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1 ole neurons revealed that (RS)-3,5-dihydroxy-phenylglycine 0.5 H(2)O (DHPG)-stimulated fluorescence w
2 (cat)/K(M) for the enantiomers of N-succinyl phenylglycine, 2.0 x 10(5) M(-1) s(-1), is comparable to
3 horyl]oxy]ethyl]sulfonyl]propionyl]-(R)-(-)-phenylglycine (3) have been designed, synthesized, and e
4 lyzed reaction to access 3,4,5-trifluoro-(S)-phenylglycine, a 1-pot activation/displacement/deprotect
6 type and position of the substituents on the phenylglycine and phenylalanine side chains has a signif
7 clearly demonstrate that S-phenylglycine (R-phenylglycine) binds only to chains rotated 19.5 degrees
8 RP with concurrent formation of 2a but not N-phenylglycine, but under anaerobic, peroxide-free condit
9 xchange the alpha-hydrogen of N-succinyl-(R)-phenylglycine, consistent with formation of a Mn2+-stabi
11 protease that incorporate phenylalanine and phenylglycine derivatives as arginine-mimicking groups w
13 of glutamate by gliomas may be prevented by phenylglycine derivatives, which may thus be useful as a
14 stage racemization of carboxylate-activated phenylglycine-derived residues, and to enlist beta-sheet
15 stage racemization of carboxylate-activated phenylglycine-derived residues, and to enlist beta-sheet
16 ion of group I mGluRs with (S)-3,5-dihydroxy-phenylglycine (DHPG) induced a Ca(2+)-calmodulin-depende
17 of P1 novaline and the aromatic ring of P2' phenylglycine formed a C-shaped clamp around the Lys136
19 phorodiamidate)-sulfonyl-propionyl-( R)- (-) phenylglycine] is a novel nitrogen mustard prodrug that
20 ses predict the incorporation of p-hydroxy-L-phenylglycine (L-pHPG) into positions 1, 3, and 5 and L-
21 I/II antagonist (+/-)-alpha-methyl-4-carboxy-phenylglycine (MCPG), and group III agonist L-2-amino-4-
22 methoxy-alpha-phenylacetic acid (MPA) or (S)-phenylglycine methyl ester (PGME) linked through anilide
25 nylacetic acids, including mandelic acid and phenylglycine, react smoothly with various aryl iodides
26 he chirality, and that the alpha-amino acid, phenylglycine, shows a strong chiral preference in its i
27 tase inhibitor difluorophenacetyl-l-alanyl-S-phenylglycine t-butyl ester (DAPT) or dimethyl sulfoxide
28 or N-(N-[3,5-difluorophenacetyl]-l-alanyl)-S-phenylglycine t-butyl ester (DAPT) or following stable t
29 N-[N-(3,5-difluorophenacetyl)-L-alanyl]-(S)-phenylglycine t-butyl ester (DAPT) preferentially inhibi
30 or N-[N-(3,5-difluorophenacetyl)-l-alanyl]-S-phenylglycine t-butyl ester (DAPT) significantly rescued
31 ly N-[N-(3,5-difluorophenacetyl)-l-alanyl]-S-phenylglycine t-butyl ester (DAPT), a chemical inhibitor
32 of N-[N-(3,5-difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester (DAPT), a gamma-secretase in
33 r, N-[N-(3,5-difluorophenacetyl)-1-alanyl]-S-phenylglycine t-butyl ester (DAPT), or Notch1 short hair
34 r, N-[N-(3,5-Difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester (DAPT), which significantly
36 or N-[N-(3,5-difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester failed to promote the direct
37 T (N-[N-(3,5-difluorophenacetyl-l-alanyl)]-S-phenylglycine t-butyl ester), reduces the survival of GC
38 N-[N-(3,5-difluorophenacetyl)-L-alanyl]-(S)-phenylglycine t-butyl ester, a potent gamma-secretase in
39 or N-(N-(3,5-difluorophenacetyl)-l-alanyl)-S-phenylglycine t-butyl ester, supporting the concept that
40 N-[N-(3,5-difluorophenylacetyl-l-alanyl)]-S-phenylglycine t-butylester (DAPT), a specific gamma-secr
41 I) N-[N-(3,5-difluorophenacetyl)-l-alanyl]-S-phenylglycine-t-butylester (DAPT), at a dose that reduce
42 tor N-[N-(3,5-Difluorophenacetyl-L-alanyl)-S-phenylglycine]-t-butyl ester, which blocks Notch signali
44 ange of the alpha-hydrogen of N-succinyl-(S)-phenylglycine with solvent hydrogen, and K263R and K263
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