GSCL Antibody | 28-903

GSCL Antibody | 28-903 | Gentaur UK, US & Europe Distribution

Host: Rabbit

Reactivity: Human

Homology: N/A

Immunogen: Antibody produced in rabbits immunized with a synthetic peptide corresponding a region of human GSCL.

Research Area: Transcription

Tested Application: E, WB, IHC

Application: GSCL antibody can be used for detection of GSCL by ELISA at 1:1562500. GSCL antibody can be used for detection of GSCL by western blot at 1.25 μg/mL, and HRP conjugated secondary antibody should be diluted 1:50, 000 - 100, 000.

Specificiy: N/A

Positive Control 1: Cat. No. 1211 - HepG2 Cell Lysate

Positive Control 2: N/A

Positive Control 3: N/A

Positive Control 4: N/A

Positive Control 5: N/A

Positive Control 6: N/A

Molecular Weight: 22 kDa

Validation: N/A

Isoform: N/A

Purification: Antibody is purified by protein A chromatography method.

Clonality: Polyclonal

Clone: N/A

Isotype: N/A

Conjugate: Unconjugated

Physical State: Liquid

Buffer: Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose.

Concentration: batch dependent

Storage Condition: For short periods of storage (days) store at 4˚C. For longer periods of storage, store GSCL antibody at -20˚C. As with any antibody avoid repeat freeze-thaw cycles.

Alternate Name: GSCL, GSCL

User Note: Optimal dilutions for each application to be determined by the researcher.

BACKGROUND: Goosecoidlike (GSCL) resides in the critical region for VCFS/DGS on 22q11. Velocardiofacial syndrome (VCFS) is phenotypically related to DiGeorge syndrome (DGS) and both syndromes are associated with hemizygous 22q11 deletions. Because many of the tissues and structures affected in VCFS/DGS derive from the pharyngeal arches of the developing embryo, it is believed that haploinsufficiency of a gene involved in embryonic development may be responsible for its etiology.Goosecoidlike (GSCL) , a homeodomain-containing gene, resides in the critical region for VCFS/DGS on 22q11. Velocardiofacial syndrome (VCFS) is a developmental disorder characterized by conotruncal heart defects, craniofacial anomalies, and learning disabilities. VCFS is phenotypically related to DiGeorge syndrome (DGS) and both syndromes are associated with hemizygous 22q11 deletions. Because many of the tissues and structures affected in VCFS/DGS derive from the pharyngeal arches of the developing embryo, it is believed that haploinsufficiency of a gene involved in embryonic development may be responsible for its etiology. The gene is expressed in a limited number of adult tissues, as well as in early human development.