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Human Dystroglycan Protein expressed in Wheat germ - ABIN1351078
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
Show all 2 Pubmed References
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
Dg is required for correct laminin assembly, for cell polarization during mediolateral intercalation and for proper differentiation of vacuoles during notochord development.
Dystroglycan is involved in skin morphogenesis downstream of the Notch signaling pathway
Dystroglycan is required for proper retinal layering
These data indicate that dystroglycan plays a key role for laminin-1 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 bears the potentiality to cleave alpha-DG enriched from rabbit skeletal muscle indicating that this degradation indeed might also occur in vivo.
Study identified beta-dystroglycan as a substrate of WWP1 and found that the muscular dystrophy-causing mutation of WWP1 renders the enzyme hyperactive by relieving autoinhibition.
ISPD and FKTN are essential for the incorporation of ribitol into alpha-dystroglycan.
N-terminal alpha Dystroglycan 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 is involved in the regulation of AQP4 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.
alpha-DG-N removal as an important posttranslational control of endometrial receptivity and uterine fluid alpha-DG-N as a potential biomarker for receptivity in women.
Phosphorylation within the cysteine-rich region of dystrophin 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.
Reduction of alpha-dystroglycan expression is correlated with glioma.
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.
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.
T192M point-mutation in dystroglycan leads to a weaker interactions with laminin-1, which leads to hypoglycosylation and which finally leads to the limb girdle disease.
GTDC2 generates CTD110.6 antibody-reactive N-acetylglucosamine epitopes on the O-mannosylated alpha-dystroglycan.
the Dystroglycan-mediated cortical microtubule anchoring, the disruption of which initiates gastrulation EMT.
Loss of alpha-dystroglycan and increased CD133 expression are frequent events in human colon cancer and evaluation of CD133 expression could help to identify high-risk colon cancer patients.
alpha-DG hypoglycosylation, together with an increased protein instability, reduces the membrane dynamics of the beta-subunit and its clustering within the actin-rich domains, influencing cell migration and spontaneous cell movement.
Utrn KO mdx mice but not mdx 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.
These results reveal a role for DG in maintaining the stability of the sarcomeric cytoskeleton during contraction.
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 and MMP-9 were knocked out in gamma - sarcoglycan-deficient mice. The study found that up-regulation of MMP-14 is capable of cleaving beta-DG, and it may be involved in the pathogenesis of sarcoglycanopathy.
The extracellular environment plays a critical role in coordinating neuronal migration and neurite outgrowth during neural circuit development.
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 deficient mice express moderate to severe muscular dystrophy; glycosylated alpha-dystroglycan has a unique role in muscle regeneration in these mice
A glucuronic acid beta1,4-xylose disaccharide synthesized by B4GAT1 acts as an acceptor primer that can be elongated by LARGE with the ligand-binding heteropolysaccharide.
This study demonstrated that the Postnatal development of the molecular complex underlying astrocyte polarization.
The X-ray crystal structure of the missense variant T190M of the murine N-terminal domain of alpha-dystroglycan (50-313) has been determined.
5-amino-4-imidazolecarboxamide riboside treatment increases utrophin A and beta-dystroglycan expression in mdx mouse muscle.
Results suggest that by interfering in the cross-talk between the transmembrane form of the laminin receptor dystroglycan and F-actin, AHNAK1 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 required for functional modification of alpha-dystroglycan in cells and tissues.
Beta-dystroglycan can respond to ezrin driven cytoskeletal and cell morphology changes,by translocating from the cytoplasm to the nucleus.
in Drosophila the microRNA complex miR-310s acts as an executive mechanism to buffer levels of the muscular dystrophy-associated extracellular matrix receptor dystroglycan via its alternative 3'-UTR
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-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.
establish a central role for Dg in maintaining integrity in Drosophila larval muscles and demonstrate the importance of glycosylation to Dg function in Drosophila
The synaptic role of Dystroglycan (Dg) in Drosophila, is studied.
Study finds that both WW binding sites are important for maintaining full Dg function in the establishment of oocyte polarity in Drosophila.
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