ライフサイエンスコーパス: abnormal protein

1 olytic degradation of certain regulatory and abnormal proteins.

2 r ubiquitin-dependent degradation of certain abnormal proteins.

3 r inability to scavenge structurally damaged abnormal proteins.

4 nt mechanisms that normally repair or remove abnormal proteins.

5 old symmetry imposed by the spindle assembly abnormal protein 6 (SAS-6) family.

6 ues to uncover molecular mechanisms by which abnormal proteins accumulate in degenerating brain tissu

7 xperimental glomerular disease, resulting in abnormal protein accumulation and compensatory upregulat

8 mitochondrial dysfunction, oxidative damage, abnormal protein accumulation and protein phosphorylatio

9 occur in the absence of neurodegeneration or abnormal protein accumulation within the substantia nigr

10 herapeutic potentials in reducing ER stress, abnormal protein accumulation, and neurological deficits

11 (Atg) genes results in neurodegeneration and abnormal protein accumulation.

12 sp70 serves as a "sensor" of the build-up of abnormal proteins after heat shock and other stresses.

13 , which are characterized by accumulation of abnormal protein aggregates (e.g. tau and alpha-synuclei

14 sequence of an attempt of the cell to remove abnormal protein aggregates and damaged organelles.

15 e huntingtin (HTT) gene, is characterized by abnormal protein aggregates and motor and cognitive dysf

16 alpha-syn) as the primary constituent of the abnormal protein aggregates observed in the brains of MS

17 m allowing recycling of long-lived proteins, abnormal protein aggregates, and damaged organelles unde

18 ar Hcy levels predisposes neurons to develop abnormal protein aggregates, which are hallmarks of AD a

19 components, including damaged organelles and abnormal protein aggregates.

20 lected neuronal populations and formation of abnormal protein aggregates.

21 e etiology of ALS remains poorly understood, abnormal protein aggregation and altered proteostasis ar

22 defects in the protein degradation pathway, abnormal protein aggregation and neurodegeneration, indi

23 thione self-recognition in such processes as abnormal protein aggregation and the thiol-disulfide exc

24 in the hearts of iDCM patients, pointing to abnormal protein aggregation as a determinant of iDCM.

25 Abnormal protein aggregation is a hallmark of many neuro

26 Abnormal protein aggregation is emerging as a common the

27 Abnormal protein aggregation is observed in an expanding

28 n global protein homoeostasis resulting from abnormal protein aggregation or a defect in the protein

29 rain dopamine neurons from oxidative stress, abnormal protein aggregation, and genetic predisposition

30 ay be applicable to other diseases caused by abnormal protein aggregation, such as Alzheimer's diseas

31 n neurodegenerative diseases associated with abnormal protein aggregation.

32 pathogenic process in cardiac disorders with abnormal protein aggregation.

33 mechanism underlying cardiac disorders with abnormal protein aggregation.

34 c model of Parkinson disease that emphasizes abnormal protein aggregation.

35 The almost complete absence of abnormal protein and near-normal accumulation of microfi

36 nol that is known to cause the production of abnormal proteins and affect the cell membrane.

37 accessory factor is apparently necessary for abnormal proteins and for RcsA.

38 otease Lon (La) of Escherichia coli degrades abnormal proteins and is involved in the regulation of c

39 g of the cellular mechanisms for disposal of abnormal proteins and of the effects of toxic protein ac

40 play an essential role in the degradation of abnormal proteins and organelles.

41 malian stress proteins in the recognition of abnormal proteins and provide supporting evidence for re

42 a serine protease involved in proteolysis of abnormal proteins and required for resistance to oxidati

43 to the accumulation of sufficient amounts of abnormal proteins and/or the inhibition of degradation o

44 not perfect overlap among the cells in which abnormal proteins are deposited and the cells that degen

45 Noninvasive methods to detect these abnormal proteins are potentially useful in developing s

46 We analyzed abnormal protein bands (APB), distinct from the presenti

47 t distinct subsets of misfolded or otherwise abnormal proteins based primarily on degradation signal

48 ones are necessary for the breakdown of many abnormal proteins, but their functions in this process h

49 ould be preferentially used in patients with abnormal protein concentrations.

