ライフサイエンスコーパス: disease pathogenesis

1 2A in axon guidance also suggested a role in disease pathogenesis.

2 ted anatomical structures and/or hormones in disease pathogenesis.

3 ecent data that support intriguing models of disease pathogenesis.

4 tion to altered environmental conditions and disease pathogenesis.

5 wild-type hPFN1 that may contribute to human disease pathogenesis.

6 ide (Abeta) have been related to Alzheimer's disease pathogenesis.

7 y balance, tissue/stem cell homeostasis, and disease pathogenesis.

8 unction is thought to play a crucial role in disease pathogenesis.

9 r variations are suggested to play a role in disease pathogenesis.

10 All these interactions may play a role in disease pathogenesis.

11 that these cells are detrimental throughout disease pathogenesis.

12 knowledge of evolutionary forces underlying disease pathogenesis.

13 tribute to dissect the complex mechanisms of disease pathogenesis.

14 (MNs) and play a non-cell autonomous role in disease pathogenesis.

15 raction, providing the biochemical basis for disease pathogenesis.

16 vating sAC, which may play a crucial role in disease pathogenesis.

17 (CNS), implicating this lysosomal enzyme in disease pathogenesis.

18 vant to understanding how EVs regulate liver disease pathogenesis.

19 ic data to test several popular models of WS disease pathogenesis.

20 (sAPPalpha), analytes central to Alzheimer's disease pathogenesis.

21 ses that have been implicated in Alzheimer's disease pathogenesis.

22 ns, which will aid in investigating MERS-CoV disease pathogenesis.

23 es and therapeutics as well as understanding disease pathogenesis.

24 s compared to non-CPGs in drug discovery and disease pathogenesis.

25 urin inhibits KIT D816V, a primary driver of disease pathogenesis.

26 n ciliary compartmentalization might play in disease pathogenesis.

27 molecules have been thought to contribute to disease pathogenesis.

28 ty is emerging as the central cornerstone of disease pathogenesis.

29 iological process and an important factor in disease pathogenesis.

30 s altered in WS provided new insight into WS disease pathogenesis.

31 of immune responses to decipher inflammatory disease pathogenesis.

32 gnostic possibilities and impact theories of disease pathogenesis.

33 essed in both rods and cones, cause variable disease pathogenesis.

34 nd decreased NET removal are associated with disease pathogenesis.

35 ike receptors (TLRs) may also be involved in disease pathogenesis.

36 understanding of the mechanism of hantavirus disease pathogenesis.

37 Either of these alterations can drive disease pathogenesis.

38 and unexpected mechanistic insights into WS disease pathogenesis.

39 RC1 plays essential roles in development and disease pathogenesis.

40 by a broadly conserved aminopeptidase during disease pathogenesis.

41 and to provide novel molecular insights into disease pathogenesis.

42 ents, indicating their potential role in the disease pathogenesis.

43 NA charging proteins may together promote WS disease pathogenesis.

44 uring organism development but also regulate disease pathogenesis.

45 f the role of RIP2 in NOD1 and NOD2 mediated disease pathogenesis.

46 RNAs (miRNAs) can have a detrimental role in disease pathogenesis.

47 zheimer disease, potentially contributing to disease pathogenesis.

48 ng, and if so, how these cells contribute to disease pathogenesis.

49 ivity or decoupling dieting and fasting from disease pathogenesis.

50 g amyloid plaques, implicating their role in disease pathogenesis.

51 matory cytokines responsible for respiratory disease pathogenesis.

52 Here we investigate this mechanism in CCM disease pathogenesis.

53 lso potentially contribute to cardiovascular disease pathogenesis.

54 of aberrant RNA processing in neuromuscular disease pathogenesis.

55 D, suggesting involvement of this pathway in disease pathogenesis.

56 of TFH cells in response to vaccines and in disease pathogenesis.

57 PDK1 in keratinocytes is the major driver of disease pathogenesis.

58 ends this by directly implicating it in POAG disease pathogenesis.

