ライフサイエンスコーパス: EACA

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1 EACA potently inhibited the binding of Glu-Pg to SK (K(i

2 with the ligands epsilon-aminocaproic acid (EACA) and trans-4-(aminomethyl)cyclohexane-1-carboxylic

3 ic acid (TXA) and epsilon-aminocaproic acid (EACA) are structurally similar to the inhibitory neurotr

4 oading dose of 5 grams of aminocaproic acid (EACA) intravenously 3 hours prior to the surgery.

5 ding constants of epsilon-aminocaproic acid (EACA), 7-aminoheptanoic acid (7-AHpA), and trans-(aminom

6 activation, e.g., epsilon-aminocaproic acid (EACA), or plasminogen antiserum.

7 analogues such as epsilon-aminocaproic acid (EACA).

8 anded and ligand [epsilon-aminocaproic acid (EACA)] bound modes and the structure of recombinant KIV-

9 ide-chain mimic, epsilon amino caproic acid (EACA), enhances the activation of Pg by urinary-type and

10 cinoma (ESCC) and esophageal adenocarcinoma (EACA) and 100% in metastasis, but no EpCAM overexpressio

11 overall molecular tumbling for both apo and EACA-bound K1(Pg).

12 Here we demonstrate that TXA and EACA are competitive antagonists of glycine receptors in

13 auses seizures, we hypothesized that TXA and EACA inhibit the activity of glycine receptors.

14 In assays simulating substrate binding, EACA also potently inhibited the binding of Glu-Pg to th

15 Both EACA structures were in the embedded binding mode utiliz

16 he Lp(a) was found to resist dissociation by EACA (0.2 M).

17 The KIV-10/M66, KIV-10/M66/EACA, and KIV-10/T66/EACA molecular structures are highl

18 Addition of EACA resulted in increases (approximately 12 degrees C)

19 rom the similar geometries of the binding of EACA and AMCHA, it appears that the kon is an important

20 uanidinium group close to the carboxylate of EACA to assist R71 in stabilizing the anionic group of t

21 A and r-[W63S]-K2tPA, high concentrations of EACA had little effect on the Tm of thermal denaturation

22 ngles in mediating the inhibitory effects of EACA: mini-Pg which lacks kringles 1-4 of Glu-Pg and mic

23 t the beginning of the extractions 1 gram of EACA per hour continuous infusion and a 6 pack of platel

24 binding mode, where only the amino group of EACA interacted with the anionic center of the LBS.

25 groove parallel to the expected position of EACA toward the anionic center (D55/D57) and makes a sal

26 A similar proportion of EACA resistant binding of Lp(a) was found with endotheli

27 KIV-10/M66, KIV-10/M66/EACA, and KIV-10/T66/EACA molecular structures are highly isostructural, indi

28 The KIV-10/T66/EACA structure determined in this work differs from one

29 human population) was reexamined (KIV-10/T66/EACA).

30 Taken together, these studies indicate that EACA inhibits Pg activation by blocking activator comple

31 e mechanism of this inhibition revealed that EACA (IC(50) 10 microM) also potently blocked amidolytic

32 tPA and r-[W63Y]K2tPA, a result showing that EACA stabilized the native conformations adopted by thes

33 The EACA resistant binding of Lp(a) was time and concentrati

34 In addition, the EACA liganded structure of a sequence polymorph (M66T in

35 splacement of three water molecules from the EACA binding groove and a movement of R35 bringing the g

36 igher binding energy of AMCHA as compared to EACA.

37 ter binding of AMCHA to Klpg, as compared to EACA.

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