ライフサイエンスコーパス: Gln residue

1 of a Thr side chain to the alpha-carbon of a Gln residue.

2 ng a strict requirement for either an Asn or Gln residue.

3 pin the specificity of the enzyme for the P2 Gln residue.

4 rotein beyond the active site is a conserved Gln residue.

5 often contain catalytically essential Asp or Gln residues.

6 h site-directed mutagenesis of these Asn and Gln residues.

7 the cross-linking reaction of at least three Gln residues (221, 237, 328) in the NH2-terminal region

8 lography of the V52Q protein showed that the Gln residue adopts the same configuration relative to th

9 an disease include deamidation of glutamine (Gln) residues, amine incorporation into Gln residues, an

10 Bank voles have a high number of Asn and Gln residues and a high Asn:Gln ratio.

11 ine (Gln) residues, amine incorporation into Gln residues, and protein crosslinking.

12 The Gln residues appear to be essential for the proliferatio

13 rnifin beta can function through some of its Gln residues as an amine acceptor in transglutaminase-ca

14 A Gln residue at position 192 in the US11 TMD is crucial f

15 other mutant, DAB389 IL-2(Q514D), in which a Gln residue at position 514 was changed to an Asp, was 2

16 was 3-fold more active as a substrate than a Gln residue at this position.

17 Remarkably, Gln residues at positions 49 and 139 could not be replac

18 ndings suggest that a high number of Asn and Gln residues at specific positions may stabilize beta-sh

19 Thr, Val, Ile, Leu, Met, Arg, Lys, Glu, and Gln residues correlate with both the number of heavy ato

20 d mutagenesis was used to substitute Ala and Gln residues for the conserved Lys residue of the Walker

21 ession which was retained upon deletion of a Gln residue from the inserted 2B/2C cleavage site.

22 ectroscopy and (3)J(HN-C alpha) constants of Gln residues from constant time correlation spectroscopy

23 , we identified that mutation at a conserved Gln residue impedes the interaction of PNKP with importi

24 G46 and V48 that alter dynamic motions of a Gln residue implicated in signal transduction in all LOV

25 sts an analogous catalytic function for this Gln residue in HisKA_3 members.

26 n-glycan profiling revealed that a conserved Gln residue in the GnTI TMD is essential for its cis/med

27 catalyzes transfer of gamma-acyl moieties of Gln residues in peptides or protein substrates to either

28 Gln residues in positions 6 and 17 produce a polar face,

29 HsIPMK activities rely on a preponderance of Gln residues, in contrast to the larger Lys and Arg resi

30 Substituting a Gln residue into the P2 of the activation site of MASP-3

31 The P(1) site being occupied by a Gln residue is a nonarchetype with respect to known prot

32 Results show that the Gln residue is critical for transmitter phosphatase acti

33 diate vicinity of the FMN binding site, this Gln residue is provided by the Ibeta strand that interac

34 Deamidation of glutamine (Gln) residues is a spontaneous or enzymatic process with

35 Since mutations of the Gln residues located within the BH4 domain appear to con

36 that multiple PrP(C) segments containing Asn/Gln residues may act in concert along a replicative inte

37 ard PPII, increasing the threshold number of Gln residues needed for fibrillation.

38 Mechanisms for expanded (>36 Gln residues) poly(Gln) toxicity include the formation o

39 pound I in 5,8-LDS are influenced by Asn and Gln residues, respectively, of the I-helices.

40 ydrogen bonding interactions of an invariant Gln residue that has been proposed to flip its amide sid

41 te-directed mutants of the conserved Asn and Gln residues that form hydrogen bonds with water molecul

42 Composed only of Ala, Leu, and Gln residues, the amino acid sequences of the peptides w

43 y occurring TM domains that contain a Glu or Gln residue (Tnf5/CD40 ligand, C79a/Ig-alpha, C79b/Ig-be

44 which show that substitution of the Asn and Gln residues to Ala compromises the Sup35 fibril stabili

45 lpha C30K fragment, lacking the NH2-terminal Gln residues, was not able to form polymers or internall

46 Four of the five conserved Asn/Gln residues were changed in six mutants generated in th

47 of each labeled peptide showed that 4 of 35 Gln residues were labeled with the following reactivitie

48 For two of the four positions, Asn and Gln residues were not interchangeable, revealing a stric

49 nique to the PTPase family are two invariant Gln residues which are located at the active site.

50 Substitution of the crucial Gln residue with other amino acids resulted in mislocali

51 ich proteins occurred preferentially after a Gln residue with predominant specificity for the tripept

52 tion of heat-labile, surface-exposed Asn and Gln residues with thermoadaptation.

53 anding (Asp, Glu) and poorly liganding (Asn, Gln) residues with significant native-like tetrahedral m