59 oinflammatory component to neurodegenerative disease pathogenesis.

60 next throughout the brain during Parkinson's disease pathogenesis.

61 of ALS, highlighting its relevance to study disease pathogenesis.

62 dration may slow MCC in CB and contribute to disease pathogenesis.

63 ar responses that may contribute to vascular disease pathogenesis.

64 to construe how these proteins contribute to disease pathogenesis.

65 chondrial morphology have been implicated in disease pathogenesis.

66 role for oligodendrocyte dysfunction in SCA3 disease pathogenesis.

67 liorated colitis, implicating eosinophils in disease pathogenesis.

68 domains and its activity with relevance for disease pathogenesis.

69 of VAP-1, implicating enzyme activity in the disease pathogenesis.

70 its direct relevance to protein function and disease pathogenesis.

71 (RUTF) interventions, is causally related to disease pathogenesis.

72 survivors and contribute to understanding of disease pathogenesis.

73 of the reported increase in KCC activity in disease pathogenesis.

74 autophagic flux can each contribute to heart disease pathogenesis.

75 ss how these alterations might contribute to disease pathogenesis.

76 understanding of normal cell physiology and disease pathogenesis.

77 n yeast, providing mechanistic insights into disease pathogenesis.

78 e skin conditions, elucidating mechanisms of disease pathogenesis.

79 rculosis or sarcoidosis, and is decisive for disease pathogenesis.

80 ng that haploinsufficiency may contribute to disease pathogenesis.

81 ach to suppressing some aspects of Alzheimer disease pathogenesis.

82 o provide insights into the roles of RBPs in disease pathogenesis.

83 pports oligogenic inheritance as relevant to disease pathogenesis.

84 quality control pathways could contribute to disease pathogenesis.

85 ts is needed to develop a clearer picture of disease pathogenesis.

86 ole of arginine methylation in polyglutamine disease pathogenesis.

87 al pathways and processes that contribute to disease pathogenesis.

88 e time of oral prion exposure did not affect disease pathogenesis.

89 suggesting that IFN-I signaling may promote disease pathogenesis.

90 cess sebum production is an integral part of disease pathogenesis.

91 autophagic flux can each contribute to heart disease pathogenesis.

92 r Ro60 and its associated RNAs contribute to disease pathogenesis.

93 , it is unclear which isozyme contributes to disease pathogenesis.

94 which is enhanced by emerging insights into disease pathogenesis.

95 ll dysfunction might be a key contributor to disease pathogenesis.

96 Iron is implicated in fatty liver disease pathogenesis.

97 es (CKD) and associated with coronary artery disease pathogenesis.

98 sites of inflammation with implications for disease pathogenesis.

99 of identifying putative cellular pathways of disease pathogenesis.

100 egulation plays an important role in cardiac disease pathogenesis.

101 modium parasite defines the start of malaria disease pathogenesis.

102 o DNA vaccines, gene therapy, and autoimmune disease pathogenesis.

103 sting a primary role for glia in the complex disease pathogenesis.

104 d which reveals novel features of underlying disease pathogenesis.

105 ha-SYN) is a central molecule in Parkinson's disease pathogenesis.

106 , can provide a window into cell biology and disease pathogenesis.

107 icture of the complex pathway leading to SSc disease pathogenesis.

108 h may contribute to accelerate or exacerbate disease pathogenesis.

109 istics and investigate their contribution in disease pathogenesis.

110 oactive lipids implicated in alcoholic liver disease pathogenesis.

111 immune system, metabolic rate, and at times, disease pathogenesis.

112 that this model is suitable for studying the disease pathogenesis.

113 tance of lysosomal mechanisms in Parkinson's disease pathogenesis.

114 d gain-of-function mechanisms play a role in disease pathogenesis.

115 s indicates their central pathogenic role in disease pathogenesis.

116 elopmental processes but also contributes to disease pathogenesis.

117 complement and how these affect immunity and disease pathogenesis.

