BMP-2 Protein, Human/Mouse/Rat (Tag Free)

Bone morphogenetic protein 2 (BMP-2) is a pleiotropic ligand protein belonging to TNFβ family, and is involved in key embryonic development of vascular and valvular homeostasis. BMP-2 binds to type I receptors (ALK-2/-3/-6) and type II receptors (BMPR2, ACVR2A) to regulate various types of calcification, including atherosclerosis, chronic kidney disease, diabetes, and valve calcification^[1]. BMP-2 is overexpressed by myofibroblast and preosteoblast in the calcified area of human calcified valve, which are densely infiltrated by B lymphocytes and T lymphocytes^[2]. BMP-2 is the junction between atherosclerotic vascular calcification and normal bone formation mechanism^[3]. BMP-2 Protein, Human/Mouse/Rat is 104 a.a. (Q283-R396), expressed in E. coli.

Bone Morphogenetic Protein 2 (BMP-2) is a ligand protein with pleiotropic, belongs to TNFβ family. BMP-2 formats BMP/TGFβ signaling to involve in vascular and valvular homeostasis, which is a critical process of embryonic development^[1].
BMP-2/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^[4].
BMP-2 is widely found in different animals, while the sequence in human is similar to Rat (91.86%), and mouse (92.13%).
BMPs exhibits critical contributions to the pathophysiology of atherosclerosis, pulmonary vascular disease, and vascular and valvular calcification^[1].
BMP-2 binds different receptor, such as type I receptors (ALK-2/-3/-6) and type II receptors (BMPR2, ACVR2A), to regulate various calcification type including Atherosclerosis, Chronic Kidney Disease, Diabetes, Valvular Calcification^[1].
BMP-2 promotes monocyte infiltration and inflammation of atherosclerotic legions^[5].
It is linked to increased plaque formation via pro-inflammatory and pro-atherogenic effects, promoting oxidative stress, endothelial dysfunction and osteogenic differentiation^[6].
BMP-2 is overexpressed in ossified regions of human calcified valves by myofibroblasts and pre-osteoblasts in areas densely infiltrated with B- and T-lymphocytes^[2].
And it serves as the linkers between atherosclerotic vascular calcification with mechanisms of normal bone formation^[3].
BMP-2 induces angiogenesis, endothelial cells (ECs) proliferation, and migration^[7].
And BMP-2 also enhances the expression of the osteoblast and chondrocyte master transcriptional regulator RUNX2 to promote the mineralization of cultured human coronary vascular SMCs in a manner that was dependent on oxidative stress and endoplasmic reticulum (ER) stress^[8].

Measured by its ability to induce alkaline phosphatase production by ATDC5 mouse chondrogenic cells. The ED₅₀ for this effect is ≤0.5 μg/mL, corresponding to a specific activity is ≥2×10³ U/mg.

• 
  Measured by its ability to induce alkaline phosphatase production by ATDC5 mouse chondrogenic cells. The ED₅₀ for this effect is 0.2579 μg/mL, corresponding to a specific activity is 3.877×10³ U/mg.

Rat; Mouse; Human

E. coli

Tag Free

P12643 (Q283-R396)

650

QAKHKQRKRLKSSCKRHPLYVDFSDVGWNDWIVAPPGYHAFYCHGECPFPLADHLNSTNHAIVQTLVNSVNSKIPKACCVPTELSAISMLYLDENEKVVLKNYQDMVVEGCGCR

Approximately 12-13 kDa

• 
  Greater than 95% as determined by reducing SDS-PAGE.

Lyophilized powder

Lyophilized from sterile 50 mM Tris-HCL, 200 mM NaCL, 500 mM arginine, pH 8.0 or 50 mM Tris-HCL, 200 mM NaCl, 500 mM arginine, pH 8.0, 5% trehalose or 0.1% TFA, 30% Acetonitrile, pH 2.5 or pH 2.4.

<1 EU/μg, determined by LAL method.

It is not recommended to reconstitute to a concentration less than 100 μg/mL in ddH₂O. For long term storage it is recommended to add a carrier protein (0.1% BSA, 5% HSA, 10% FBS or 5% Trehalose).

Stored at -20°C for 2 years. After reconstitution, it is stable at 4°C for 1 week or -20°C for longer (with carrier protein). It is recommended to freeze aliquots at -20°C or -80°C for extended storage.

Room temperature in continental US; may vary elsewhere.