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anti-Human Dystroglycan Antibodies:
anti-Rat (Rattus) Dystroglycan Antibodies:
anti-Mouse (Murine) Dystroglycan Antibodies:
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Cow (Bovine) Monoclonal Dystroglycan Primary Antibody for IA, ICC - ABIN4279745
Annese, Corsi, Ruggieri, Tamma, Marinaccio, Picocci, Errede, Specchia, De Luca, Frassanito, Desantis, Vacca, Ribatti, Nico: Isolation and characterization of neural stem cells from dystrophic mdx mouse. in Experimental cell research 2016
Show all 2 Pubmed References
Human Monoclonal Dystroglycan Primary Antibody for ELISA, WB - ABIN560555
Hesse, Johansson, Mattsson, Bremell, Andreasson, Halim, Anckarsäter, Blennow, Anckarsäter, Zetterberg, Larson, Hagberg, Grahn: The N-terminal domain of ?-dystroglycan, released as a 38 kDa protein, is increased in cerebrospinal fluid in patients with Lyme neuroborreliosis. in Biochemical and biophysical research communications 2011
We find that the dystroglycan ortholog DGN-1 mediates the fidelity of follower lumbar commissure axon extension along the pioneer axon route
C. elegans dystroglycan (DG) DGN-1 functions to maintain the position of lumbar neurons during late embryonic and larval development.
ten-1 is required for gonadal and pharyngeal basement membrane integrity and acts redundantly with integrin ina-1 and dystroglycan dgn-1
Dystroglycan is involved in skin morphogenesis downstream of the Notch (show NOTCH1 Antibodies) signaling pathway
Dystroglycan is required for proper retinal layering
These data indicate that dystroglycan plays a key role for laminin-1 (show LAMA1 Antibodies) assembly and pronephric cell anchoring to the basement membrane during early development of the pronephros.
Results show that dystroglycan is critical for both proliferation and elongation of somitic cells and that the Dg-cytoplasmic domain is required for laminin assembly at intersomitic boundaries.
Results provide evidence that MMP-2 (show MMP2 Antibodies) bears the potentiality to cleave alpha-DG enriched from rabbit skeletal muscle indicating that this degradation indeed might also occur in vivo.
ISPD (show ISPD Antibodies) and FKTN (show FKTN Antibodies) are essential for the incorporation of ribitol into alpha-dystroglycan.
N-te (show UTRN Antibodies)rminal (show DMD Antibodies)alpha Dystroglyca (show DMD Antibodies)n ELISA signals were significantly reduced in Duchenne muscular dystrophy serum relative to serum from otherwise normal controls.
TMEM5 is a UDP-xylosyl transferase that elaborates the O-mannose glycan structure on alpha-dystroglycan. The authors demonstrate in a zebrafish model as well as in a human patient that defects in TMEM5 result in muscular dystrophy in combination with abnormal brain development.
Our results strongly suggest that the balance and integrity between the dystroglycan alpha and beta subunits are indispensable and responsible for the cell differentiation and proliferation in acute leukemia cells.
interation of DG with laminin and dynamin (show DNM1 Antibodies) is involved in the regulation of AQP4 (show AQP4 Antibodies) internalization
The Muscular Dystrophy Gene TMEM5 Encodes a Ribitol beta1,4-Xylosyltransferase Required for the Functional Glycosylation of Dystroglycan.
Data show that CD93 antigen proved to be phosphorylated on tyrosine 628 and 644 following cell adhesion on laminin through dystroglycan.
Phosphorylation within the cysteine-rich region of dystrophin (show DMD Antibodies) enhances its association with beta-dystroglycan and identifies a potential novel therapeutic target for skeletal muscle wasting.
Novel mutations in DAG1 are associated with asymptomatic hyperCKemia with hypoglycosylation of alpha-dystroglycan.
Depletion of DAG resulted in altered morphology and reduced properties of differentiated HL-60 cells, including chemotaxis, respiratory burst, phagocytic activities and markers of differentiation, implicating DAG as a protein involved in differentiation.
Utrn (show UTRN Antibodies) KO mdx (show DMD Antibodies) mice but not mdx (show DMD Antibodies) mice show decreased expression of serum N-terminal alpha Dystroglycan compared to normal mice.
Loss of dystroglycan glycosylation is associated with dystroglycanopathies leading to a breakdown of muscle cell membrane integrity and eventual degeneration.
Integrin beta1 and dystroglycan compensate each other to mediate laminin-dependent basement membrane assembly and epiblast polarization.
