Anti-S100B Antibody, Mouse Monoclonal General Information
Anti-S100B Antibody, Mouse Monoclonal
Reacts with: Human
Recombinant Human S100B Protein (Catalog#10181-H07E)
This antibody was produced from a hybridoma resulting from the fusion of a mouse myeloma with B cells obtained from a mouse immunized with purified, recombinant Human S100B (rh S100B; Catalog#10181-H07E; NP_006263.1; Ser2-Glu92). The IgG fraction of the cell culture supernatant was purified by Protein A affinity chromatography.
Monoclonal Mouse IgG2a Clone #60
0.2 μm filtered solution in PBS
This antibody is shipped as liquid solution at ambient temperature. Upon receipt, store it immediately at the temperature recommended below.
This antibody can be stored at 2℃-8℃ for one month without detectable loss of activity. Antibody products are stable for twelve months from date of receipt when stored at -20℃ to -80℃. Preservative-Free. Avoid repeated freeze-thaw cycles.
S1B is a member of the S1 family of proteins containing two EF-hand-type calcium-binding motifs. S1B exerts both intracellular and extracellular functions. Intracellular S1B acts as a stimulator of cell proliferation and migration and an inhibitor of apoptosis and differentiation, which might have important implications during brain, cartilage and skeletal muscle development and repair, activation of astrocytes in the course of brain damage and neurodegenerative processes, and of cardiomyocyte remodeling after infarction, as well as in melanomagenesis and gliomagenesis. As an extracellular factor, S1B engages RAGE (receptor for advanced glycation end products) in a variety of cell types with different outcomes (i.e. beneficial or detrimental, pro-proliferative or pro-differentiative) depending on the concentration attained by the protein, the cell type and the microenvironment. This calcium binding astrocyte-specific cytokine, presents a marker of astrocytic activation and reflects CNS injury. The excellent sensitivity of S1B has enabled it to confirm the existence of subtle brain injury in patients with mild head trauma, strokes, and after successful resuscitation from cardiopulmonary arrest. Recent findings provide evidence, that S1B may decrease neuronal injury and/or contribute to repair following traumatic brain injury (TBI). Hence, S1B, far from being a negative determinant of outcome, as suggested previously in the human TBI and ischemia literature, is of potential therapeutic value that could improve outcome in patients who sustain various forms of acute brain damage.
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