ライフサイエンスコーパス: secretion defect

1 pleted insulin content and evoked an insulin secretion defect.

2 ing LQT2 missense mutations, with incomplete secretion defect.

3 xin-4 single- or double-knockout mice had no secretion defect.

4 priming factor, Munc13-4, and have a severe secretion defect.

5 oplasm led to incomplete cleavage and a mild secretion defect.

6 ne 57-to-lysine mutant had the most dramatic secretion defect.

7 increase in F-actin, but did not rescue the secretion defect.

8 the conditioned medium, suggesting a modest secretion defect.

9 elevated [Ca2+]i, and corrected the insulin secretion defect.

10 een these two Abs to assess the basis of the secretion defect.

11 b/ob islets consistently revealed an insulin secretion defect.

12 sporter EspP have been shown to cause strong secretion defects.

13 Mycobacterium marinum transposon mutants for secretion defects.

14 with a range in severity of cell growth and secretion defects.

15 s in severe temperature-sensitive growth and secretion defects.

16 mmon properties of the suppressors relate to secretion defects.

17 to differentiate black subjects with insulin secretion defects.

18 the mutant protein is able to overcome this secretion defect and improve glomerular permselectivity.

19 mmon in patients with platelet dense granule secretion defects and mild thrombocytopenia.

20 These secretion defects appear to be caused, in part, by reduc

21 The secretion defect appeared to reflect an impaired ability

22 Insulin secretion defects are central to the development of type

23 The cellular secretion defect arises from failure of the aberrant gra

24 on may have profound implications in insulin secretion defects associated with diabetes.

25 Previously, we identified severe secretion defects because of mutations in the heavy chai

26 ed glucose intolerance and beta-cell insulin secretion defect but showed no changes in beta-cell mass

27 ons at the conserved positions in CD2 caused secretion defects, but had little effect on growth at 37

28 te manifestation of the two opposite insulin secretion defects by altering the expression levels of t

29 s critical for virion secretion and that the secretion defect caused by mutations in the S protein ca

30 The M133T mutation could also overcome the secretion defect caused by the G145R immune-escape mutat

31 Persistent insulin secretion defects culminate in progressive deficits in b

32 As predicted, the secretion defect decreased pea and vetch nodulation but

33 glucose and glyburide, suggesting an insulin secretion defect either at the level or upstream of the

34 overexpression of Pep12p suppressed the CPY secretion defect exhibited by vti1-1 cells at 36 degrees

35 ine substitution at yscU codon 263 displayed secretion defects for some substrates (LcrV, YopB and Yo

36 er, without further worsening of the insulin secretion defect, glucose homeostasis deteriorates in ag

37 Aeromonas homologue, ExeE, to complement the secretion defect in both epsL and exeL mutant strains.

38 The secretion defect in each mutant can be suppressed by inc

39 The secretion defect in exo70 mutants was most pronounced du

40 e molecular mechanism underlying the insulin secretion defect in Hnf-1alpha(-/-) mice.

41 ed calcium mobilization rescued the TNFalpha secretion defect in Syk-deficient cells.

42 Moreover, mutations in FRW2 caused secretion defects in 24% (8 of 33), a frequency twice th

43 here, and mistargeting of the exocyst led to secretion defects in cells.

44 We previously described secretion defects in four mutants of the murine anti-pho

45 ing the prevalence of insulin resistance and secretion defects in minorities, especially in African-A

46 e SAR1 pre-mRNA is the specific cause of the secretion defects in prp2-13 and rse1-1.

47 Secretion defects in STXBP5-deficient platelets were con

48 ve new approach for the treatment of insulin secretion defects in type 2 diabetes.

49 bstitutions at Tyr-326 showed strong protein secretion defects in vivo and were completely defective

50 ti1a phenotype, and vti1b null cells show no secretion defects, indicating that vti1b does not partic

51 All six had evidence of protein secretion defects involving two proteins, a 40-kDa prote

52 ing of N1922S-fVIII is a novel mechanism for secretion defects leading to hemophilia A.

53 The magnitude of the secretion defect observed for signal sequence-containing

54 for these genes were determined by comparing secretion defects observed after RNA interference under

55 erase faithfully recapitulates mutant EFEMP1 secretion defects observed previously using more cumbers

56 nt a sec31Delta mutant and cannot rescue the secretion defect of a temperature-sensitive sec31 mutant

57 The secretion defect of the secA2 mutation appears to be lim

58 NARE protein Sft1p suppresses the growth and secretion defects of this mutation.

59 in partially rescued both the behavioral and secretion defects of unc-13 mutants in C. elegans.

60 The ESX-1 secretion defect prevents several virulence factors from

61 In parallel, these mice develop an insulin-secretion defect resulting in a progressive glucose into

62 man beta cell line recapitulated the insulin secretion defect seen in vivo.

63 anum cell lysates, suggesting a modest ESX-1 secretion defect unrelated to the Rv3879c mutation.

64 This apparent secretion defect was completely rescued by inhibition of

65 The secretion defect was not due to altered expression of SN

66 ent TolC substitutions displaying this toxin secretion defect were scattered throughout the protein,

67 Similar neuropeptide secretion defects were found in mutants lacking unc-31 (

68 The same assembly and secretion defects were observed when these mutations wer