50 r neurodegenerative diseases associated with abnormal protein conformation and toxicity.

51 reflecting a propensity for codeposition of abnormal protein conformers, remains to be determined.

52 gella revealed that the mutant flagella have abnormal protein content, including abnormal levels of i

53 ized that mutations that are translated into abnormal proteins could affect the transcription of GATA

54 Certain NKX2-5 homeodomain mutations show abnormal protein degradation via the Ubiquitin-proteasom

55 development of corneal dystrophies in which abnormal protein deposition in the cornea leads to a los

56 completely understood, changes in the brain: abnormal protein deposition, synaptic dysfunction, neuro

57 en rate of brain atrophy and the presence of abnormal protein deposits in the brain in dementia, and

58 a small group of psychiatrists described the abnormal protein deposits in the brain that define the m

59 As the mice aged, we observed abnormal protein deposits on the cartilage surface and d

60 encephalopathies (TSEs) are characterized by abnormal protein deposits, often with large amyloid fibr

61 nt of therapies that specifically target the abnormal proteins derived from these mutations.

62 These chimeric transcripts encode abnormal proteins, designated CP1, CP60 and CP69, consis

63 mptoms of patients with these mutations, the abnormal proteins displayed diminished capacities to act

64 crease of cathepsin V/L2 mRNA (P < 0.03) and abnormal protein distribution; and a 1.8-fold decrease o

65 Abnormal protein distributions were reversed in cultured

66 g terminally differentiated cells accumulate abnormal proteins due to chronic environmental or physio

67 s with an abnormal free light-chain ratio or abnormal protein electrophoresis results from the origin

68 ifts, premature cessation of translation and abnormal protein expression.

69 Amyloidoses are diseases characterized by abnormal protein folding and self-assembly, for which no

70 We predict that abnormal protein folding or aggregation or both contribu

71 in impaired troponin solubility, suggesting abnormal protein folding.

72 roduct of a broken mRNA; the tag targets the abnormal protein for proteolysis.

73 as many diverse functions, including tagging abnormal proteins for degradation, supporting phage grow

74 ognized mechanism for the production of some abnormal proteins found in cancer cells.

75 d, these systems must be able to distinguish abnormal proteins from normal ones, yet be capable of re

76 with PAX6 missense mutations originate from abnormal protein function in a restricted number of ocul

77 ime a correlation between RAI1 mutations and abnormal protein function plus they suggest that a reduc

78 eculated that the expansion primarily causes abnormal protein functioning, which in turn causes HD pa

79 ere found between MRP inhibitor exposure and abnormal protein, glucose, or phosphate handling in the

80 ers of glycosylation (CDGs) are disorders of abnormal protein glycosylation that affect multiple orga

81 ion and aggregation of potentially cytotoxic abnormal proteins have been identified in the substantia

82 ed proteins as a result of gene mutations or abnormal protein homeostasis.

83 sequence of the amino acid glutamine in the abnormal protein huntingtin (Htt).

84 hology and tissue levels and function of the abnormal protein in order to explore consequences of the

85 work describes the presence of an additional abnormal protein in pancreatic cancer and describes a ne

86 Here, we report the presence of the same abnormal protein in pancreatic carcinoma and explore the

87 identified alpha-synuclein (SNCA) as a major abnormal protein in PDC but not AD.

88 ns offer the potential to detect or treat an abnormal protein in the presence of the wild type (WT).

89 addition, we have found that accumulation of abnormal proteins in cells upon incubation with amino ac

90 The role of aggregation of abnormal proteins in cellular toxicity is of general imp

91 tivates mTORC1 to inhibit autophagy and form abnormal proteins in human neurons and mice.

92 logically characterized by the deposition of abnormal proteins in the brain.

93 regulatory proteins as well as defective and abnormal proteins in the cell.

94 Intracellular accumulation of abnormal proteins in these diseases, a pathological hall

95 ons about the relative levels of genetically abnormal proteins in tumors, this approach could prove u

96 hies due to the accelerating accumulation of abnormal proteins including TDP-43 proteinopathy, tauopa

97 f protein products resulting in a buildup of abnormal proteins, including beta-amyloid and phospho-Ta

98 t vesicular and receptor trafficking via its abnormal protein interactions, suggesting that impairmen

99 sis describes neurological diseases where an abnormal protein is misfolded and accumulated as deposit

100 ggesting that the cellular ability to handle abnormal proteins is compromised.