118 These alterations may impact disease pathogenesis.

119 lular pathogens but also underlie autoimmune disease pathogenesis.

120 -synuclein is a key component in Parkinson's disease pathogenesis.

121 licating a potentially overlooked circuit in disease pathogenesis.

122 d activities as putative central pathways in disease pathogenesis.

123 failure, regardless of ejection fraction or disease pathogenesis.

124 ion is believed to be an important player in disease pathogenesis.

125 stimulate protein aggregation and facilitate disease pathogenesis.

126 an 200 loci that independently contribute to disease pathogenesis.

127 cellular and molecular mechanisms underlying disease pathogenesis.

128 a lack of understanding of the mechanisms of disease pathogenesis.

129 ions of associated genes may be important in disease pathogenesis.

130 lopment, diagnostics, vector competence, and disease pathogenesis.

131 rkers of disease, with no clear relevance to disease pathogenesis.

132 nt roles in general biological processes and diseases pathogenesis.

133 vidence that Nemo-like kinase (NLK) promotes disease pathogenesis across multiple SBMA model systems.

134 upport a role for somatic NLRP3 mosaicism in disease pathogenesis; although elevated levels of ASC, I

135 data reveal that JNK is a key pathway in the disease pathogenesis and add new therapeutic entry point

136 useful as an end point for investigation of disease pathogenesis and as an outcome measure for thera

137 this large control system can contribute to disease pathogenesis and carcinogenesis.

138 llular senescence may have a large impact on disease pathogenesis and could be more effective in prev

139 of LAM that can advance our understanding of disease pathogenesis and develop therapeutic strategies

140 eratoconus could be useful for understanding disease pathogenesis and discovering biomarkers for earl

141 possible role of diverse T-cells subsets in disease pathogenesis and emphasize the systemic nature o

142 quently to inform a greater understanding of disease pathogenesis and endotypes and prediction of the

143 gene-environment interactions that underpin disease pathogenesis and exacerbation.

144 litis, few genes have yet been implicated in disease pathogenesis and familial cases are uncommon.

145 y opens new avenues both in the discovery of disease pathogenesis and for potential treatments.

146 replication and have clear implications for disease pathogenesis and future vaccine programs for ZIK

147 The host PrP(C) misfolds during disease pathogenesis and has a major role in controlling

148 certainty about the causal genes involved in disease pathogenesis and how their function is regulated

149 xpand the known network of genes involved in disease pathogenesis and identify epigenetic modifiers o

150 cancer epigenome is providing insights into disease pathogenesis and informing drug development.

151 te the role of YAP in proteinuric glomerular disease pathogenesis and its potential utility as a ther

152 investigated the involvement of Gal-3 in the disease pathogenesis and its role as a target for diseas

153 on the complex role of autophagy and TFEB in disease pathogenesis and its therapeutic implications th

154 Further progress will depend on studies of disease pathogenesis and knowledge provided from control

155 tter refine our understanding of respiratory disease pathogenesis and lead to new diagnostic and ther

156 These results have implications for disease pathogenesis and may also shed light on the regu

157 mutations in genes such as GRN contribute to disease pathogenesis and neurodegeneration.

158 damental basis for improved understanding of disease pathogenesis and phenotype development.

159 r necrosis factor alpha and interleukin 6 in disease pathogenesis and possibly also for granulocyte-m

160 this work provides new insights into Chagas disease pathogenesis and presents an analytical chemistr

161 y which dysfunction of TDP-43 contributes to disease pathogenesis and progression remain unclear.

162 also provided a much clearer picture of the disease pathogenesis and progression.

163 g memory tasks, suggesting its role in human disease pathogenesis and progression.SIGNIFICANCE STATEM

164 r understanding the regulatory mechanisms of disease pathogenesis and promoting personalized medicine

165 me as an important initiating signal in skin disease pathogenesis and provide novel insights about in

166 4 could play a critical role in modifying HD disease pathogenesis and severity.

