BMP-5 Protein, Human (HEK293, hFc)

Bone morphogenetic protein 5 (BMP-5) is a pleiotropic ligand protein belonging to the TGFβ family, which is mainly expressed in the lung and liver. After BMP-5 silencing, the activity of p38/ERK signaling pathway can be down-regulated to inhibit chondrocyte senescence and apoptosis and knee arthritis (OA)^[1]. Bmp-5 initiates typical BMP signaling cascades by binding to type I receptor BMPR1A and type II receptor BMPR2^[2], or triggers signals through atypical pathways such as MAPK p38 signaling cascades to promote chondrogenic differentiation^[3].

Bone Morphogenetic Protein 5 (BMP-5) is a ligand protein with pleiotropic, belongs to TGFβ family and expresses mainly in the lung and liver. BMP/TGFβ signaling to involve in vascular and valvular homeostasis, which is a critical process of embryonic development^[4]. And BMP/TGFβ signaling can be terminated by inhibitory SMADs including SMAD6 and SMAD7, which are activated and induced by BMP signaling and switch off BMP signaling via multiple mechanisms^[5].
BMP-5 silencing inhibits chondrocyte senescence and apoptosis as well as osteoarthritis (OA) progression by downregulating activity in the p38/ERK signaling pathway^[1].
BMP-5 initiates the canonical BMP signaling cascade by associating with type I receptor BMPR1A and type II receptor BMPR2^[2].
BMP-5 also triggers signal through non-canonical pathway such as MAPK p38 signaling cascade to promote chondrogenic differentiation^[3].
BMP-5 specific expressing in neural crest progenitor cells is sufficient to induce cell proliferation through the MEK-ERK-ID3 signaling cascade, whereas disruption of this signaling cascade had no effect on cell survival^[6].

BMP-5 (3 ng/mL; 1, 3, 5, 7, and 17 d) induces SCG neurons dendritic growth^[2].
BMP-5 (1 ng/mL; , 3, and 6 min) induces phosphorylation of Smad-1 in cultured sympathetic neurons^[2].
BMP-5 (.1-1 ng/mL; 6 d) is less potent than BMP-7 in dendritic growth in cultured sympathetic neurons, but equally efficacious in promoting dendritic growth in cultured sympathetic neurons^[2].

Measured by its ability to induce alkaline phosphatase production by ATDC5 mouse chondrogenic cells. The ED₅₀ for this effect is 0.7568 µg/mL, corresponding to a specific activity is 1.32×10³ U/mg.

Human

HEK293

N-hFc

NP_066551.1 (Q324-H454)

653  [NCBI]

Partial

QNRNKSSSHQDSSRMSSVGDYNTSEQKQACKKHELYVSFRDLGWQDWIIAPEGYAAFYCDGECSFPLNAHMNATNHAIVQTLVHLMFPDHVPKPCCAPTKLNAISVLYFDDSSNVILKKYRNMVVRSCGCH

Approximately 50-55 kDa, based on SDS-PAGE under reducing conditions, due to the glycosylation.

≥ 90%, as determined by reducing SDS-PAGE.

Solution

Supplied as a 0.22 μm filtered solution of PBS, pH 7.4.

<1 EU/μg, determined by LAL method.

N/A.

Stored at -80°C for 1 year from date of receipt. It is stable at -20°C for 3 months after opening. It is recommended to freeze aliquots at -80°C for extended storage. Avoid repeated freeze-thaw cycles.

Shipping with dry ice.

• [1]. Shao Y, et al. BMP5 silencing inhibits chondrocyte senescence and apoptosis as well as osteoarthritis progression in mice. Aging (Albany NY). 2021 Mar 19;13(7):9646-9664.  [Content Brief]

  [2]. Beck HN, et al. Bone morphogenetic protein-5 (BMP-5) promotes dendritic growth in cultured sympathetic neurons. BMC Neurosci. 2001;2:12.  [Content Brief]

  [3]. Snelling SJ, et al. BMP5 activates multiple signaling pathways and promotes chondrogenic differentiation in the ATDC5 growth plate model. Growth Factors. 2010 Aug;28(4):268-79.  [Content Brief]

  [4]. Yang P, et al. The role of bone morphogenetic protein signaling in vascular calcification. Bone. 2020 Dec;141:115542.  [Content Brief]

  [5]. Miyazawa K, et al. Regulation of TGF-β Family Signaling by Inhibitory Smads. Cold Spring Harb Perspect Biol. 2017 Mar 1;9(3):a022095.  [Content Brief]

  [6]. Shih HY, et al. Bmp5 Regulates Neural Crest Cell Survival and Proliferation via Two Different Signaling Pathways. Stem Cells. 2017 Apr;35(4):1003-1014.  [Content Brief]