Key features and details
- Rabbit polyclonal to Fibulin 5
- Suitable for: IHC-P
- Reacts with: Human
- Isotype: IgG
Product nameAnti-Fibulin 5 antibody
See all Fibulin 5 primary antibodies
DescriptionRabbit polyclonal to Fibulin 5
Specificityab198212 detects endogenous levels of total Fibulin 5 protein.
Tested applicationsSuitable for: IHC-Pmore details
Species reactivityReacts with: Human
Predicted to work with: Mouse, Rat
Synthetic peptide corresponding to Human Fibulin 5 (internal sequence).
Database link: Q9UBX5
- Human lung cancer tissue.
Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term. Avoid freeze / thaw cycle.
Storage bufferpH: 7.30
Preservative: 0.05% Sodium azide
Constituents: 49% PBS, 50% Glycerol
Concentration information loading...
PurityImmunogen affinity purified
Our Abpromise guarantee covers the use of ab198212 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|IHC-P||1/50 - 1/200. Perform heat mediated antigen retrieval with citrate buffer pH 6 before commencing with IHC staining protocol.|
FunctionPromotes adhesion of endothelial cells through interaction of integrins and the RGD motif. Could be a vascular ligand for integrin receptors and may play a role in vascular development and remodeling.
Tissue specificityExpressed predominantly in heart, ovary, and colon but also in kidney, pancreas, testis, lung and placenta. Not detectable in brain, liver, thymus, prostate, or peripheral blood leukocytes.
Involvement in diseaseDefects in FBLN5 are a cause of autosomal dominant cutis laxa (ADCL) [MIM:123700]. Hereditary cutis laxa refers to a heterogeneous group of connective tissue disorders characterized by cutaneous abnormalities and variable systemic manifestations. The most constant clinical feature is loose skin, sagging over the face and trunk. Hereditary cutis laxa is inherited in both autosomal dominant and autosomal recessive modes. Autosomal dominant cutis laxa is a relatively benign inherited and acquired connective tissue disorder.
Defects in FBLN5 are a cause of cutis laxa autosomal recessive type 1 (ARCL1) [MIM:219100]. Hereditary cutis laxa refers to a heterogeneous group of connective tissue disorders characterized by cutaneous abnormalities and variable systemic manifestations. The most constant clinical feature is loose skin, sagging over the face and trunk. Hereditary cutis laxa is inherited in both autosomal dominant and autosomal recessive modes. ARCL1 shows the most severe phenotype and has the poorest prognosis. In addition to the skin, internal organs enriched in elastic fibers, such as the lung and arteries, are affected.
Defects in FBLN5 are the cause of age-related macular degeneration type 3 (ARMD3) [MIM:608895]. ARMD is a multifactorial disease and the most common cause of irreversible vision loss in the developed world. In most patients, the disease is manifest as ophthalmoscopically visible yellowish accumulations of protein and lipid (known as drusen) that lie beneath the retinal pigment epithelium and within an elastin-containing structure known as Bruch membrane.
Sequence similaritiesBelongs to the fibulin family.
Contains 6 EGF-like domains.
- Information by UniProt
- ADCL2 antibody
- ARCL1A antibody
- ARMD3 antibody
ab198212 has not yet been referenced specifically in any publications.