ライフサイエンスコーパス: cellular dysfunction

1 they are formed and proliferate to generate cellular dysfunction.

2 racellular aggregates that initiate profound cellular dysfunction.

3 ds may impair normal cell signaling, causing cellular dysfunction.

4 together with lipofuscin, may contribute to cellular dysfunction.

5 e is enriched, OXPHOS declines, resulting in cellular dysfunction.

6 terocyte viability, increased apoptosis, and cellular dysfunction.

7 l significance of these reaction pathways to cellular dysfunction.

8 ey then penetrate these live cells and cause cellular dysfunction.

9 nstead are part of a coordinated response to cellular dysfunction.

10 ir capacity to cause membrane disruption and cellular dysfunction.

11 ral role for PRC in the adaptive response to cellular dysfunction.

12 ransient dysynchrony without whole heart and cellular dysfunction.

13 nce, two major protective mechanisms against cellular dysfunction.

14 mal trafficking, substrate accumulation, and cellular dysfunction.

15 ation of spurious oxidative damage can cause cellular dysfunction.

16 ent observed phenotypes represent reversible cellular dysfunction.

17 endothelial cells, which is associated with cellular dysfunction.

18 (GPCRs) involved in host defense and sensing cellular dysfunction.

19 e arise from Purkinje cell death rather than cellular dysfunction.

20 ceptors involved in host defense and sensing cellular dysfunction.

21 ccumulates within the islet to contribute to cellular dysfunction.

22 ls of mitochondrial fusion and escaped major cellular dysfunction.

23 ential as a therapeutic target to ameliorate cellular dysfunction.

24 comprise a catalytic A-subunit that induces cellular dysfunction and a B-pentamer that recognizes ho

25 Genomic instability leads to mutations, cellular dysfunction and aberrant phenotypes at the tiss

26 ansduction pathways, which can contribute to cellular dysfunction and age-related reductions in stres

27 sruption is a novel mechanism to account for cellular dysfunction and apoptosis in T2DM.

28 delicate quality-control system can lead to cellular dysfunction and apoptosis.

29 mitochondrial Ca(2+) homeostasis can lead to cellular dysfunction and apoptosis.

30 c role of p53 in the mitochondria-associated cellular dysfunction and behavioral abnormalities of Hun

31 hat lipotoxicity in Schwann cells results in cellular dysfunction and cell death that involves a robu

32 This lipid overload is associated with cellular dysfunction and cell death, which contribute to

33 hronic diseases and has been associated with cellular dysfunction and cell death.

34 nergistic disruptive mechanisms that lead to cellular dysfunction and cell death.

35 ellular calcium may play a role in mediating cellular dysfunction and death following central nervous

36 Hepatocyte cellular dysfunction and death induced by lipids and mac

37 euronal signaling but can also contribute to cellular dysfunction and death under pathological condit

38 echanisms whereby mutant huntingtin leads to cellular dysfunction and death.

39 is known to induce lipotoxicity resulting in cellular dysfunction and death.

40 ely results in global oxidative stress (OS), cellular dysfunction and death.

41 ygen and nitrogen species capable of causing cellular dysfunction and death.

42 Inadequate oxygenation can cause cellular dysfunction and death.

43 an overproduction of ceramide and consequent cellular dysfunction and death.

44 ed as a key mechanism underlying age-related cellular dysfunction and disease progression.

45 be cytoprotective, it can also contribute to cellular dysfunction and disease progression.

46 cellular components that may play a role in cellular dysfunction and disease.

47 ry incurred during liver surgery can lead to cellular dysfunction and elevations in proinflammatory c

48 mation of oxidized LDL in the artery wall to cellular dysfunction and formation of lesions.

49 sult of cell death per se, but the result of cellular dysfunction and morphological alterations that

50 of the mutant protein is expected to prevent cellular dysfunction and neurodegeneration in HD.

51 s valuable new insight into mTORC1-dependent cellular dysfunction and neurodevelopmental disorders.

52 ts to nuclear proteins eventually leading to cellular dysfunction and neuronal death.

53 eta42) lead to a series of events that cause cellular dysfunction and neuronal death.

54 gical mechanisms do not explain the basis of cellular dysfunction and organ failure, the ultimate cau

55 understanding into how these defects lead to cellular dysfunction and organ pathology is still incomp

56 dation may play a role in the development of cellular dysfunction and other complications of diabetes

57 anisms by which protein aggregation mediates cellular dysfunction and overt cell death are unknown.

58 ation of misfolded proteins and to potential cellular dysfunction and pathological consequences.

59 prevent Abeta42 aggregation protects against cellular dysfunction and reduces the production/accumula

60 ial stress, inflammation, pulmonary vascular cellular dysfunction and structural dysregulation, iron

61 are considered as toxic metabolites causing cellular dysfunction and tissue damage, the enzymology o

62 lar NAD(+) and subsequently, ATP, leading to cellular dysfunction and, ultimately, cell death.

63 er-ordered aggregates, and cause a myriad of cellular dysfunctions and neuronal death.

64 n (AL-LC) proteins provoke oxidative stress, cellular dysfunction, and apoptosis in isolated adult ca

65 y attenuated AL-LC-induced oxidative stress, cellular dysfunction, and apoptosis.

