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1  equilibrium is strongly in the direction of pyroglutamate.
2  were blocked by cyclization of glutamine to pyroglutamate.
3 N-terminal residue was glutamine rather than pyroglutamate.
4 ate, cysteine, glutamine, lysine, malate and pyroglutamate.
5 %), and a compound tentatively identified as pyroglutamate (22%).
6 dialysis, radioactivity was recovered in 14C-pyroglutamate (88%) and 14C-glutamine (11%).
7                    However, it confirms that pyroglutamate, a known constituent in brain, is actively
8 o improving mAb specificity and affinity for pyroglutamate Abeta.
9                   N-terminally truncated and pyroglutamated Abeta peptides were recently shown to see
10 -length Abeta1-42 and Abeta1-40, N-truncated pyroglutamate Abeta3-42 and Abeta4-42 are major variants
11 a starting with position four in addition to pyroglutamate Abeta3-x is a relevant target to fight Alz
12 ith both the free N-terminus of Abeta4-x and pyroglutamate Abeta3-X mitigated neuron loss in Tg4-42 m
13                                 NT4X reduced pyroglutamate Abeta3-x, Abetax-40 and Thioflavin-S posit
14 e for the removal of pyroglutamate (pGlu) by pyroglutamate aminopeptidase (PGAP) and demonstrate its
15 in chains of immunoglobulins with the enzyme pyroglutamate aminopeptidase requires the use of chaotro
16                   Following injection of 14C-pyroglutamate and microdialysis, radioactivity was recov
17 w peptide is: [sequence: see text] where Z = pyroglutamate and O = 4-trans-hydroxyproline.
18 studies indicated that 14C-glutamine and 14C-pyroglutamate are not subject to significant non-enzymat
19            Our data do not support a role of pyroglutamate as an intermediate in the formation of ext
20 eavy chains of immunoglobulins such that the pyroglutamate at the amino terminal was accessible to en
21 Amyloid-beta (Abeta) peptides, starting with pyroglutamate at the third residue (pyroGlu-3 Abeta), ar
22                     In one of these changes, pyroglutamate can form on the N terminus of the polypept
23 t ADan-(1-34) and its N-terminally modified (pyroglutamate) counterpart together with Abeta-(1-42) an
24 um l-pyroglutamate (l-MSpG) and monosodium d-pyroglutamate (d-MSpG).
25 d an improved method for the halogenation of pyroglutamate derivatives in high yield with enhanced st
26              Reverse microdialysis with 1 mM pyroglutamate did not increase interstitial glutamate le
27 n this study, we determined if non-enzymatic pyroglutamate formation from glutamine contributed to th
28                                              Pyroglutamate formation increases the rate of Abeta olig
29                                              Pyroglutamate formation was additionally found to increa
30 oxicity of Abeta3-40 and Abeta3-42 and their pyroglutamated forms.
31                    Typically, the removal of pyroglutamate from the protein chains of immunoglobulins
32 -Ala-Thr-Lys-Lys-Pro-Tyr-Ile-Leu-OH, pGlu is pyroglutamate) from Conus geographus venom.
33 he N terminus, which can be cyclized to form pyroglutamate in mammalian cells, the IL17A neutralizati
34       Cyclization of N-terminal glutamine to pyroglutamate is a common modification of recombinant mo
35                                 Methyl N-Boc-pyroglutamate is cleaved with vinylmagnesium bromide to
36                                              Pyroglutamate is in chemical equilibrium with glutamate,
37 mi intensity were identified as monosodium l-pyroglutamate (l-MSpG) and monosodium d-pyroglutamate (d
38                                              Pyroglutamate levels increased over time after injection
39                                              Pyroglutamate-modified Abeta peptides at amino acid posi
40                                              Pyroglutamate-modified amyloid-beta (pE-Abeta) is a high
41                                              Pyroglutamate-modified amyloid-beta (pEAbeta) has been d
42 ic conversion of the N-terminal glutamine to pyroglutamate not only provides an identification of the
43                      Glutamate conversion to pyroglutamate occurs more slowly than from glutamine but
44                             The NH2-terminal pyroglutamate of onconase, a residue essential for ribon
45 erminal cyclization of glutamine residues to pyroglutamate on the light and heavy chains are the majo
46 t against oligomeric assemblies of Abeta and pyroglutamate or oxidized residues, and IgGs specific fo
47 onal antibodies can cyclize spontaneously to pyroglutamate (pE) in vitro.
48                  Cyclization of Gln1 to form pyroglutamate (pE) limited the site of cross-linking in
49 o and in vivo Because N-terminally truncated pyroglutamate (pE)-modified Abeta species (AbetapE3) exh
50                             Juxtaposition of pyroglutamate pE3 and the F4 side chain (the "pEF head")
51 , PFA1 binds the toxic N-terminally modified pyroglutamate peptide pyro-Glu3-Abeta with a 77-fold los
52 rt an optimized procedure for the removal of pyroglutamate (pGlu) by pyroglutamate aminopeptidase (PG
53 eine and glutamate residues and results in a pyroglutamate product.
54 sultant N-terminal glutamine was cyclized to pyroglutamate (pyrGln(23)), and several C-terminal pepti
55 ue disulfide connectivity, and an N-terminal pyroglutamate rendered copsin extremely stable against h
56 bohydrate group, and the identification of a pyroglutamate residue at the sequence N-terminus.
57 the blocked CHH suggests that the N-terminal pyroglutamate residue has no obvious biological signific
58 teine residues is evident but the N-terminal pyroglutamate residue is replaced by a six-residue exten
59 evealing that the function of the N-terminal pyroglutamate residue is to secure Lys9.
60 ed successfully to facilitate the removal of pyroglutamate residues.
61 )]Ser or [Met-(-1)]Tyr instead of the native pyroglutamate results in recombinant onconase derivative
62 lective annulation of an oxolane ring onto a pyroglutamate scaffold to construct either a gamma,gamma
63 th the native protein lacking the N-terminal pyroglutamate (the numbering system used has Asp2 as the
64 characterized by cyclization of glutamine to pyroglutamate; the N-terminus of ZP2 was identified by E
65 ated bicyclic lactam substrates derived from pyroglutamate using aqueous hydrogen peroxide and tertia
66 erase to convert the N-terminal glutamine to pyroglutamate was developed in the current study.
67 ost-translational modification, glutamate to pyroglutamate, was not present in soluble circulating AD
68  terminus was post-translationally modified (pyroglutamate), whereas Abeta was mainly Abeta-(4-42).

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