Human BMP-5 Antibody Summary
Accession # P22003
Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
Alkaline Phosphatase Production Induced by BMP‑5 and Neutralization by Human BMP‑5 Antibody. Recombinant Human BMP-5 (Catalog # 615-BMC) induces alkaline phosphatase production in the ATDC5 mouse chondrogenic cell line in a dose-dependent manner (orange line). Alkaline phosphatase production elicited by Recombinant Human BMP-5 (1.5 µg/mL) is neutralized (green line) by increasing concen-trations of Mouse Anti-Human BMP-5 Monoclonal Antibody (Catalog # MAB7151). The ND50 is typically 2-10 µg/mL.
Preparation and Storage
- 12 months from date of receipt, -20 to -70 °C as supplied.
- 1 month, 2 to 8 °C under sterile conditions after reconstitution.
- 6 months, -20 to -70 °C under sterile conditions after reconstitution.
Bone Morphogenetic Protein-5 (BMP-5) is one of at least 15 structurally and functionally related BMPs which are members of the transforming growth factor beta (TGF-beta ) superfamily (1). BMP-5 is synthesized as a 454 amino acid (aa) precursor protein that is cleaved at the dibasic cleavage site (RxxR) to release the 20 kDa C-terminal mature protein (2). Mature BMP-5 contains seven conserved cysteine residues involved in formation of the cysteine knot and the single interchain disulfide bond. Biologically active BMP-5 is a disulfide-linked homodimer of the C-terminal mature protein. Mature human BMP-5 shares 96% aa sequence identity with mouse and rat BMP-5. Cellular responses to BMP-5 are mediated by the formation of hetero-oligomeric complexes of type I and type II serine/threonine kinase receptors (1). BMP-5 is expressed by chondrocytes in proliferating and hypertrophic zones of bone growth plates (3). It contributes to limb development by promoting proliferation and differentiation of chondrocytes as well as apoptosis of undifferentiated mesoderm (3, 4). Genetic defects in BMP-5 which cause C-terminal truncation or loss of the proteolytic cleavage site result in multiple skeletal abnormalities, including the short ear phenotype in mice (5, 6). BMP-5 is also expressed by ovarian granulosa cells where it functions as an autocrine factor to promote GC proliferation and inhibit their production of progesterone (7). In the nervous system, BMP-5 promotes dendrite outgrowth and dopaminergic neuronal differentiation (8, 9). It is upregulated in oral squamous carcinoma cells and induces the apoptosis of some myeloma cell lines (10, 11).
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- Jin, Y. et al. (2001) Oral Oncol. 37:225.
- Ro, T.B. et al. (2004) Oncogene 23:3024.
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