Cleavage of beta-DG still occurred when both MMP-2 (show MMP2 Antibodies) and MMP-9 (show MMP9 Antibodies) were knocked out in gamma - sarcoglycan (show SGCG Antibodies)-deficient mice. The study found that up-regulation of MMP-14 (show MMP14 Antibodies) is capable of cleaving beta-DG, and it may be involved in the pathogenesis of sarcoglycanopathy.
we provide evidence that a subset of GABAergic interneurons requires dystroglycan for formation and maintenance of axonal terminals on pyramidal cells
These findings reveal a role for dystroglycan in orchestrating both the assembly and function of the subventricular zone neural stem cell niche
Fktn (show FKTN Antibodies) deficient mice express moderate to severe muscular dystrophy; glycosylated alpha-dystroglycan has a unique role in muscle regeneration in these mice
5-amino-4-imidazolecarboxamide riboside treatment increases utrophin (show UTRN Antibodies) A and beta-dystroglycan expression in mdx (show DMD Antibodies) mouse muscle.
Results suggest that by interfering in the cross-talk between the transmembrane form of the laminin receptor dystroglycan and F-actin, AHNAK1 (show AHNAK Antibodies) influences the cytoskeleton organization of Schwann cells
in Drosophila the microRNA complex miR (show MYLIP Antibodies)-310s acts as an executive mechanism to buffer levels of the muscular dystrophy-associated extracellular matrix receptor dystroglycan via its alternative 3'-UTR (show UTS2R Antibodies)
photoreceptor(R) cell differentiation defects appear at the same stage in a deficiency line Df(2R)Dg(248) that affects Dystroglycan (DG) and the neighboring mitochondrial ribosomal gene, mRpL34; findings discussed in view of recent work implicating DG as a regulator of cell metabolism and its genetic interaction with mRpL34
Nrk, mbl, capt and Cam genetically interact with dystrophin and/or dystroglycan in the process of axon path-finding in the eye.
differential splicing of Dystroglycan is developmentally regulated and tissue-specific
only dystroglycan, but not dystrophin deficiency causes myodegeneration induced by energetic stress suggesting that dystroglycan might be a component of the low-energy pathway and act as a transducer of energetic stress in normal and dystrophic muscles
the primary function of Dystroglycan in oogenesis is to organize cellular polarity
Dystroglycan links EGF receptor (show EGFR Antibodies)-induced repression of the anterior follicle cell fate and anterior-posterior polarity formation in the oocyte
The interaction of perlecan and dystroglycan at the basal side of the epithelium promotes basal membrane differentiation and is required for maintenance of cell polarity in the follicle-cell epithelium.
The synaptic role of Dystroglycan (Dg) in Drosophila, is studied.
reduced expression of dystroglycan induced tolerance to cold as well as preference for low temperature; sustained increase in mitochondrial oxidative metabolism caused by reduced expression of DmDG accounted for the cryophilic phenotype of the atu mutant
Patchytail fish contain a point mutation (c.1700T>A) in dag1, resulting in a missense change leading to skeletal muscle defects, brain abnormalities and ocular defects in posterior as well as anterior chambers.
Removal of dystroglycan causes severe muscular dystrophy in zebrafish embryos.
genetic evidence that neuromuscular synapse formation can occur in the absence of MuSK and that the combinatorial function of UnpFL/MuSK and dystroglycan generates diverse patterns of vertebrate neuromuscular innervation
Dystroglycan is a laminin binding component of the dystrophin-glycoprotein complex which provides a linkage between the subsarcolemmal cytoskeleton and the extracellular matrix. Dystroglycan 1 is a candidate gene for the site of the mutation in autosomal recessive muscular dystrophies. The dramatic reduction of dystroglycan 1 in Duchenne muscular dystrophy leads to a loss of linkage between the sarcolemma and extracellular matrix, rendering muscle fibers more susceptible to necrosis. Dystroglycan also functions as dual receptor for agrin and laminin-2 in the Schwann cell membrane. The muscle and nonmuscle isoforms of dystroglycan differ by carbohydrate moieties but not protein sequence. Alternative splicing results in multiple transcript variants all encoding the same protein.
DystroGlycaN family member (dgn-1)
, DystroGlycaN family member (dgn-2)
, DystroGlycaN family member (dgn-3)
, dystrophin-associated glycoprotein 1
, dystroglycan 1
, dystroglycan 1 (dystrophin-associated glycoprotein 1)
, RAB7, member RAS oncogene family
, glycine cleavage system T-protein
, dystrophin associated glycoprotein 1
, dystrophin-associated glycoprote