ライフサイエンスコーパス: GID

1 "GID" is a collection of E3 ligase complexes; a core scaf

2 GID/CTLH-Ubc8/UBE2H-mediated ubiquitylation regulates bi

3 ytical sample comprised only veterans with a GID diagnosis code (n = 9,608).

4 itory effect of the fractions obtained after GID on PL and a-amylase activities using a fluorescence

5 thermal treatments on peptide profiles after GID.

6 The results presented suggest that after GID, a variety of peptides with biological activities we

7 ve alpha-GID mutants (alpha-GID[A10V], alpha-GID[V13I], and alpha-GID[V13Y]) and one inactive variant

8 (alpha-GID[A10V], alpha-GID[V13I], and alpha-GID[V13Y]) and one inactive variant (alpha-GID[A10Q]).

9 Two mutants, alpha-GID[A10V] and alpha-GID[V13Y], had substantially reduced potency at the huma

10 k correctly identified three bioactive alpha-GID mutants (alpha-GID[A10V], alpha-GID[V13I], and alpha

11 therapy, and the 19-residue conotoxin alpha-GID that antagonizes it.

12 ensive conformational sampling to dock alpha-GID and its analogs to an alpha4beta2 nAChR homology mod

13 to alpha-GID, a desirable feature for alpha-GID analogs.

14 ied three bioactive alpha-GID mutants (alpha-GID[A10V], alpha-GID[V13I], and alpha-GID[V13Y]) and one

15 Two mutants, alpha-GID[A10V] and alpha-GID[V13Y], had substantially reduced

16 homology models, as exemplified by the alpha-GID:alpha4beta2 nAChR complex, and is extendable to othe

17 at the human alpha7 nAChR relative to alpha-GID, a desirable feature for alpha-GID analogs.

18 a-GID[V13Y]) and one inactive variant (alpha-GID[A10Q]).

19 ts inhibited alpha-amylase after cooking and GID, and the peptide fraction <3 kDa was responsible for

20 lopment of levodopa-induced dyskinesias, and GID-like behaviors occur regardless of pregraft levodopa

21 Both GID and non-GID data elements were applied to a sample o

22 vators, these interactions are unaffected by GID mutations, revealing an unanticipated specificity of

23 In yeast, the evolutionarily conserved GID E3 ligase mediates glucose-induced degradation of fr

24 The Global Image Database (GID) is a web-based structured central repository for sc

25 th Gal4 in vivo [Gal4 interaction defective (GID) mutants].

26 low-up of at-risk individuals for developing GID post infection.

27 otection against gastrointestinal digestion (GID) exerted by an O:W emulsion on the integrity of the

28 released during gastrointestinal digestion (GID) of A1 beta-CN variant, in comparison to the A2 vari

29 ect of simulated gastrointestinal digestion (GID) on phenolic content, composition and antioxidant ca

30 d for artificial gastrointestinal digestion (GID).

31 -vitro simulated gastrointestinal digestion (GID; oral, gastric and intestinal phases) was performed

32 during in vitro gastro-intestinal digestion (GID) of six sterilised model systems of infant formula.

33 ested (simulated gastrointestinal digestion, GID) green pea, chickpea, and navy beans were evaluated,

34 ciated with canine gastrointestinal disease (GID).

35 Gender identity disorder (GID) is the diagnostic term to describe persons disconte

36 sides diagnoses of gender identity disorder (GID), a combination of non-GID data elements was used to

37 iduals (defined as gender identity disorder [GID], endocrine disorder not otherwise specified, sex-di

38 k factors of new gastrointestinal disorders (GID) associated with SARS-CoV-2 infection up to 3.5 year

39 is a conserved GSK3beta interaction domain (GID), which is also present in GSKIP.

40 kinase 3beta (GSK-3beta) interaction domain (GID).

41 The release of this peptide during GID was hindered by protein glycation.

42 ft efficacy and/or graft-induced dyskinesia (GID) induction.

