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Data (including data from studies in knockout mice) suggest that S100b acting as a humoral factor impairs glycolysis in muscle (myoblasts, myotubes, and skeletal muscles) independent of insulin action; this effect appears to be due to inhibition of Gapdh activity from enhanced poly(ADP-ribosyl)ation of Gapdh. (S100B = S100 protein, beta polypeptide, neural; Gapdh = glyceraldehyde-3-phosphate dehydrogenase)
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S100B inhibits C3H/10T1/2 murine embryonic mesenchyma.l cells into osteoblasts. S100B stimulates C3H/10T1/2 cell differentiation into adipocytes.
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The results of this study showed that S100B affects behavioral despair in female mice through functional interaction with the 5-HT7 receptor.
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Data show that S100B has direct effects on macrophages, enhancing particularly CCL22 and IL-1beta expression and modulates the inflammatory response in uveoretinitis and this is likely to be, at least in part, via a direct effect on macrophages.
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Data show that high glucose increased protein-protein interaction between Steap4 and S100B in mesangial (MES13) cells.
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high glucoseinduced profibrotic genes (TGFbeta, type IV collagen and fibronectin) and cell hypertrophyrelated p21WAF1 are dependent on S100B.
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S100A1 and S100B are dispensable for endochondral ossification during skeletal development.
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Data suggest up-regulation of S100b/RAGE (advanced glycosylation end-product receptor) signaling plays role in inflammatory interaction between adipocytes/macrophages; adipocyte secretion of S100b is up-regulated by Tnf (tumor necrosis factor-alpha).
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Gioma production of S100B enhancestumor growth through CCL2 upregulation and tumor-associated macrophages chemoattraction.
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HMGB1, S100B, and RAGE signaling modulate the hippocampal inflammatory response and might play key roles in surgery-induced cognitive decline.
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S100B is a proinflammatory cytokine bridging RAGE and CD166/ALCAM downstream effector mechanisms, both being compensatory upregulated after genetic deletion of its counterpart.
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S100B expression may serve to modulate cardiac metabolism and adverse consequences of AGE in diabetic post-MI remodeling and function
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S100B is expressed in mouse photoreceptor cone outer segments but not in rods.
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The RAGE pathway may play an important role in STAT3 induction in glioma-associated macrophages and microglia, a process that may be mediated through S100B.
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S100B and APP levels are simultaneously increased within Down syndrome neural progenitors, their secretions are synergistically enhanced in a paracrine fashion, and their overexpressions disrupt mitochondrial membrane potentials and redox states.
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Unlike in the hippocampus-dependent tasks, S100B-KO mice were indistinguishable from wild-type mice in both cerebellum-dependent motor coordination and delay eyeblink conditioning.
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Data support S100B inhibition as a novel strategy for reducing cortical plaque load, gliosis and neuronal dysfunction in Alzheimer disease (AD) and suggest that both extracellular as well as intracellular S100B contribute to AD histopathology.
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These results suggest that S100beta is important for brain development and establishment of proper brain functions.
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Given the crucial roles of COX-2, IL-1beta and TNF-alpha in the inflammatory response, we propose that, by engaging RAGE, S100B might play an important role in microglia activation in the course of brain damage.
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Intracellular S100B might modulate myoblast differentiation by interfering with MyoD expression in an NF-kappaB-dependent manner.
