Product Name: GSCL Antibody
Species Reactivity: Human
Tested Applications: ELISA, IHC, WB
Applications: 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.
User Note: Optimal dilutions for each application to be determined by the researcher.
Predicted Molecular Weight: 22 kDa
Immunogen: Antibody produced in rabbits immunized with a synthetic peptide corresponding a region of human GSCL.
Host Species: Rabbit
Purification: Antibody is purified by protein A chromatography method.
Physical State: Lyophilized
CAS NO.: 61477-94-9
SB 525334
Buffer: Antibody is lyophilized in PBS buffer with 2% sucrose. Add 100 μL of distilled water. Final antibody concentration is 1 mg/mL.
Concentration: 1 mg/ml
Storage Conditions: 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.
Clonality: Polyclonal
Conjugate: Unconjugated
Alternate Names: GSCL, GSCL
Accession NO.: NP_005306
Protein Ino: 4885363
Official Symbol: GSC2
Geneid: 2928
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.
PubMed ID:http://aac.asm.org/content/20/3/314.abstract
