ライフサイエンスコーパス: copper deficiency

1 ction of Heph expression and activity during copper deficiency).

2 nduction of cum1(+)-lacZ transcription under copper deficiency.

3 motifs in the MIR408 promoter in response to copper deficiency.

4 the most common neurological complication of copper deficiency.

5 activates genes necessary during periods of copper deficiency.

6 ctivation of Mac1 in response to an external copper deficiency.

7 e zebrafish embryo identical to that seen in copper deficiency.

8 between up- and down-regulated genes in iron copper deficiency.

9 mentation, and seizures because of perinatal copper deficiency.

10 under growth conditions of excess copper or copper deficiency.

11 me c(6) and coprogen oxidase) in response to copper deficiency.

12 ies and growth retardation characteristic of copper deficiency.

13 ripheral blood is reduced in cases of severe copper deficiency.

14 s is also reduced in both overt and marginal copper deficiency.

15 and families facing this troublesome form of copper deficiency.

16 smorphogenesis associated with developmental copper deficiency.

17 ow bioavailability from the diet may lead to copper deficiency.

18 mbranes suggested a tendency toward moderate copper deficiency.

19 d, suggesting that the apoSOD was not due to copper deficiency.

20 Both are signs of copper deficiency.

21 er, the observations argue for a specialized copper-deficiency adaptation for iron uptake in Chlamydo

22 compound to moist air is shown to result in copper deficiency and a decrease in the size of the orde

23 fatty liver disease reveals onset of hepatic copper deficiency and altered expression levels of centr

24 recent developments in our understanding of copper deficiency and copper homeostasis outlined in thi

25 n the genes encoding ATP7A and ATP7B lead to copper deficiency and copper toxicity disorders, Menkes

26 KEY MESSAGE: Copper deficiency and excess differentially affect iron

27 lly meaningful regulatory connection between copper deficiency and hypoxia.

28 arch showed that interleukin 2 is reduced in copper deficiency and is likely the mechanism by which T

29 stasis in mitochondria even in situations of copper deficiency and mitochondrial metallochaperone mal

30 the effects of mild short-term and long-term copper deficiency and the role of copper in other physio

31 The best characterized are the copper deficiency and toxicity disorders Menkes and Wils

32 ation nutritional evaluation revealed severe copper deficiency, and her hematologic abnormalities res

33 ces cerevisiae, transcriptional responses to copper deficiency are mediated by the copper-responsive

34 neurologic findings in adults with acquired copper deficiency as well as the development of novel mo

35 chondrial metallochaperones lead to a global copper deficiency at the whole cell level, total copper

36 athy has been recognised in association with copper deficiency but has not been well characterised.

37 Chlamydomonas reinhardtii adapts to copper deficiency by degrading apoplastocyanin and induc

38 Copper deficiency can result in anemia, neutropenia, ske

39 Thus, copper deficiency could explain the unexpectedly low pop

40 s underscored by Menkes disease, an X-linked copper deficiency disorder caused by mutations in the co

41 rting P-type ATPase that is defective in the copper deficiency disorder, Menkes disease.

42 ndrome (OHS) are allelic, X-linked recessive copper-deficiency disorders resulting from mutations in

43 otype are X-linked diseases that result from copper deficiency due to mutations in a copper-effluxing

44 Copper deficiency during embryonic and fetal development

45 Acquired copper deficiency has been documented in conditions pred

46 The diagnosis of marginal copper deficiency has not been perfected despite an incr

47 Copper deficiencies have been linked with photoreceptor

48 Acquired copper deficiency in adults is reported with increasing

49 omes suggest that the canned formula induced copper deficiency in infant monkeys.

50 and that its knockdown partially rescues the copper deficiency in patient cells.

51 The copper deficiency in SCO patient fibroblasts is rescued

52 Importantly, we find that copper deficiency in these mutants promotes aggregation

53 Copper deficiency in wild-type cells does not change the

54 In contrast with purely nutritional copper deficiency, in which copper replacement can be cu

55 We report that copper deficiency induced by tetrathiomolybdate (TM) sig

56 or mechanism of the antiangiogenic effect of copper deficiency induced by TM is suppression of NFkapp

57 previously for Cyc6 and is restricted to the copper deficiency-induced Cpx1 transcript.

58 re models to study the mechanisms underlying copper deficiency-induced teratogenesis.

59 Copper deficiency is an under-recognized cause of revers

60 use copper is an essential micronutrient and copper deficiency is detrimental to many important cellu

61 Overt copper deficiency is not believed to be a widespread pub

62 tudies may yield important insights into how copper deficiency is sensed and appropriate cellular res

63 anism that operates in microalgae faced with copper deficiency is the replacement of the abundant cop

64 Patients with simultaneous copper deficiency (<0.78 mug/mL) and peripheral neuropat

65 y copper transport protein, as well as other copper-deficiency markers are down-regulated by copper.

66 osis, and anemia, and the effects of genetic copper deficiency (Menkes syndrome) and copper overload

67 The impact of copper deficiency on the expression of several O(2)-depe

68 ldiglycerides, indicating a global impact of copper deficiency on the photosynthetic apparatus.

69 ns may predispose individuals to the risk of copper deficiency or copper excess.

70 atients could be at risk for either moderate copper deficiency or copper toxicity.

71 Copper deficiency or excess results in severe neuro-path

72 s in live cells and mice under situations of copper deficiency or overload.

73 supplementation, which normally activate the copper deficiency regulon in wild-type cells.

74 Mercuric ions, which antagonize the copper-deficiency response, also antagonize the oxygen-d

75 st, COPT2 participates in the attenuation of copper deficiency responses driven by iron limitation, p

76 se observations suggest that the oxygen- and copper-deficiency responses share signal transduction co

77 onditions for copper detoxification, whereas copper deficiency results in a redistribution of CUA-1 t

78 e study by Peled and coworkers suggests that copper deficiency results in the inhibition of different

79 This case shows that copper deficiency should be an integral part of the diff

80 ese cells exhibited biochemical signature of copper deficiency, suggesting that GSH functions as an i

81 is more active in cells that are adapted to copper deficiency than to cells grown in a medium contai

82 ved in both models due to a combined COX and copper deficiency that resulted in a dilated cardiomyopa

83 Cs remains cubic regardless of the degree of copper deficiency (that is, "x") in the NC lattice.

84 ected patients exhibit signs and symptoms of copper deficiency, the mechanisms resulting in neurologi

85 same genes are activated also in response to copper-deficiency through copper-response elements that

86 Genetic and genomic studies indicate that copper deficiency triggers changes in the expression of

87 adequate copper stores, are prone to develop copper deficiency unless given higher provisions of copp

88 causing sensory ataxia is characteristic of copper deficiency usually co-occurring with myelopathy.

89 uned by actively controlling their degree of copper deficiency via oxidation and reduction experiment

90 In the 25 y since copper deficiency was first delineated in persons with M

91 Perinatal copper deficiency was studied in young rats in rapidly f

92 t and may modulate Cu transport rates during copper deficiency, Wilson's disease, and other copper to

93 studies have reported on the association of copper deficiency with the development of concomitant ne