|Basic FGF (E9S5A) Rabbit mAb 98658||20 µl||
||H||18, 22, 24||Rabbit IgG|
|IGF-I (E6B7O) Rabbit mAb 73034||20 µl||
||H M||9, 13, 18, 20||Rabbit IgG|
|HGF β (D6S7D) XP® Rabbit mAb 52445||20 µl||
||H||35, 85||Rabbit IgG|
|TGF-β (56E4) Rabbit mAb 3709||20 µl||
|HBEGF (E5L5T) Rabbit mAb 27450||20 µl||
||H||18, 21, 27||Rabbit IgG|
|MIF (E7T1W) Rabbit mAb 87501||20 µl||
||H M R||12||Rabbit IgG|
|EREG (D4O5I) Rabbit mAb 12048||20 µl||
||H||17,19, 30||Rabbit IgG|
|Angiopoietin-2 (D200) Antibody 50697||20 µl||
|Anti-rabbit IgG, HRP-linked Antibody 7074||100 µl||
|VEGF-A (E9X8Q) Rabbit mAb 50661||20 µl||
||H||16, 20, 23, 26||Rabbit IgG|
Monoclonal antibodies are produced by immunizing animals with recombinant protein specific to the mature full-length human basic FGF protein, with recombinant protein fragment specific to human mature HBEGF protein, with recombinant protein specific to the carboxy terminus of human HGF protein, with synthetic peptides corresponding to residues surrounding Ser83 of human IGF-I protein, Tyr100 of human MIF protein, and Glu155 of human EREG protein, and with synthetic peptides corresponding to a region in the carboxy terminus of TGF-β1 protein.
Polyclonal antibodies are produced by immunizing animals with a synthetic peptides corresponding to residues surronding His38 of human VEGFA protein and Asp200 of human angiopoietin-2 protein. Antibodies are purified by peptide affinity chromatography.
The tumor microenvironment (TME) is composed of a heterogenous mixture of tumor cells, blood vessels, fibroblasts, stromal cells, infiltrating immune cells, and extracellular matrix (ECM) components, whose collective interactions play important roles in tumor development (1). Cells in the TME secrete a variety of bioactive molecules, including growth factors, cytokines, ECM proteins, and proteases (e.g., MMPs), many of which play critical roles in regulating growth and development of the tumor (2,3). Growth factors play particularly important roles in the TME, serving as cellular messengers that trigger activation or suppression of signaling pathways that govern tumor development, either directly via the tumor cells, or indirectly by way of effects on the TME. Binding of growth factors to their cognate receptors leads to activation of intracellular signaling pathways, resulting in changes in the expression of target genes that regulate cell behavior. Many growth factors (e.g., IGFs, HGFs, FGFs, HBEGF, EREG) are known to promote tumor development by way of direct effects on tumor cells; other growth factors can affect tumor development indirectly, through effects in the TME that influence tumor angiogenesis (e.g., VEGFs, angiopoietins), ECM deposition (TGF-β), or immune cell signaling (e.g., TGF-β, HBEGF, MIF) (4). The diverse and complex role played by growth factors in promoting tumorigenesis makes them important therapeutic targets in oncology, while elucidating the functions of specific growth factors in the context of tumor development remains an active area of cancer research (5).
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