ライフサイエンスコーパス: abnormal protein

1 a better predictor of FA-M/E positivity than abnormal protein.

2 olytic degradation of certain regulatory and abnormal proteins.

3 r ubiquitin-dependent degradation of certain abnormal proteins.

4 thological pathways and prion-like spread of abnormal proteins.

5 r inability to scavenge structurally damaged abnormal proteins.

6 nt mechanisms that normally repair or remove abnormal proteins.

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

8 Oligomerisation of the spindle assembly abnormal protein 6 (SAS-6) is an essential step in the c

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

10 a group of diseases commonly associated with abnormal protein accumulation and aggregation in the cen

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

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

13 ent work has established the primary role of abnormal protein accumulation and the spread of disease-

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

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

16 n 1 antibody did not have rimmed vacuoles or abnormal protein accumulation.

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

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

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

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

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

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

23 disorders are defined by the accumulation of abnormal protein aggregates that impair synaptic functio

24 which may increase the risk of accumulating abnormal protein aggregates, a hallmark of most neurodeg

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

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

27 components, including damaged organelles and abnormal protein aggregates.

28 lected neuronal populations and formation of abnormal protein aggregates.

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

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

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

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

33 More recently, such abnormal protein aggregation has been reported to spread

34 rt in vivo patterns of neuroinflammation and abnormal protein aggregation in seven cases of familial

35 progressive neurological disorder featuring abnormal protein aggregation in the brain, including the

36 Abnormal protein aggregation is a hallmark of many neuro

37 Abnormal protein aggregation is emerging as a common the

38 Abnormal protein aggregation is observed in an expanding

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

40 Cells utilize protein disaggregases to avoid abnormal protein aggregation that causes many diseases.

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

42 neurodegenerative diseases characterized by abnormal protein aggregation, including amyotrophic late

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

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

45 n neurodegenerative diseases associated with abnormal protein aggregation.

46 f neurodegenerative diseases associated with abnormal protein aggregation.

47 binatory of motor and cognitive symptoms and abnormal protein aggregation.

48 stress, dopaminergic neurodegeneration, and abnormal protein aggregation.

49 pathogenic process in cardiac disorders with abnormal protein aggregation.

50 mechanism underlying cardiac disorders with abnormal protein aggregation.

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

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

53 autophagic pathways leads to accumulation of abnormal proteins and damaged organelles in many neurode

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

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

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

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

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

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

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

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

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

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

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

65 oteasome is pivotal to the timely removal of abnormal proteins but its functional capacity often beco

66 l disease was not due to cell toxicity of an abnormal protein, but rather to haploinsufficiency and l

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

68 translation results in the production of an abnormal protein, called FMRpolyG.

69 "Dysregulated" and "Undifferentiated", with abnormal protein concentrations and adverse outcomes in

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

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

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

73 s, including reduced synaptic plasticity and abnormal protein content by 8-10 months of age.

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

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

76 The abnormal protein degradation implicated in the pathogene

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

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

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

80 roteinopathies are disorders associated with abnormal protein depositions in brain neurons.

81 brain glucose metabolism and accumulation of abnormal protein deposits called plaques and tangles are

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

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

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

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

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

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

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

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

90 Abnormal protein distributions were reversed in cultured

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

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

93 ine-rich dipeptide repeats (DPRs), mimicking abnormal proteins expressed from the hexanucleotide expa

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

95 Our study reveals that the abnormal protein folding and N-glycosylation can cause w

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

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

98 in impaired troponin solubility, suggesting abnormal protein folding.

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

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

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

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

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

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

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

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

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

108 enic variants in VMA21 in male patients with abnormal protein glycosylation that result in mild chole

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

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

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

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

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

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

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

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

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

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

119 al for breaking down most of the damaged and abnormal proteins in human cells.

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

121 act mechanisms underlying the propagation of abnormal proteins in the brain are only partially unders

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

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

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

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

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

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

128 nesis of the TNNI3 variant is not related to abnormal protein incorporation within the sarcomere.

129 ocesses and functions presumably mediated by abnormal protein interactions of mutant HTT.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

144 is a chronic inflammatory disease driven by abnormal protein modifications.

145 n gene which results in the production of an abnormal protein, mutant huntingtin (mHtt).

146 ses and for advancing therapeutics targeting abnormal protein oligomerization.

147 mprehensive protein information and identify abnormal proteins/peptides.

148 nd identifying a misclassified case based on abnormal proteins phenotype.

149 d other neurodegenerative diseases involving abnormal protein polymerization.

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

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

152 Abnormal protein processing and modification is associat

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

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

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

156 Additionally, Abeta deposits and abnormal protein responses have been observed in cardiom

157 The abnormal proteins resulting from these fusion genes aber

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

159 We hypothesized that the spread of these abnormal proteins selectively affects vulnerable areas,

160 tif 1 (RRM1) of TDP-43, which is involved in abnormal protein self-aggregation and interaction with p

161 Small-molecule inhibitors of abnormal protein self-assembly are promising candidates

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

163 iverse methodological approaches to describe abnormal protein signalling across distinct intra-tumour

164 s in the urine of CKD patients and extracted abnormal protein signals comparing with the healthy cont

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

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

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

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

169 Genetic mutations, abnormal protein synthesis, environmental stress, and ag

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

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

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

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

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

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

176 The abnormal proteins that partitioned to the insoluble pell

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

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

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

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

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

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

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

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

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

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

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

188 Abnormal protein tyrosine kinases (PTKs) cause many huma

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

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

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

192 Abnormal proteins, which escape chaperone-mediated refol