Anti-Fibulin 5 antibody - C-terminal (ab151298)

Overview

  • Product name
    Anti-Fibulin 5 antibody - C-terminal
    See all Fibulin 5 primary antibodies
  • Description
    Rabbit polyclonal to Fibulin 5 - C-terminal
  • Tested applications
    Suitable for: WBmore details
  • Species reactivity
    Reacts with: Human
    Predicted to work with: Mouse, Rat, Cow
  • Immunogen

    Synthetic peptide corresponding to a region within C terminal amino acids 384-448 of Human Fibulin 5 (Uniprot ID: Q9UBX5)

  • Positive control
    • HeLa whole cell lysate

Properties

Applications

Our Abpromise guarantee covers the use of ab151298 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

Application Abreviews Notes
WB 1/500 - 1/3000. Predicted molecular weight: 50 kDa.

Target

  • Function
    Promotes 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 specificity
    Expressed 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 disease
    Defects 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 similarities
    Belongs to the fibulin family.
    Contains 6 EGF-like domains.
  • Cellular localization
    Secreted.
  • Information by UniProt
  • Database links
  • Alternative names
    • ADCL2 antibody
    • ARCL1A antibody
    • ARMD3 antibody
    • Dance antibody
    • Developmental arteries and neural crest EGF like protein antibody
    • Developmental arteries and neural crest EGF-like protein antibody
    • EVEC antibody
    • Fbln5 antibody
    • FBLN5_HUMAN antibody
    • FIBL 5 antibody
    • FIBL-5 antibody
    • Fibulin-5 antibody
    • FLJ90059 antibody
    • UP50 antibody
    • Urine p50 protein antibody
    see all

Images

  • Anti-Fibulin 5 antibody - C-terminal (ab151298) at 1/1000 dilution + HeLa whole cell lysate at 30 µg

    Predicted band size : 50 kDa

References

ab151298 has not yet been referenced specifically in any publications.

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