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Angiogenesis

Angiogenesis is the process by which new blood vessels are formed from pre-existing vessels. Almost all tissues develop a network of blood vessels in order to provide cells with nutrients and oxygen and to eliminate waste products. Angiogenesis occurs during embryo development, wound healing, and ovulation. Pathological angiogenesis is the abnormal and rapid proliferation of blood vessels. Typically, pathological angiogenesis is sustained in almost all forms of cancer and even other non-cancerous diseases. Cancerous tumors have the ability to develop and maintain a network of blood vessels to supply necessary nutrients to the expanding cancer cells. The angiogenic process is activated by a cell’s lack of oxygen and release of angiogenic molecules. These molecules attract inflammatory and endothelial cells which secrete other angiogenic stimuli. The attracted endothelial cells form the new blood vessel and several enzymes will digest part of the current blood vessel while proteins join the new fragment to the old branch. This process is called anastomosis. The entire angiogenesis process is highly regulated by growth factors, cytokines, and integrins. In cancer, small tumors do not need to have their own blood supply. As the tumor grows, however, blood vessels are needed to provide oxygen and nutrients to the rapidly growing cells. Anti-cancer therapy focuses on the time between the promotion of angiogenesis by cancer and the progression of it. This is useful in addition to traditional cancer treatments which mainly focus on inhibiting the cell cycle and reproduction of the cancer cells.

Anti-BMP5 antibody binds against the target bone morphogeneteic protein 5. BMP 5 induces cartilage and bone formation. BMP5 is secreted by cells and expressed in the lung and liver. BMPs may also play a role in certain cancers. Anti-FGFR2 antibody binds against the target fibroblast growth factor receptor 2. FGFR2 is a receptor for acidic and basic fibroblast growth factors. Fibroblast growth factor receptor 2 is localized on the cell membrane of cells and is also secreted. Defects in FGFR2 are the cause of Crouzon syndrome, Apert syndrome, Pfeiffer syndrome, and familial scaphocephaly syndrome. Crouzon syndrome, also known as branchial arch syndrome, is a genetic disorder in which some of the skull bones fuse together prematurely which prevents normal skull growth. Affected individuals have distinct facial features like bulging eyes, a beaked nose, and underdeveloped jaws. Apert syndrome is similar to Crouzon syndrome. It is a genetic disorder that causes the skull bones to close earlier than normal and affects the shape of the head and face. Affected individuals may often also have fused fingers and fused toes. Pfeiffer syndrome and familial scaphocephaly syndrome, as well, have facial and cranial symptoms similar to those affected with Crouzon syndrome and branchial arch syndrome.

 
Product Number Title Applications Host Clonality
AC15-0116 Anti-TGF beta Antibody ELISA, WB, IHC, ICC, IF Chicken Polyclonal
AC16-0012 Anti-TIMP1 Antibody ELISA, WB, IHC(F), IHC(P), IP Mouse Monoclonal (7-6C1)
AC16-0013 Anti-TIMP1 Antibody WB, IHC(F), IHC(P), ICC, IF, IP, FC Mouse Monoclonal (147-6D11)
AC16-0020 Anti-MMP3 Antibody ELISA, WB, IHC(F), IHC(P) Mouse Monoclonal (55-2A4)
AC16-0021 Anti-MMP2 Antibody IHC(F), IHC(P), FC Mouse Monoclonal (42-5D11)
AC16-0022 Anti-MMP9 Antibody WB, IHC(F), IHC(P) Mouse Monoclonal (56-2A4)
AC16-0023 Anti-MMP14 Antibody ELISA, WB, IHC(P) Mouse Monoclonal (114-1F2)
AC16-0024 Anti-MMP7 Antibody ELISA, WB, IHC(P), IP Mouse Monoclonal (141-7B2)
AC16-0025 Anti-MMP14 Antibody WB, IHC(P) Mouse Monoclonal (113-5B7)
AC16-0026 Anti-MMP15 Antibody ELISA, WB, IHC(F), IHC(P), IP Mouse Monoclonal (162-22G5)
AC16-0027 Anti-MMP13 Antibody WB, IHC(F), IHC(P) Mouse Monoclonal (181-15A12)
AC16-0028 Anti-MMP7 Antibody WB, IHC(P) Mouse Monoclonal (176-5F12)
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