Promotional price valid on web orders only. Your contract pricing may differ. Interested in signing up for a dedicated account number?
Learn More

DUX4 Mouse anti-Human, Mouse, Clone: P2B1, Invitrogen™

Mouse Monoclonal Antibody

Manufacturer:  Invitrogen MA527584

Catalog No. PIMA527584


Add to cart

Description

Description

DUX4 (also known as Double homeobox 4) is the leading candidate causative gene for facioscapulohumeral dystrophy (FSHD), a degenerative skeletal muscle disease and one of the most common muscular dystrophies. FSHD is caused by the deletion of a subset of D4Z4 macrosatellite repeats on chromosome 4. Each repeat contains a retrogene encoding the double-homeobox factor DUX4. DUX4 expression is epigenetically suppressed in differentiated tissues and the residual DUX4 transcripts are spliced to remove the carboxyterminal domain that has been associated with cell toxicity. In FSHD individuals, the expression of the full-length DUX4 transcript is not completely suppressed in skeletal muscle, and possibly other differentiated tissues, and results in a small percentage of cells expressing relatively abundant amounts of the full-length DUX4 mRNA and protein.
Specifications

Specifications

DUX4
Monoclonal
1 mg/ml
PBS with 50% glycerol and 0.09% sodium azide; pH 7.4
Q9UBX2
Double homeobox 4, Double homeobox 10, DUX10, Double homeobox protein 4/10, DUX4L, DUX4L1
Mouse
IgG1
100 μg
-20°C
Primary
100288687, 664783
Immunocytochemistry, Immunofluorescence, Immunohistochemistry, Western Blot
P2B1
Unconjugated
DUX4
Liquid
DUX4
C-terminal 76 amino acids of DUX4 with glutathione-s-transferase (gst) tag
Protein G
RUO
Antibody
Monoclonal
Human, Mouse
Documents
Provide Content Correction

We continue to work to improve your shopping experience and your feedback regarding this content is very important to us. Please use the form below to provide feedback related to the content on this product.

Product Title

By clicking Submit, you acknowledge that you may be contacted by Fisher Scientific in regards to the feedback you have provided in this form. We will not share your information for any other purposes. All contact information provided shall also be maintained in accordance with our Privacy Policy.

Cancel Submit