66 alcineurin inhibitors benefit axonal damage, cellular dysfunction, and cognitive outcomes in animal m

67 Fibrosis, cellular dysfunction, and gap junction protein alteratio

68 sequent activation of inflammatory pathways, cellular dysfunction, and lipoapoptosis.

69 Accumulated protein damage and resultant cellular dysfunction are consequences of limited protein

70 e and untreatable, and mechanisms underlying cellular dysfunction are poorly understood.

71 iapoptotic effects on beta-cells and prevent cellular dysfunction associated with mitoNEET overexpres

72 g of the relative contribution of reversible cellular dysfunction at different stages in disease.

73 ing that the DA subgenomic segment can cause cellular dysfunction but not death, possibly similar to

74 ations to a variety of stress conditions and cellular dysfunction, but how the energetic demands are

75 ontaining expanded CUG or CCUG repeats cause cellular dysfunction by altering the processing or metab

76 f mutant huntingtin in the nucleus may cause cellular dysfunction by binding to Sp1 and thus reducing

77 We propose a novel mechanism for cellular dysfunction by the HD mutation arising from the

78 twi/twi Schwann cells that may be reflecting cellular dysfunctions by inhibition of the PKC.

79 ease hypothesis that protein aggregation and cellular dysfunction can occur at a threshold of approxi

80 Mutant HTT expression leads to a myriad of cellular dysfunctions culminating in neuronal loss and c

81 In addition to its role in cellular dysfunction during metabolic stress, the period

82 deficiencies contribute to microvascular and cellular dysfunction following critical illness.

83 citotoxicity has been shown to contribute to cellular dysfunction following traumatic brain injury (T

84 s involving cells, chemokines and cytokines, cellular dysfunctions, growth factors, and viral protein

85 Although many cellular dysfunctions have been described in cystinosis,

86 AD-related cellular dysfunctions have been linked to this ApoE4 mis

87 impairs neuronal energetics, contributing to cellular dysfunction in AD.

88 y, autophagy is tightly regulated to prevent cellular dysfunction in all eukaryotic cells.

89 nal MT stability and suggest a mechanism for cellular dysfunction in dynein-linked disease.

90 al mutant fragments that aggregate and cause cellular dysfunction in HD.

91 tect LDL oxidation and prevent oxLDL-induced cellular dysfunction in HUVECs.

92 contributes to free fatty acid (FFA)-induced cellular dysfunction in nonislet tissues in type 2 diabe

93 quantity of ectopic fat could contribute to cellular dysfunction in obesity and type 2 diabetes.

94 nisms and, potentially, provides a basis for cellular dysfunction in pathologic situations in which i

95 portant questions about common mechanisms of cellular dysfunction in these disorders.

96 The first indication of cellular dysfunction in treated SC cultures was a decrea

97 (mtHtt), and is associated with a variety of cellular dysfunctions including excessive mitochondrial

98 ty, leading to aberrant chromatin states and cellular dysfunction, including those related to morphog

99 g accumulation of amyloid A and for limiting cellular dysfunction induced by amyloid A.

100 consistent with the hypothesis that adipose cellular dysfunction is a primary contributor to systemi

101 A major cellular dysfunction is insufficient apical plasma membr

102 ing in displacement of normal structures and cellular dysfunction is the characteristic feature of sy

103 oteins, which occur naturally or result from cellular dysfunction, might be more common than recogniz

104 ll enable us to directly test whether common cellular dysfunction or behavioural outcomes of a geneti

105 the application of gene products that reduce cellular dysfunction or death represent new therapeutic

106 ough reactive oxygen species toxicity) drive cellular dysfunction or demise.

107 ngton's disease (HD), cognitive symptoms and cellular dysfunction precede the onset of classical moto

108 the early cognitive deficits may be due to a cellular dysfunction rather than being a consequence of

109 nature of species responsible for mediating cellular dysfunction remain unclear.

110 ich was associated with their development of cellular dysfunction; second, when peritoneal macrophage

111 pects of Alzheimer's disease (AD)-associated cellular dysfunction, suggesting a pivotal role for this

112 d or prolonged tissue injury, can exacerbate cellular dysfunction, suggesting that it may contribute

113 hronic exposure to hyperglycemia can lead to cellular dysfunction that may become irreversible over t

114 onal regulation is one of the main causes of cellular dysfunction that underlies different disease st

115 tion and parenchymal inflammation leading to cellular dysfunction, thrombosis, and fibrosis.

116 mia causes myocardial insulin resistance and cellular dysfunction via IRS1 and IRS2, we generated hea

117 GPCR/G protein interfaces and counteracting cellular dysfunctions via focused tuning of GPCR signali

118 HADH II enzymatic activity to Abeta-mediated cellular dysfunction was studied by site-directed mutage

119 ng several cellular biological mechanisms of cellular dysfunction, we and others have recently propos

120 the presence of misfolded proteins leads to cellular dysfunction, we employed Caenorhabditis elegans

121 d colleagues demonstrated a toxic cascade of cellular dysfunctions which may underlie Parkinson's dis

122 L expression (which can persist) can lead to cellular dysfunction with survival.

123 protein, are responsible for a wide range of cellular dysfunctions within the vessel wall.

124 adily express protein aggregates, leading to cellular dysfunction without concomitant up-regulation o