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H4791

Sigma-Aldrich

Bone Morphogenetic Protein 2 human

BMP-2, recombinant, expressed in HEK 293 cells, HumanKine, suitable for cell culture

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Synonym(s):
BMP-2
MDL number:
UNSPSC Code:
12352202
NACRES:
NA.77

biological source

human

Quality Level

recombinant

expressed in HEK 293 cells

form

lyophilized powder

potency

≤60 ng/mL EC50

quality

endotoxin tested

mol wt

dimer 30-38 kDa (glycosylated)

packaging

pkg of 10 μg

storage condition

avoid repeated freeze/thaw cycles

technique(s)

cell culture | mammalian: suitable

impurities

≤1 EU/μg Endotoxin level

UniProt accession no.

storage temp.

−20°C

Gene Information

human ... BMP2(650)

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General description

Bone Morphogenetic Protein 2 is a member of the TGF-β superfamily of cytokines that affect bone and cartilage formation. It is important for skeletal development during embryogenesis. BMP-2 induces chondrocyte formation, osteoblast differentiation, and is involved in embryo dorsal-ventral patterning and organogenesis.

Biochem/physiol Actions

It has been reported that Bone Morphogenetic Protein 2 (BMP-2) inhibits estradiol induced proliferation of human breast cancer cells. BMP-2 signaling mediates apoptosis by activation of the TAK1-p38 kinase pathway that is negatively regulated by Smad6. Cellular responses to BMP-2 are mediated by the formation of hetero-oligomeric complexes of type I and type II serine/threonine kinase receptors, which play significant roles in BMP binding and signaling. One BMP type II receptor and two BMP type I receptors have been identified. Both BMP type I receptors bind BMP-2 with high-affinity in the absence of BMP receptor type II.

Physical form

Lyophilized from a 0.2 μm filtered solution of 2x PBS + 6% Ethanol.

Preparation Note

This Bone Morphogenetic Protein 2 (BMP-2) is produced from a DNA sequence encoding the human BMP-2 protein, expressed in HEK 293 cells. It is a glycosylated homodimer linked by a single disulfide bond with an apparent molecular mass of 30-38 kDa.

Analysis Note

The specific activity was determined by its ability to induce alkaline phosphatase production in a dose response to BMP-2 in the ATDC-5 cell line (mouse chondrogenic cell line).

Legal Information

HumanKine is a registered trademark of Proteintech Group, Inc. and Humanzyme, Inc

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Regulatory Information

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Moulay Hicham Alaoui-Ismaili et al.
Cytokine & growth factor reviews, 20(5-6), 501-507 (2009-11-17)
Bone morphogenetic proteins (BMPs) are growth factors belonging to the TGF beta super family. To date, more than twenty human BMPs have been identified. Of these, BMP-2 and BMP-7 (also known as osteogenic protein 1 or OP-1) are the only
Zhi-Jie Xia et al.
Frontiers in cell and developmental biology, 10, 979096-979096 (2022-11-18)
Saul-Wilson syndrome is a rare skeletal dysplasia caused by a heterozygous mutation in COG4 (p.G516R). Our previous study showed that this mutation affected glycosylation of proteoglycans and disturbed chondrocyte elongation and intercalation in zebrafish embryos expressing the COG4p.G516R variant. How
Yinbo Xiao et al.
Materials today. Bio, 16, 100367-100367 (2022-08-09)
Mesenchymal stem cell (MSC)-based tissue engineering strategies are of interest in the field of bone tissue regenerative medicine. MSCs are commonly investigated in combination with growth factors (GFs) and biomaterials to provide a regenerative environment for the cells. However, optimizing
Thorsten Pfirrmann et al.
Human molecular genetics, 24(11), 3119-3132 (2015-02-26)
Chordin-Like 1 (CHRDL1) mutations cause non-syndromic X-linked megalocornea (XMC) characterized by enlarged anterior eye segments. Mosaic corneal degeneration, presenile cataract and secondary glaucoma are associated with XMC. Beside that CHRDL1 encodes Ventroptin, a secreted bone morphogenetic protein (BMP) antagonist, the
Ernst B Hunziker et al.
Tissue engineering. Part A, 21(13-14), 2089-2098 (2015-04-22)
The articular cartilage layer of synovial joints is commonly lesioned by trauma or by a degenerative joint disease. Attempts to repair the damage frequently involve the performance of autologous chondrocyte implantation (ACI). Healthy cartilage must be first removed from the

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