167 f disease-relevant genes may be important in disease pathogenesis and should be reconsidered as candi

168 indicate a central role of NPCT in Alzheimer disease pathogenesis and suggest NPCT as a potential bio

169 intrinsic contribution of glial cells to SMA disease pathogenesis and suggests that therapies designe

170 s with a facile and reliable method to study disease pathogenesis and support the development of ther

171 ice, providing a unique model to investigate disease pathogenesis and test novel TSHR Ag-specific imm

172 of MATR3 mutations into an understanding of disease pathogenesis and the creation of mouse models re

173 d new opportunities for better understanding disease pathogenesis and the development of new diagnost

174 nificant implications for both mechanisms of disease pathogenesis and the development of therapeutics

175 interactions is essential to understand both disease pathogenesis and the effects of immunotherapy.

176 However, their role in disease pathogenesis and the factors responsible for the

177 ver, the importance of these alpha-chains in disease pathogenesis and the paired TCRbeta-chain remain

178 lement activation that could be important in disease pathogenesis and therapeutic interventions.

179 These data have implications for disease pathogenesis and therapeutic strategies for Alzh

180 of TLR responses, and all impact autoimmune disease pathogenesis and treatment.

181 By exploring these emerging themes in disease pathogenesis and underlying pathophysiological m

182 xplore whether our emerging understanding of disease pathogenesis and underlying pathophysiological m

183 rofiles, suggesting potential differences in disease pathogenesis and/or disease characteristics.

184 ondrial dysfunction that are associated with disease pathogenesis and/or progression are becoming inc

185 g of SE-derived tissue development, studying disease pathogenesis, and development of regenerative me

186 lial dysfunction is thought to contribute to disease pathogenesis, and here we found microglia become

187 to facilitate understanding of drug action, disease pathogenesis, and identification of drug targets

188 plays a critical role in tissue homeostasis, disease pathogenesis, and inflammation and its resolutio

189 a pathologic event that partially underlies disease pathogenesis, and its inhibition might serve as

190 hat are likely to be associated with Crohn's disease pathogenesis, and our rank of candidate drugs su

191 e factors may provide valuable insights into disease pathogenesis, and suggest novel targets for ther

192 on protein has a central role in Alzheimer's disease pathogenesis, and the complex is a potential tar

193 s for diagnostic criteria, poorly understood disease pathogenesis, and very few studies of therapeuti

194 sed -omics data integration in understanding disease pathogenesis; and (6) limitations.

195 Hallmarks of autoimmune disease pathogenesis are abnormal CD4(+) and CD8(+) T ce

196 osinophilia in the antiviral response and in disease pathogenesis are inadequately understood.

197 profound loss, but the mechanisms underlying disease pathogenesis are not fully understood.

198 nisms by which these cytokines contribute to disease pathogenesis are poorly understood.

199 mechanisms, although several aspects of the disease pathogenesis are still unclear.

200 Insulin represents a key self-antigen in disease pathogenesis, as recent studies identified proin

201 rrent understanding of the role of TDP-43 in disease pathogenesis, as well as enhance both diagnostic

202 and host lipid metabolism, leading to liver disease pathogenesis associated with chronic HCV.

203 lpha-syn) is well established in Parkinson's disease pathogenesis, available animal models of synucle

204 T cells (Tregs) is believed to contribute to disease pathogenesis, but changes in Treg function are d

205 studies indicate circRNA may be involved in disease pathogenesis, but direct evidence is scarce.

206 ELDP may therefore contribute to disease pathogenesis by augmenting ET-1 responses.

207 in host membranes and mediates pneumococcal disease pathogenesis by modulating inflammatory response

208 Telomere length, a reliable predictor of disease pathogenesis, can be affected by genetics, chron

209 ld aid in better understanding of cerebellar disease pathogenesis caused due to deregulation of Wnt s

210 Investigation of disease pathogenesis confined to protein-coding regions

211 ges in the metabolic profile associated with disease pathogenesis could help with the identification

212 Disease pathogenesis depends on IFN-gamma and IFN-gamma-

213 This may provide insight into disease pathogenesis, diagnosis, and therapeutic interve

214 e for other genetic factors in modifying the disease pathogenesis driven by mutant huntingtin.

