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1 RAGE is a central cell surface receptor for amphoterin, a polypeptide linked to outgrowth of culture
3 phosphacan are also high affinity ligands of amphoterin and HB-GAM (Kd = 0.3-8 nM), two heparin-bindi
5 tenascin-R and two heparin-binding proteins, amphoterin and the heparin-binding growth-associated mol
6 Receptor for AGE (RAGE) and the polypeptide amphoterin are highly expressed and co-localized in neur
9 Here we demonstrate that blockade of RAGE-amphoterin decreased growth and metastases of both impla
10 ere with RAGE including administration of an amphoterin-derived peptide known to antagonize RAGE acti
15 point to Sp1-dependent mechanisms underlying amphoterin-mediated increases in RAGE expression in neur
16 sion, thereby providing a mechanism by which amphoterin-mediated regulation of RAGE might contribute
19 sistent with this, we show that depletion of amphoterin mRNA from cultured adult rat DRG neurons atte
23 tioning nerve injury increases the levels of amphoterin protein in axons without a corresponding incr
24 sion in neuroblastoma cells and further link amphoterin-RAGE interaction to development of the nervou
25 er RAGE or its ligands, S100/calgranulins or amphoterin, reduced functional recovery as assessed by m
26 ubation of cultured neuroblastoma cells with amphoterin resulted in increased transcription and trans
28 We tested the hypothesis that interaction of amphoterin with neuronal cells enhances RAGE expression,
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