DUX4 antibody (AA 53-120) (Biotin)

Catalog No. ABIN1699985

The Rabbit Polyclonal anti-DUX4 antibody has been validated for WB, ELISA, IHC (p) and IHC (fro). It is suitable to detect DUX4 in samples from Human.

Quick Overview for DUX4 antibody (AA 53-120) (Biotin) (ABIN1699985)

Target: DUX4 (Double Homeobox 4 (DUX4))

Reactivity: Human

Host: Rabbit

Clonality: Polyclonal

Conjugate: This DUX4 antibody is conjugated to Biotin

Application: Western Blotting (WB), ELISA, Immunohistochemistry (Paraffin-embedded Sections) (IHC (p)), Immunohistochemistry (Frozen Sections) (IHC (fro))

Product Details anti-DUX4 Antibody (Biotin)

Binding Specificity: AA 53-120

Predicted Reactivity: Human

Purification: Purified by Protein A.

Immunogen: KLH conjugated synthetic peptide derived from human DUX4

Isotype: IgG

Application Details

Application Notes: WB 1:300-5000
IHC-P 1:200-400
IHC-F 1:100-500

Restrictions: For Research Use only

Handling

Format: Liquid

Concentration: 1 μg/μL

Buffer: Aqueous buffered solution containing 0.01M TBS ( pH 7.4) with 1 % BSA, 0.03 % Proclin300 and 50 % Glycerol.

Preservative: ProClin

Precaution of Use: This product contains ProClin: a POISONOUS AND HAZARDOUS SUBSTANCE, which should be handled by trained staff only.

Storage: -20 °C

Storage Comment: Store at -20°C for 12 months.

Expiry Date: 12 months

Target Details for DUX4

Target: DUX4 (Double Homeobox 4 (DUX4))

Alternative Name: DUX4

Background:

Synonyms: Double homeobox protein 10, Double homeobox protein 4, Double homeobox protein 4/10, DUX10, DUX4_HUMAN.

Background: DUX4 is a homeodomain protein with a similar protein sequence to Pax3 and Pax7. Defects in DUX4 may be the cause of facioscapulohumeral muscular dystrophy (FSHD). FSHD is characterized by weakness of the muscles of the face, upper-arm and shoulder girdle. Severity is highly variable. Weakness is slowly progressive and about 20 % of affected individuals eventually require a wheelchair. Approximately 70-90 % of individuals have inherited the disease-causing deletion from a parent, and approximately 10-30 % of affected individuals have FSHD as the result of a de novo deletion. Offsprings of an affected individual have a 50 % chance of inheriting the deletion.