VIA41

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$40.00
SKU: VIA41-s
View product citations for antibody VIA41 on CiteAb

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Available: 176

DSHB Data Sheet

Catalog Fields

Antigen: Dystroglycan, alpha-
Hybridoma Cells Available: No
Antigen Species: Rabbit
Depositor: Campbell, K.P.
Isotype: MIgG1
Antigen Sequence:
Host Species: mouse
Depositors Institution: University of Iowa
Positive Tested Species Reactivity: Human, Mouse, Rabbit
Depositors Notes:
Antigen Molecular Weight: Apparent: 156 kDa
Human Protein Atlas:  
Predicted Species Reactivity:  
Gene: DAG1
Immunogen: Dystrophin complex isolated from detergent-solubilized skeletal muscle membranes using wheat-germ agglutinin-Sepharose.
Alternate Gene Names:
Alternate Antibody Name: VIA4-1
Clonality: Monoclonal
Alternate Antigen Name:
Epitope Mapped: No
Myeloma Strain:
Epitope Location or Sequence:
Uniprot ID: Q28685 
Immunogen Sequence: Full length protein
Entrez Gene ID: 100009278 
Additional Characterization:  
Antibody Registry ID: AB_2617217 
Additional Information: VIA41 recognizes a glycoconjugate on the LARGE fully glycosylated form of alphaDG. Dystroglycan is a central component of the dystrophin-glycoprotein complex that links the extracellular matrix and the cytoskeleton in the skeletal muscle. RRID:AB_2617217
Recommended Applications: Immunofluorescence, Immunoprecipitation, Western Blot
These hybridomas were created by your colleagues. Please acknowledge the hybridoma contributor and the Developmental Studies Hybridoma Bank (DSHB) in the Materials and Methods of your publications. Please email the citation to us.
For your Materials & Methods section:
VIA41 was deposited to the DSHB by Campbell, K.P. (DSHB Hybridoma Product VIA41)
Storage and Handling Recommendations
Although many cell products are maintained at 4°C for years without loss of activity, shelf-life at 4°C is highly variable. For immediate use, short term storage at 4°C up to two weeks is recommended. For long term storage, divide the solution into volumes of no less than 20 ul for freezing at -20°C or -80°C. The small volume aliquot should provide sufficient reagent for short term use. Freeze-thaw cycles should be avoided. For concentrate or bioreactor products, an equal volume of glycerol, a cryoprotectant, may be added prior to freezing.
Usage Recommendations
Although the optimal Ig concentration for an application varies for each product and must be optimized for each laboratory, a good starting concentration for immunohistochemistry (IHC), immunofluorescence (IF), and immunocytochemistry (ICC) is 2-5 ug/ml. For western blots, the recommended concentration range is 0.2-0.5 ug/ml.
All cell products contain the antimicrobial ProClin. Click here for additional information.

11 References

  • Initial Publication
  • IF References
  • WB References
  • IP References
  • All References
  • Initial Publication
    IF References
    WB References
    IP References
    All References

    Deficiency of a glycoprotein component of the dystrophin complex in dystrophic muscle.
    Campbell KP
    Nature 345.6273 (1990 May 24): 315-9.

    ISPD loss-of-function mutations disrupt dystroglycan O-mannosylation and cause Walker-Warburg syndrome.
    Campbell KP
    Nature genetics 44.5 (2012 May): 575-80.

    Post-translational disruption of dystroglycan-ligand interactions in congenital muscular dystrophies.
    Campbell KP
    Nature 418.6896 (2002 Jul 25): 417-22.

    GMPPB-Associated Dystroglycanopathy: Emerging Common Variants with Phenotype Correlation.
    Mathews KD
    Human mutation 36.12 (2015 Dec): 1159-63.

    Congenital disorder of glycosylation due to DPM1 mutations presenting with dystroglycanopathy-type congenital muscular dystrophy.
    Mehta L
    Molecular genetics and metabolism 110.3 (2013 Nov): 345-351.

    Membrane organization of the dystrophin-glycoprotein complex.
    Campbell KP
    Cell 66.6 (1991 Sep 20): 1121-31.

    Dystrophin-associated proteins are greatly reduced in skeletal muscle from mdx mice.
    Campbell KP
    The Journal of cell biology 115.6 (1991 Dec): 1685-94.

    Endogenous glucuronyltransferase activity of LARGE or LARGE2 required for functional modification of α-dystroglycan in cells and tissues.
    Campbell KP
    The Journal of biological chemistry 289.41 (2014 Oct 10): 28138-48.

    Pompe disease results in a Golgi-based glycosylation deficit in human induced pluripotent stem cell-derived cardiomyocytes.
    Kamp TJ
    The Journal of biological chemistry 290.5 (2015 Jan 30): 3121-36.

    Laminin-α1 LG4-5 domain binding to dystroglycan mediates muscle cell survival, growth, and the AP-1 and NF-κB transcription factors but also has adverse effects.
    Jarrett HW
    American journal of physiology. Cell physiology 302.6 (2012 Mar 15): C902-14.

    Differential glycosylation of α-dystroglycan and proteins other than α-dystroglycan by like-glycosyltransferase.
    Hu H
    Glycobiology 22.2 (2012 Feb): 235-47.

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