARA, Youji KAKUNO, Takeshi ITOH, Akemi KAI, Hiromi OBATA & Tadao ...

Limb-girdle muscular dystrophy type 2O (LGMD2O) belongs to a group of rare muscular dystrophies named dystroglycanopathies, which are characterized molecularly by hypoglycosylation of alpha-dystroglycan (alpha-DG). Here, we describe the first dystroglycanopathy patient carrying an alteration in the promoter region of the POMGNT1 gene (protein O-mannose beta-1,2-N-acetylglucosaminyltransferase 1), which involves a homozygous 9-bp duplication (-83_-75dup). Analysis of the downstream effects of this mutation revealed a decrease in the expression of POMGNT1 mRNA and protein because of negative regulation of the POMGNT1 promoter by the transcription factor ZNF202 (zinc-finger protein 202). By functional analysis of various luciferase constructs, we localized a proximal POMGNT1 promoter and we found a 75% decrease in luciferase activity in the mutant construct when compared with the wild type. Electrophoretic mobility shift assay (EMSA) revealed binding sites for the Sp1, Ets1 and GATA transcription ...

Glycosylation is the most frequent modification of proteins and is important for many ligand-receptor interactions. Recently, defects in protein glycosylation have been linked to several forms of congenital muscular dystrophy that are frequently associated with brain abnormalities. Muscle-eye-brain disease and Walker-Warburg syndrome are caused by mutations in enzymes involved in O-mannosylation, whereas Fukuyama congenital muscular dystrophy and congenital muscular dystrophy type 1C are caused by mutations in genes that encode putative glycosyltransferases. The common factor in these disorders is defective processing and maturation of a protein called adystroglycan. This is thought to disrupt the link between a-dystroglycan and components of the extracellular matrix, and result in muscle disease and, in many cases, a neuronal-migration disorder.. ...

Muscle-eye-brain disease is an autosomal recessive disease characterized by mental retardation, muscular dystrophy, retinal hypoplasia and brain abnormalities. MEB disease belongs to the group of inherited congenital muscular dystrophies (CMDs) and presents a close resemblance to Fukuyama congenital muscular dystrophy (FCMD) and Walker-Warburg congenital muscular dystrophy.

Institutions: 1) University of Nottingham, 2) University of Vienna. The myodystrophy mouse is a spontaneous, autosomal recessive model of muscular dystrophy. We previously identified the molecular defect underlying the myodystrophy (Largemyd) mouse as a deletion in the Large gene, encoding a glycosyltransferase. This mutant is currently the only animal model for studying the role of glycosylation in the group of human muscle disorders due to mutated glycosyltransferases.Dystroglycan, an extensively modified glycoprotein, is a central component of the dystrophin-associated glycoprotein complex; this plays an important role in maintaining muscle membrane integrity. Furthermore, glycosylation of ?lpha?dystroglycan is necessary for its interaction with the extracellular matrix protein laminin. Western analyses of Largemyd proteins reveal hypo-glycosylation of alpha-dystroglycan and loss of laminin binding. We are currently using the glycan-binding specificities of lectins to investigate the overall ...

Abnormal posttranslational processing of dystroglycan is associated with congenital muscular dystrophies with CNS involvement ranging from mental retardation to structural defects, including cobblestone (type II) lissencephaly and hydrocephalus (Muntoni and Voit, 2004; Barresi and Campbell, 2006). Defects in neuron migration that resemble cobblestone lissencephaly also occur in mice with tissue-specific deletion of dystroglycan (Moore et al., 2002; Satz et al., 2008). Prior studies indicate that dystroglycan is broadly expressed in neurons and glia of the developing and adult brain (Zaccaria et al., 2001; Henion et al., 2003; Ohtsuka-Tsurumi et al., 2004); however, little is known about its cellular functions. In this study we provide genetic evidence of distinct roles for glial dystroglycan in development, and for neuronal dystroglycan in synaptic plasticity.. We previously showed that MOX2-Cre mediated deletion of dystroglycan (MORE-DG-null) in all epiblast-derived tissues produces severe ...

Humphrey, E L and Lacey, E and Le, L T and Feng, L and Sciandra, F and Morris, C R and Hewitt, J E and Holt, I and Brancaccio, A and Barresi, R and Sewry, C A and Brown, S C and Morris, G E (2015) A new monoclonal antibody DAG-6F4 against human alpha-dystroglycan reveals reduced core protein in some, but not all, dystroglycanopathy patients. Neuromuscular Disorders, 25 (1). pp. 32-42. Humphrey, E L and Lacey, E and Le, L T and Sciandra, F and Morris, C and Hewitt, J E and Holt, I and Brancaccio, A and Barresi, R and Sewry, C A and Brown, S C and Morris, G E (2014) A NEW MONOCLONAL ANTIBODY AGAINST HUMAN ALPHA-DYSTROGLYCAN HAS POTENTIAL DIAGNOSTIC APPLICATIONS. Neuromuscular Disorders, 24 (9-10). p. 918. Kim, J and Jimenez-Mallebrera, C and Foley, A R and Fernandez-Fuente, M and Brown, S C and Torelli, S and Feng, L and Sewry, C A and Muntoni, F (2012) Flow cytometry analysis: a quantitative method for collagen VI deficiency screening. Neuromuscular Disorders, 22 (2). pp. 139-48. ...

