1 ve alpha-GID mutants (alpha-GID[A10V],
alpha-
GID[V13I], and alpha-GID[V13Y]) and one inactive variant
2 (alpha-GID[A10V], alpha-GID[V13I], and
alpha-
GID[V13Y]) and one inactive variant (alpha-GID[A10Q]).
3 Two mutants, alpha-GID[A10V] and
alpha-
GID[V13Y], had substantially reduced potency at the huma
4 k correctly identified three bioactive
alpha-
GID mutants (alpha-GID[A10V], alpha-GID[V13I], and alpha
5 therapy, and the 19-residue conotoxin
alpha-
GID that antagonizes it.
6 ensive conformational sampling to dock
alpha-
GID and its analogs to an alpha4beta2 nAChR homology mod
7 to alpha-GID, a desirable feature for
alpha-
GID analogs.
8 ied three bioactive alpha-GID mutants (
alpha-
GID[A10V], alpha-GID[V13I], and alpha-GID[V13Y]) and one
9 Two mutants,
alpha-
GID[A10V] and alpha-GID[V13Y], had substantially reduced
10 homology models, as exemplified by the
alpha-
GID:alpha4beta2 nAChR complex, and is extendable to othe
11 at the human alpha7 nAChR relative to
alpha-
GID, a desirable feature for alpha-GID analogs.
12 a-GID[V13Y]) and one inactive variant (
alpha-
GID[A10Q]).
13 lopment of levodopa-induced dyskinesias,
and GID-like behaviors occur regardless of pregraft levodopa
14 vators, these interactions are unaffected
by GID mutations, revealing an unanticipated specificity of
15 The Global Image
Database (
GID) is a web-based structured central repository for sc
16 th Gal4 in vivo [Gal4 interaction
defective (
GID) mutants].
17 ect of simulated gastrointestinal
digestion (
GID) on phenolic content, composition and antioxidant ca
18 during in vitro gastro-intestinal
digestion (
GID) of six sterilised model systems of infant formula.
19 Gender identity
disorder (
GID) is the diagnostic term to describe persons disconte
20 is a conserved GSK3beta interaction
domain (
GID), which is also present in GSKIP.
21 kinase 3beta (GSK-3beta) interaction
domain (
GID).
22 The release of this peptide
during GID was hindered by protein glycation.
23 ft efficacy and/or graft-induced
dyskinesia (
GID) induction.
24 Approaches to therapy
for GID and task force guidelines are noted.
25 diffraction at grazing angles of
incidence (
GID) were conducted to determine the structure of synthe
26 hat the Gid4 subunit of the ubiquitin
ligase GID in the yeast Saccharomyces cerevisiae targeted the g
27 Coexpression
of GID-JLP disrupts ternary complex formation in addition t
28 bute to suboptimal efficacy and/or
postgraft GID behaviors.
29 Our results show that the
simulated GID modified the health-promoting properties of the stud
30 a-subunits via its C-terminal domain (
termed GID-JLP), spanning amino acids 1165-1307, and this inter
31 The GID annotations are searchable by field or globally.
32 The GID was designed to manage images from a wide spectrum o
33 The annotations in
the GID define the source experiment of the images by descri
34 In addition, the entries in
the GID reference these imaging protocols with the probe seq
35 The development of
the GID continues, aiming at facilitating the management and
36 Analysis of
the GID reveals that the monomolecular film, at the crystall
37 d for degradation by the Gid4 subunit of
the GID ubiquitin ligase.
38 ied Gid4 as the recognition component of
the GID-based proteolytic system termed the Pro/N-end rule p
39 been shown to antagonize Wnt signaling,
the GID inhibits GSK-3beta in vivo and activates Wnt signali
40 der behavior, and CNS differences related
to GID and bi-gender descriptions.
41 In yeast strains expressing a
Tra1 GID mutant, binding of Gal4 to the promoter is unexpecte
42 In contrast to WT Tra1,
Tra1 GID mutants are not recruited by Gal4 to the promoter an
43 n (3kDa) permeates before and after in
vitro GID of model IFs.
44 After the in
vitro GID of the samples, only the inhibition of alpha-glucosi
45 Protein degradation during in
vitro GID was evaluated by SDS-PAGE and by measuring the nitro
46 ased by about 50% at the end of the in
vitro GID.