43 ain unknown, including those for RING-family GID/CTLH E3 ubiquitin ligases and their dedicated E2, Ub

44 ifies the catalytic centers within a flexing GID E3-substrate assembly, and facilitates substrate col

45 Approaches to therapy for GID and task force guidelines are noted.

46 ased on a high positive predictive value for GID-coded veterans (83%, 95% confidence interval: 77, 89

47 Meanwhile, Mtb isolated from GID/CTLH knockout macrophages are nutritionally starved

48 nges in the composition of crude extracts in GID aliquots were followed by analysis with HPLC-DAD-MS(

49 diffraction at grazing angles of incidence (GID) were conducted to determine the structure of synthe

50 hat the Gid4 subunit of the ubiquitin ligase GID in the yeast Saccharomyces cerevisiae targeted the g

51 cose Induced Degradation/C-Terminal to LisH (GID/CTLH) complex is a highly conserved E3 ubiquitin lig

52 COVID-19 positive patients who developed new GID compared to 38,928 (5.70%) controls.

53 ients had an elevated risk of developing new GID (adjusted HR = 1.18 (95% CI 1.12-1.25) compared to p

54 The primary outcome was new GID which included peptic ulcer, inflammatory bowel dise

55 Both GID and non-GID data elements were applied to a sample of 13,233,529

56 dentity disorder (GID), a combination of non-GID data elements was used to identify potentially trans

57 95% confidence interval: 77, 89) versus non-GID-coded veterans (2%, 95% confidence interval: 1, 11)

58 Coexpression of GID-JLP disrupts ternary complex formation in addition t

59 -19 patients without past medical history of GID (controls) from the Montefiore Health System in the

60 These findings highlight the importance of GID conditions which may affect the outcomes for possibl

61 es and degradation assays with substrates of GID, we show that Gid10 can function as a specific N-rec

62 he BCM7 release depended on both the type of GID enzymes and the P/S ratio.

63 y, findings suggest that relying entirely on GID diagnosis codes is the most reliable approach for id

64 bute to suboptimal efficacy and/or postgraft GID behaviors.

65 itional cellular factors directly regulating GID-type E3s remains rudimentary.

66 Our results show that the simulated GID modified the health-promoting properties of the stud

67 uring the intestinal step of in vitro static GID of bovine milk and cheeses with A1 or A2 beta-CN phe

68 a-subunits via its C-terminal domain (termed GID-JLP), spanning amino acids 1165-1307, and this inter

69 The GID annotations are searchable by field or globally.

70 The GID was designed to manage images from a wide spectrum o

71 Our study identifies the GID/CTLH complex activity as broadly suppressive of host

72 f a single deletion or point mutation in the GID complex on the global proteome, allowing the identif

73 The annotations in the GID define the source experiment of the images by descri

74 In addition, the entries in the GID reference these imaging protocols with the probe seq

75 The development of the GID continues, aiming at facilitating the management and

76 lly characterize Gid12 as a modulator of the GID E3 ligase complex.

77 ed carbon source-dependent regulation of the GID E3 ligase, an important regulator of cellular metabo

78 ntification and validation of targets of the GID E3 ligase.

79 This unveiled regulatory targets of the GID ligase during a metabolic switch.

80 Analysis of the GID reveals that the monomolecular film, at the crystall

81 Gid4, a subunit of the GID ubiquitin ligase in the yeast Saccharomyces cerevisi

82 d for degradation by the Gid4 subunit of the GID ubiquitin ligase.

83 ied Gid4 as the recognition component of the GID-based proteolytic system termed the Pro/N-end rule p

84 he recognition component (N-recognin) of the GID-mediated Pro/N-degron pathway.

85 2H, MAEA) of the 12 predicted members of the GID/CTLH complex as determinants of intracellular growth

86 ow that the anti-microbial properties of the GID/CTLH complex knockout macrophages are mediated by en

87 been shown to antagonize Wnt signaling, the GID inhibits GSK-3beta in vivo and activates Wnt signali

88 der behavior, and CNS differences related to GID and bi-gender descriptions.

89 In yeast strains expressing a Tra1 GID mutant, binding of Gal4 to the promoter is unexpecte

90 In contrast to WT Tra1, Tra1 GID mutants are not recruited by Gal4 to the promoter an

91 n (3kDa) permeates before and after in vitro GID of model IFs.

92 After the in vitro GID of the samples, only the inhibition of alpha-glucosi

93 Protein degradation during in vitro GID was evaluated by SDS-PAGE and by measuring the nitro

94 ased by about 50% at the end of the in vitro GID.

95 2 milk based on BCM7 release during in vitro GID.

96 214 from Thailand (107 healthy and 107 with GID).

97 luding 113 from Vietnam (46 healthy, 67 with GID) and 214 from Thailand (107 healthy and 107 with GID