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1 ate, cysteine, glutamine, lysine, malate and pyroglutamate.
2 equilibrium is strongly in the direction of pyroglutamate.
3 were blocked by cyclization of glutamine to pyroglutamate.
4 N-terminal residue was glutamine rather than pyroglutamate.
10 uctures for TAP01 family antibodies bound to pyroglutamate AB3-14, we identified a novel pseudo B-hai
11 42 and AB1-40 - and the N-truncated species, pyroglutamate AB3-42 and AB4-42, which appear to play a
14 -length Abeta1-42 and Abeta1-40, N-truncated pyroglutamate Abeta3-42 and Abeta4-42 are major variants
15 a starting with position four in addition to pyroglutamate Abeta3-x is a relevant target to fight Alz
16 ith both the free N-terminus of Abeta4-x and pyroglutamate Abeta3-X mitigated neuron loss in Tg4-42 m
18 ed higher levels of Abeta1-40 and N-terminal pyroglutamated Abetax-42 compared to diffuse plaques and
19 observed that diffuse plaques have increased pyroglutamated Abetax-42 levels in s-AD but not CU-AP, s
20 e for the removal of pyroglutamate (pGlu) by pyroglutamate aminopeptidase (PGAP) and demonstrate its
21 in chains of immunoglobulins with the enzyme pyroglutamate aminopeptidase requires the use of chaotro
24 KD and 12 matched healthy subjects) received pyroglutamated apelin-13 ([Pyr(1)]apelin-13, 1 nmol/min
26 studies indicated that 14C-glutamine and 14C-pyroglutamate are not subject to significant non-enzymat
27 gical roles of some PTMs, such as N-terminal pyroglutamate, are poorly understood due to a dearth of
29 eavy chains of immunoglobulins such that the pyroglutamate at the amino terminal was accessible to en
30 anslationally modified Abeta peptides with a pyroglutamate at the N-terminus (pGlu3, pE3), are attrac
31 Amyloid-beta (Abeta) peptides, starting with pyroglutamate at the third residue (pyroGlu-3 Abeta), ar
32 mab (an antibody specific for the N-terminal pyroglutamate beta-amyloid epitope) dosing was every 4 w
36 t ADan-(1-34) and its N-terminally modified (pyroglutamate) counterpart together with Abeta-(1-42) an
38 d an improved method for the halogenation of pyroglutamate derivatives in high yield with enhanced st
40 n this study, we determined if non-enzymatic pyroglutamate formation from glutamine contributed to th
41 deamidation in the Fc domain and N-terminal pyroglutamate formation in the heavy chain are the main
48 for direct labeling and identification of a pyroglutamate hormone present in porcine intestinal extr
49 he N terminus, which can be cyclized to form pyroglutamate in mammalian cells, the IL17A neutralizati
50 f anticancer activity through the N-terminal pyroglutamate in naturally occurring asperigimycins C an
55 mi intensity were identified as monosodium l-pyroglutamate (l-MSpG) and monosodium d-pyroglutamate (d
60 oredox catalysis process that enables direct pyroglutamate N-H arylation in peptides and proteins, us
61 ic conversion of the N-terminal glutamine to pyroglutamate not only provides an identification of the
64 erminal cyclization of glutamine residues to pyroglutamate on the light and heavy chains are the majo
65 t against oligomeric assemblies of Abeta and pyroglutamate or oxidized residues, and IgGs specific fo
68 o and in vivo Because N-terminally truncated pyroglutamate (pE)-modified Abeta species (AbetapE3) exh
70 cine comprising two Abeta peptides (1-14 and pyroglutamate pE3-14) and three tau peptides (centered o
71 , PFA1 binds the toxic N-terminally modified pyroglutamate peptide pyro-Glu3-Abeta with a 77-fold los
72 rt an optimized procedure for the removal of pyroglutamate (pGlu) by pyroglutamate aminopeptidase (PG
75 sultant N-terminal glutamine was cyclized to pyroglutamate (pyrGln(23)), and several C-terminal pepti
76 ue disulfide connectivity, and an N-terminal pyroglutamate rendered copsin extremely stable against h
78 the blocked CHH suggests that the N-terminal pyroglutamate residue has no obvious biological signific
79 teine residues is evident but the N-terminal pyroglutamate residue is replaced by a six-residue exten
82 ts provide the first chemical tool to modify pyroglutamate residues within complex polypeptides in bi
86 )]Ser or [Met-(-1)]Tyr instead of the native pyroglutamate results in recombinant onconase derivative
87 lective annulation of an oxolane ring onto a pyroglutamate scaffold to construct either a gamma,gamma
88 th the native protein lacking the N-terminal pyroglutamate (the numbering system used has Asp2 as the
89 characterized by cyclization of glutamine to pyroglutamate; the N-terminus of ZP2 was identified by E
90 ated bicyclic lactam substrates derived from pyroglutamate using aqueous hydrogen peroxide and tertia
92 ost-translational modification, glutamate to pyroglutamate, was not present in soluble circulating AD
93 terminus was post-translationally modified (pyroglutamate), whereas Abeta was mainly Abeta-(4-42).