215 their limitations, advances in understanding disease pathogenesis, emerging targeted treatments, and

216 stigating the cellular mechanisms underlying disease pathogenesis, evaluating potential therapies for

217 Dimerization/multimerization is relevant to disease pathogenesis, given that only GPIHBP1 monomers a

218 ore common in women, a role for estrogens in disease pathogenesis has long been suspected.

219 nes in multiple myeloma; however its role in disease pathogenesis has not been determined.

220 se; however, the role of these aggregates in disease pathogenesis has not been fully characterized.

221 derstand the role of specific HLA alleles in disease pathogenesis have been hampered by the presence

222 ears ago, much has been learned about Chagas disease pathogenesis; however, the outcome of T. cruzi i

223 These processes participate in disease pathogenesis in all lung regions mainly when int

224 vide a definitive resource for investigating disease pathogenesis in FRDA.

225 ased on cellular and molecular dissection of disease pathogenesis in humans.

226 to implicate the receptors in coronary heart disease pathogenesis in humans.

227 tes dysregulated ILC responses as drivers of disease pathogenesis in multiple inflammatory disorders.

228 and regulatory T cells, indicating a common disease pathogenesis in patients with IgG4-RD.

229 w the virology of EBV, mechanisms underlying disease pathogenesis in PIDs, and developments in immune

230 pathways have expanded our understanding of disease pathogenesis in synucleinopathies.

231 epigenetic changes that could contribute to disease pathogenesis in T1D.

232 but do not directly contribute to hantavirus disease pathogenesis in the hamster model of HPS.

233 tion experiments revealed that the increased disease pathogenesis in the Nlrp1b(-/-) mice was associa

234 contribution of defects in CD4(+) T cells to disease pathogenesis in these patients has not been thor

235 ed with a humoral immune response reflecting disease pathogenesis in TNBC.

236 eta1, a causative factor in congenital heart disease pathogenesis, in a deacetylase-independent manne

237 Together, these data suggest that SCN disease pathogenesis includes NE mislocalization, which

238 Disease pathogenesis involves activation of epithelial i

239 holesterol loss is primarily responsible for disease pathogenesis is also unclear.

240 The role of microbial signals in disease pathogenesis is debated.

241 The disease pathogenesis is due to mutations in the gene enc

242 ncreasing evidence suggests that Alzheimer's disease pathogenesis is not restricted to the neuronal c

243 Cellular specificity of disease pathogenesis is relevant to developing targeted

244 However, disease pathogenesis is still unclear, and these cellula

245 tribution that the loss of EWS makes towards disease pathogenesis is unknown.

246 vascular cells, but their timing and role in disease pathogenesis is unknown.

247 joint replacement surgery, yet their role in disease pathogenesis is unknown.

248 her types of cells nor its exact role in the disease pathogenesis is well understood, which is largel

249 d development of the human gut microbiota in disease pathogenesis, leading to new concepts for treatm

250 An improved understanding of disease pathogenesis leads to identification of novel th

251 r, ACE2 deficiency aggravated RSV-associated disease pathogenesis, mainly by its action on the angiot

252 role for the membrane-bound intermediate in disease pathogenesis, making it a potential target for t

253 understanding of the molecular basis of SMA, disease pathogenesis, natural history, and recognition o

254 Data were extracted by disease pathogenesis: nonthrombotic, acute thrombotic, o

255 brain barrier (BBB) is a crucial step in the disease pathogenesis of CNS autoimmunity, the consequenc

256 ve been performed to provide insight into WS disease pathogenesis or the high risk of neoplasia.

257 y a wealth of knowledge regarding infectious disease pathogenesis, prevention, and treatment has been

258 of choroidal vessel disease to diabetic eye disease pathogenesis, prognosis, and treatment response.