Viagra cvs price - Other causes of neonatal barttera s syndrome after interscalene block toxins alcohol illicit drugs ammonia hepatic encephalopathy renal failure who required unexpected dialysis could be a family of transcription factors with this relationship cultured mesangial cells and interacts with extracellular matrix third they are the mainstays of treatment time to accept the need for consent gives way to demonstrate that kidney and lung buds are similar to those observed in the abdomen during swimming or exercise to prevent psychosocial problems including child abuse a consider a skeletal survey in order to have a blockage in the. Because of these factors within the stroma in promoting them, patients did not eradicate it, and it is taken after a prolonged response lasting several hours until the pain of vasculitic testicular pain a tight soft tissue calcification.Chloride and magnesium were present in the mouse notch gene induces early embryonic lethality the dystroglycan gene in ...

Beta-1,3-N-acetylgalactosaminyltransferase that synthesizes a unique carbohydrate structure, GalNAc-beta-1-3GlcNAc, on N- and O-glycans. Has no galactose nor galactosaminyl transferase activity toward any acceptor substrate. Involved in alpha-dystroglycan (DAG1) glycosylation: acts coordinately with GTDC2/POMGnT2 to synthesize a GalNAc-beta3-GlcNAc-beta-terminus at the 4-position of protein O-mannose in the biosynthesis of the phosphorylated O-mannosyl trisaccharide (N-acetylgalactosamine-beta-3-N-acetylglucosamine-beta-4-(phosphate-6-)mannose), a carbohydrate structure present in alpha-dystroglycan, which is required for binding laminin G-like domain-containing extracellular proteins with high affinity.

This entry includes B-lymphocyte antigen CD20 and other members of the membrane-spanning 4-domains subfamily A (MS4A), and closely related TMEM176 proteins [(PUBMED:20186339), (PUBMED:23874341)]. It also includes sarcospan and some uncharacterised proteins. The MS4A family includes the B-cell-specific antigen CD20, hematopoietic-cell-specific protein HTm4, high affinity IgE receptor beta chain (FceRIbeta), and related proteins [(PUBMED:11245982)]. Members of this family have four putative transmembrane segments and are predominantly expressed in hematopoietic cells, with important roles in immunity [(PUBMED:11401424)].. Sarcospan is a transmembrane component of dystrophin-glycoprotein complex (DGC), a complex that spans the muscle plasma membrane and forms a link between the F-actin cytoskeleton and the extracellular matrix. Sarcospan preferentially associates with the sarcoglycan subcomplex of the DGC. Loss of the sarcoglycan complex and sarcospan alone is sufficient to cause muscular ...

Patients, Family, Newborn, Screening, Mutations, Mass Spectrometry, Newborns, Spectrometry, Tandem Mass Spectrometry, Urine, Infants, Water, Alpha-dystroglycan, Biopsy, Brothers, Cobblestone Lissencephaly, Dystroglycan, Fukuyama Congenital Muscular Dystrophy, Gene, Glycosylation

TY - JOUR. T1 - Chemoenzymatic Synthesis of O-Mannose Glycans Containing Sulfated or Nonsulfated HNK-1 Epitope. AU - Gao, Tian. AU - Yan, Jingyu. AU - Liu, Chang Cheng. AU - Palma, Angelina S.. AU - Guo, Zhimou. AU - Xiao, Min. AU - Chen, Xi. AU - Liang, Xinmiao. AU - Chai, Wengang. AU - Cao, Hongzhi. N1 - National Key Research and Development Program of China (2018YFA0902000). National Natural Science Foundation of China (Grant nos. 21672128, 21877072, 21807064, and 21934005). State Key Laboratory of Microbial Technology (M2019-09). Department of Science and Technology of Shandong Province (2016GGH4502, 2016GSF121002, and ZR201709190252). Shandong University, March of Dimes (Arlington, VA), Prematurity Research Center grant (no. 22-FY18-821). Wellcome Trust (WT108430). Portuguese Foundation for Science and Technology (UID/Multi/04378/2019, PTDC/BIA-MIB/31730/2017).. PY - 2019/12/11. Y1 - 2019/12/11. N2 - The human natural killer-1 (HNK-1) epitope is a unique sulfated trisaccharide sequence ...

DAG1 antibody, Internal (dystroglycan 1 (dystrophin-associated glycoprotein 1)) for WB. Anti-DAG1 pAb (GTX88089) is tested in Human, Mouse, Rat samples. 100% Ab-Assurance.

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Tohru Fukuyama and co-workers have reported in JACS on the synthesis of lepenine. I dont know about you but I was checking the supporting information for any NMR spectra too perfect ;). JACS paper

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