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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 ELISA Kits) signaling pathway
Dystroglycan is required for proper retinal layering
These data indicate that dystroglycan plays a key role for laminin-1 (show LAMA1 ELISA Kits) 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 ELISA Kits) bears the potentiality to cleave alpha-DG enriched from rabbit skeletal muscle indicating that this degradation indeed might also occur in vivo.
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 ELISA Kits) is involved in the regulation of AQP4 (show AQP4 ELISA Kits) 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 ELISA Kits) 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.
A report of a homozygous novel DAG1 missense mutation c.2006G>T in the beta-subunit of dystroglycan in two Libyan siblings with with a novel muscle-eye-brain disease-like phenotype with multicystic leucodystrophy.
The study provides evidence for at least three separate pools of dystroglycan complexes within myofibers that differ in composition and are differentially affected by loss of dystrophin (show DMD ELISA Kits).
These data suggest that proteolysis, tyrosine phosphorylation and translocation of dystroglycan to the nucleus resulting in altered gene transcription could be important mechanisms in the progression of prostate cancer.
Cleavage of beta-DG still occurred when both MMP-2 (show MMP2 ELISA Kits) and MMP-9 (show MMP9 ELISA Kits) were knocked out in gamma - sarcoglycan (show SGCG ELISA Kits)-deficient mice. The study found that up-regulation of MMP-14 (show MMP14 ELISA Kits) 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 ELISA Kits) 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 ELISA Kits) A and beta-dystroglycan expression in mdx (show DMD ELISA Kits) 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 ELISA Kits) influences the cytoskeleton organization of Schwann cells
We evaluate the key characteristics of the mdx in comparison with other mouse mutants with inactivations in DAPC components, along with key modifiers of the disease phenotype.
results indicate a novel role for laminin-dystroglycan interactions in the cooperative integration of astrocytes, endothelial cells, and pericytes in regulating the Blood Brain Barrier.
Endogenous glucuronyltransferase activity of LARGE or LARGE2 (show GYLTL1B ELISA Kits) required for functional modification of alpha-dystroglycan in cells and tissues.
in Drosophila the microRNA complex miR (show MYLIP ELISA Kits)-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 ELISA Kits)
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 ELISA Kits)-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.
Results suggest that Perlecan signaling through Dystroglycan may determine where Myosin II can be activated by AMPK, thereby providing the basal polarity cue for the low-energy epithelial polarity pathway.
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