101 onfirmed, and a therapy directed against the abnormal protein it produces has shown promising results

102 n described; these were also associated with abnormal protein kinase A activity.

103 layed increased cytosolic Ca(2+) activation, abnormal protein kinase A phosphorylation, and increased

104 excitation-contraction coupling; furthermore abnormal protein kinase and phosphatase activities have

105 r complications of diabetes and is caused by abnormal protein kinase C activation as a result of incr

106 l or systemic inflammation and filtration of abnormal proteins known to directly injure tubules are a

107 nship among MT activity, the accumulation of abnormal protein L-isoaspartyl residues, and seed viabil

108 s seed vigor and longevity by repairing such abnormal proteins mainly in the cytosolic fraction.

109 red IGF-1 signaling in CKD not only leads to abnormal protein metabolism in muscle but also impairs s

110 th impaired insulin/IGF-1 signaling, causing abnormal protein metabolism.

111 these agents, by causing the accumulation of abnormal proteins, might stimulate the expression of cyt

112 d other neurodegenerative diseases involving abnormal protein polymerization.

113 Self-propagating abnormal proteins, prions, have been identified in yeast

114 -related proteins during the whole lifetime; abnormal protein processing and aggregation; and cellula

115 Abnormal protein processing and modification is associat

116 their vulnerability to other insults due to abnormal protein processing or changes in signaling path

117 the vast majority of these diseases and the abnormal proteins produced caused by these mutations.

118 g factors that lead to aberrant splicing and abnormal protein production.

119 The abnormal proteins resulting from these fusion genes aber

120 ons could be identified--that is, normal and abnormal protein segments were seen on SDS-PAGE gels.

121 Inhibition or modulation of abnormal protein self-assembly, therefore, is an attract

122 llows examination of mutation effects on the abnormal protein structure and function.

123 e activated in neurodegenerative diseases by abnormal protein structures, such as amyloid fibrils in

124 as for about 50% of the rapid degradation of abnormal proteins such as canavanine-containing proteins

125 ations in genes related to the prevention of abnormal protein synthesis under oxidative stress.

126 mRNA properties, adds short peptide tags to abnormal proteins, targeting these proteins for proteoly

127 ed knockout system as a tool in targeting an abnormal protein that affects growth and transformation.

128 with diffuse Lewy bodies is the result of an abnormal protein that interferes with normal protein deg

129 strates for this degradation pathway include abnormal proteins that arise from misfolding and/or muta

130 In mammalian cells, abnormal proteins that escape proteasome-dependent degra

131 ted mRNAs as templates for the production of abnormal proteins that might be toxic to bacteria.

132 The abnormal proteins that partitioned to the insoluble pell

133 thway plays a major role in the breakdown of abnormal proteins that result from oxidative stress, neu

134 tworks and, perhaps, chronic intoxication by abnormal proteins that the brain is temporarily able to

135 easomes must remove regulatory molecules and abnormal proteins throughout the cell, but how proteasom

136 These results provide further evidence for abnormal protein TKP in hyperapoB cells and suggest a po

137 mutations cause neutropenia and suggest that abnormal protein trafficking and accelerated apoptosis o

138 a loss of I(Kv11.1) through interactions of abnormal protein trafficking and channel gating.

139 These results demonstrate that abnormal protein trafficking and impairment in MVB matur

140 demonstrate the role of axonal transport and abnormal protein trafficking in causing various forms of

141 that the AtUBP1 and 2 enzymes are needed for abnormal protein turnover in Arabidopsis.

142 organization, impaired signal transduction, abnormal protein turnover, and impaired energy metabolis

143 D) and can lead to loss of protein function, abnormal protein turnover, interference with cell cycle,

144 Abnormal protein tyrosine kinases (PTKs) cause many huma

145 ause for early-onset encephalopathies due to abnormal protein ufmylation.

146 ritical role in mediating the degradation of abnormal proteins under conditions of oxidative stress a

147 Accordingly, the rate of elimination of abnormal proteins was lower in cells lacking a functiona

148 Abnormal proteins, which escape chaperone-mediated refol