BMP-2 Protein, Human/Mouse/Rat (Low Endotoxin)

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].