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1  RAGE is a central cell surface receptor for amphoterin, a polypeptide linked to outgrowth of culture
2                              The presence of amphoterin also produces a 5-fold increase in phosphacan
3 phosphacan are also high affinity ligands of amphoterin and HB-GAM (Kd = 0.3-8 nM), two heparin-bindi
4 account for at least 80% of their binding to amphoterin and HB-GAM.
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
7      Indeed, the co-localization of RAGE and amphoterin at the leading edge of advancing neurites ind
8                                    Exogenous amphoterin can increase neurite growth, suggesting that
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
11                DNA chip analysis showed that amphoterin-induced gene and open reading frame 2 (Amigo2
12                       Inhibition of the RAGE-amphoterin interaction suppressed activation of p44/p42,
13                                              Amphoterin is an HMG protein (HMGB1) that has been shown
14                            The mRNA encoding amphoterin localizes to axonal processes and we showed r
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
17                                              Amphoterin mRNA 3'-UTR is also sufficient for axonal loc
18                A 60 nucleotide region of the amphoterin mRNA 3'-UTR is necessary and sufficient for i
19 sistent with this, we show that depletion of amphoterin mRNA from cultured adult rat DRG neurons atte
20 in axons without a corresponding increase in amphoterin mRNA in the axons.
21          Overexpression of axonally targeted amphoterin mRNA increases axon outgrowth in cultured sen
22                           Here, we show that amphoterin mRNA is transported constitutively into axons
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
27 unction; however, promoter responsiveness to amphoterin was markedly attenuated.
28 We tested the hypothesis that interaction of amphoterin with neuronal cells enhances RAGE expression,
29                 In vitro, the interaction of amphoterin with neuronal RAGE induces neurite outgrowth.

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