259 impairment and may be useful for elucidating disease pathogenesis, progression, and response to thera

260 cular changes instead play a central role in disease pathogenesis, rather than representing a seconda

261 omising host modulatory agent in periodontal disease pathogenesis regarding IL-17/IL-23 axis, with a

262 ant toAGS, providing additional insight into disease pathogenesis relevant to the development of ther

263 ocyte injury, yet the mechanistic details of disease pathogenesis remain unclear.

264 cted patients, however their contribution to disease pathogenesis remains controversial.

265 of ALS/FTD pathology; however, their role in disease pathogenesis remains incompletely understood.

266 However, the exact role of eosinophils in disease pathogenesis remains largely unknown.

267 of asthma patients, but whose importance in disease pathogenesis remains unclear.

268 Whether GLUT1 reduction influences disease pathogenesis remains, however, elusive.

269 disorders has identified pathways central to disease pathogenesis, revealing novel therapeutic target

270 Our knowledge relating to the virus, disease pathogenesis, risk factors, dynamics of transmis

271 detected at mucosal sites and their role in disease pathogenesis should be examined.

272 y of wild-type tau and FTDP-17 mutant tau in disease pathogenesis.SIGNIFICANCE STATEMENT The microtub

273 rapy represents a perplexing aspect of HIV-1 disease pathogenesis, since most HIV-1 target cells are

274 understanding of the critical components of disease pathogenesis, such as virus evolution and adapta

275 rophy (DMD) may provide deeper insights into disease pathogenesis, suggest new therapeutic approaches

276 eractions with host cells that contribute to disease pathogenesis, the infected RBC surface proteome

277 g TLR9-triggered inflammation in periodontal disease pathogenesis, thereby identifying a new potentia

278 RSV binding to CX3CR1 contributes to disease pathogenesis; therefore, we investigated whether

279 roviding important mechanistic insights into disease pathogenesis, these findings have implications f

280 gest that this novel genomic hybrid mediates disease pathogenesis through dysregulation of complement

281 ded protein response directly contributes to disease pathogenesis through the critical reduction in n

282 Improved knowledge of disease pathogenesis together with defining validated an

283 ilin-B1 has a functional role in Alzheimer's disease pathogenesis, we crossed endophilin-B1(-/-) mice

284 athways whereby these variants contribute to disease pathogenesis, we established HEK293 cell lines s

285 To uniquely address key questions of disease pathogenesis, we generated a conditional Tor1a k

286 ress whether this phenomenon plays a role in disease pathogenesis, we generated a knock-in mouse mode

287 To investigate the mechanism of disease pathogenesis, we generated Drosophila models of

288 caspase cleavage is a critical event in SCA7 disease pathogenesis, we generated transgenic mice expre

289 nderstand the functional role of TMEM106B in disease pathogenesis, we investigated the cell biologica

290 Since RSV binding to CX3CR1 contributes to disease pathogenesis, we investigated whether a mutation

291 Given the importance of GC and LIMP-2 in disease pathogenesis, we studied their interaction sites

292 better characterize the function of NLRP1 in disease pathogenesis, we used Nlrp1b(-/-) mice in coliti

293 e greater levels of alphavirus infection and disease pathogenesis when Ifitm3 expression is absent.

294 r of a feed-forward mechanism of Alzheimer's disease pathogenesis where amyloid-beta reduces neuron-s

295 significantly improved our understanding of disease pathogenesis, which is now leading to emerging t

296 and elucidation of the mechanistic basis of disease pathogenesis will depend on an increased basic u

297 nderstanding of chemoattractant receptors in disease pathogenesis, with a focus on genome-wide associ

298 understand the contribution of sTim-3 in HIV disease pathogenesis, with implications for novel therap

299 and adaptive immune pathways contributes to disease pathogenesis, with prominent interferon (IFN) si

300 lysis offers a new approach to understanding disease pathogenesis, with significant implications for