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1 in binding site within 54-132 amino acids of tumstatin.
2 ng the two distinct anti-tumor properties of tumstatin.
3 essential for the antiangiogenic activity of tumstatin.
5 lpha(v)beta(3) integrin-mediated activity of tumstatin, although significant inhibition of endothelia
7 lectively, such distinct properties of human tumstatin and human endostatin provide the first insight
8 in is localized to a 25-amino acid region of tumstatin and it is independent of disulfide bond linkag
12 confirm that the anti-angiogenic activity of tumstatin and tum-5 is independent of disulfide bond req
17 suppressive action of TSP-1, endostatin, and tumstatin correlates with expression of CD36 receptor, a
19 three independent lines of mice deficient in tumstatin, endostatin, or thrombospondin-1 (TSP-1), to a
21 isite interaction with alphaVbeta3 integrin, tumstatin inhibits activation of focal adhesion kinase (
22 model in which T3, while unable to alter the tumstatin-insensitive vasculature contributed by the alp
25 suggest that the anti-angiogenic activity of tumstatin is localized to a 25-amino acid region of tums
27 emonstrate that Tum-5, a domain derived from tumstatin, is an effective inhibitor of tumor-associated
28 ndostatin) or type IV collagen alpha3 chain (tumstatin) or TSP-1 to assess the contribution of these
29 uble-knockout mice, compared with either the tumstatin- or the TSP-1-deficient mice, strongly suggest
30 Collectively, our results demonstrate that tumstatin peptide binds specifically to the tumor endoth
32 nstrate that systemic administration of this tumstatin peptide inhibits tumor growth and angiogenesis
35 es identified a 25-aa fragment of tumstatin (tumstatin peptide) with in vitro antiangiogenic activity
38 tration of endostatin, thrombospondin-1, and tumstatin peptides, as well as deletion of their genes,
42 wo distinct RGD-independent binding sites on tumstatin suggest unique alpha(v)beta(3) integrin-mediat
43 ffected by exposure to an active fragment of tumstatin (T3), whereas alpha(V)beta(3)-expressing gliom
47 l cell apoptosis accounts for the ability of tumstatin to function as an endogenous inhibitor of angi
48 Moreover, tumors grow 2-fold faster in the tumstatin/TSP-1 double-knockout mice, compared with eith
49 nesis studies identified a 25-aa fragment of tumstatin (tumstatin peptide) with in vitro antiangiogen
50 esent study, the anti-angiogenic activity of tumstatin was localized to the putative 54-132-amino aci
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