FBLN5 Antibody | 59-590

FBLN5 Antibody | 59-590 | Gentaur UK, US & Europe Distribution

Host: Rabbit

Reactivity: Human

Homology: N/A

Immunogen: This FBLN5 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 393-421 amino acids from the C-terminal region of human FBLN5.

Research Area: Signal Transduction

Tested Application: WB

Application: For WB starting dilution is: 1:1000

Specificiy: N/A

Positive Control 1: N/A

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: 50 kDa

Validation: N/A

Isoform: N/A

Purification: This antibody is purified through a protein A column, followed by peptide affinity purification.

Clonality: Polyclonal

Clone: N/A

Isotype: Rabbit Ig

Conjugate: Unconjugated

Physical State: Liquid

Buffer: Supplied in PBS with 0.09% (W/V) sodium azide.

Concentration: batch dependent

Storage Condition: Store at 4˚C for three months and -20˚C, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.

Alternate Name: Fibulin-5, FIBL-5, Developmental arteries and neural crest EGF-like protein, Dance, Urine p50 protein, UP50, FBLN5, DANCE

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

BACKGROUND: The protein encoded by this gene is a secreted, extracellular matrix protein containing an Arg-Gly-Asp (RGD) motif and calcium-binding EGF-like domains. It promotes adhesion of endothelial cells through interaction of integrins and the RGD motif. It is prominently expressed in developing arteries but less so in adult vessels. However, its expression is reinduced in balloon-injured vessels and atherosclerotic lesions, notably in intimal vascular smooth muscle cells and endothelial cells. Therefore, the protein encoded by this gene may play a role in vascular development and remodeling. Defects in this gene are a cause of autosomal dominant cutis laxa, autosomal recessive cutis laxa type I (CL type I) , and age-related macular degeneration type 3 (ARMD3) .