ALAS2 Antibody | 29-663

ALAS2 Antibody | 29-663 | 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 ALAS2.

Research Area: Other

Tested Application: E, WB, IHC

Application: ALAS2 antibody can be used for detection of ALAS2 by ELISA at 1:62500. ALAS2 antibody can be used for detection of ALAS2 by western blot at 5.0 μg/mL, and HRP conjugated secondary antibody should be diluted 1:50, 000 - 100, 000.

Specificiy: N/A

Positive Control 1: Cat. No. 1205 - Jurkat 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: 57 kDa, 65 kDa, 61 kDa, 63 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 ALAS2 antibody at -20˚C. As with any antibody avoid repeat freeze-thaw cycles.

Alternate Name: ALAS2, ANH1, ASB, PRO2399, XLSA, ALASE, XLDPP, XLEPP, ALAS-E

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

BACKGROUND: ALAS2 specifies an erythroid-specific mitochondrially located enzyme. The protein catalyzes the first step in the heme biosynthetic pathway. Defects in its gene cause X-linked pyridoxine-responsive sideroblastic anemia.The product of this gene specifies an erythroid-specific mitochondrially located enzyme. The encoded protein catalyzes the first step in the heme biosynthetic pathway. Defects in this gene cause X-linked pyridoxine-responsive sideroblastic anemia. Alternatively spliced transcript variants encoding different isoforms have been identified.