ライフサイエンスコーパス: cell metabolism

1 ional nonchemotactic cell functions, such as cell metabolism).

2 his occurs through alteration of endothelial cell metabolism.

3 repair, cell migration and invasiveness, and cell metabolism.

4 ld represent a new role for Wnt signaling in cell metabolism.

5 sregulated pathway that is critical for TNBC cell metabolism.

6 ed whether mitochondrial dynamics controls T cell metabolism.

7 ramming, naive/primed pluripotency, and stem cell metabolism.

8 ver previously unexplored roles of TDP-43 in cell metabolism.

9 are implicated in the regulation of RNA and cell metabolism.

10 ion and acts as critical regulator of tumour cell metabolism.

11 collagen-derived proline contributes to PDAC cell metabolism.

12 agy as a salvage pathway supporting leukemia cell metabolism.

13 by the DNA damage that arises during normal cell metabolism.

14 tabolic pathways with an influence on cancer cell metabolism.

15 , were predicted to be dispensable in normal cell metabolism.

16 1-alpha degradation and takes control of Tr1 cell metabolism.

17 iciency, acts as central metabolic switch in cell metabolism.

18 nt demands of cancer cannot be met by normal cell metabolism.

19 r (HIF) oxygen-sensing machinery and hypoxic cell metabolism.

20 ne function, transcriptional regulation, and cell metabolism.

21 zation stages that correlate with changes in cell metabolism.

22 findings have added another pot to the mix - cell metabolism.

23 els of gene regulation, signalling and whole-cell metabolism.

24 atidylinositol(4,5)bisphosphate content, and cell metabolism.

25 to monitor the effect of therapy on myeloma-cell metabolism.

26 te signal transduction pathways that control cell metabolism.

27 eins (SREBPs) in the acquisition of effector-cell metabolism.

28 al role in angiogenesis, erythropoiesis, and cell metabolism.

29 ycin (mTOR) complex 1 (mTORC1) signaling and cell metabolism.

30 ble of reducing N-hydroxylated substrates in cell metabolism.

31 tivation is linked to fundamental changes in cell metabolism.

32 GC-1alpha and negatively regulates brown fat cell metabolism.

33 D3 and minimized thyroid hormone effects in cell metabolism.

34 ted costimulation, accompanied by enhanced T-cell metabolism.

35 y transcripts encoding enzymes implicated in cell metabolism.

36 in live cells and gaining new insights into cell metabolism.

37 tumorigenesis acting at the level of cancer cell metabolism.

38 uggesting a role for Id1 in adipogenesis and cell metabolism.

39 ulator of IDH2-dependent functions in cancer cell metabolism.

40 rently known about compartmentation of plant-cell metabolism.

41 cess that plays a central role in eukaryotic cell metabolism.

42 ess and provide key intermediates to sustain cell metabolism.

43 ate the effect of macromolecular crowding on cell metabolism.

44 increased glycolysis, recapitulating cancer cell metabolism.

45 ociated with cell growth, proliferation, and cell metabolism.

46 s RNA processing, cytoskeletal dynamics, and cell metabolism.

47 Oncoproteins such as Akt and c-Myc regulate cell metabolism.

48 ustrating an in vitro Warburg-like effect on cell metabolism.

49 global role of riboswitch RNAs in bacterial cell metabolism.

50 R are evolutionarily conserved regulators of cell metabolism.

51 phorylation, signaling, gene regulation, and cell metabolism.

52 as long been considered a hallmark of cancer cell metabolism.

53 for HPV-associated malignancies by targeting cell metabolism.

54 ignificant alteration of pathways related to cell metabolism.

55 tions including phagocytosis, autophagy, and cell metabolism.

56 in to assess the effects of 380 compounds on cell metabolism.

57 ents that specifically interfere with cancer cell metabolism.

58 tores, increases autophagy and restores beta-cell metabolism.

59 inositol biosynthesis, with broad effects on cell metabolism.

60 ce due to specific changes in energy and fat cell metabolism.

61 nes likely to be involved in rewiring cancer cell metabolism.

62 media could revolutionize the monitoring of cell-metabolism.

63 ter, ions or nutrients that are essential to cells' metabolism.

64 lishes miR-22 as a novel regulator of tumour cell metabolism, a function that could contribute to the

65 In the conventional view of mammalian cell metabolism, AcCoA is primarily generated from gluco

66 synthetic demands of activated cells, immune cell metabolism also has direct roles in controlling the

67 Stem cell metabolism also offers a potential target for contr

68 In a recent paper in Cell Metabolism, Altman et al. (2015) report that MYC di

69 opment and implementation of drugs targeting cell metabolism and aberrant AKT signaling.

70 is as a regulator of resting CD8(+) memory T cell metabolism and activity in humans.

71 s-2 signaling preferentially regulates tumor cell metabolism and adds to our understanding of how thi

72 ated protein kinase is a master regulator of cell metabolism and an attractive drug target for cancer

73 nate cancer cells, mechanistic links between cell metabolism and apoptosis remain poorly understood.

74 cin complex 1 (mTORC1) is a key regulator of cell metabolism and autophagy.

75 himeric antigen receptor (CAR) can control T cell metabolism and balance the response toward long-liv

76 been attributed to their ability to regulate cell metabolism and cell death pathways, emerging data p

77 ishing an emerging relationship between stem cell metabolism and cell fate control.

78 R to these stimuli results in alterations to cell metabolism and cell growth.

79 t of organic acids plays a key role in plant cell metabolism and demonstrate that AtQUAC1 reduce diff

80 tylicum chromosome--with the aim of altering cell metabolism and differentiation.

81 WNT signaling in the reprogramming of cancer cell metabolism and examines the role of these signaling

82 function, the mechanisms that regulate Treg cell metabolism and function remain unclear.

83 ever, how nutrient availability influences T cell metabolism and function remains poorly understood.

84 ole of mTOR provides a direct link between T cell metabolism and function.

85 The lysosomal Ragulator complex regulates cell metabolism and growth by coordinating the activitie

86 into the impact of HDAC inhibition on cancer cell metabolism and highlight PC as a candidate noninvas

87 tions between oncogenic signaling and cancer cell metabolism and how these links may be exploited for

88 Ndfip1 restricts Treg cell metabolism and IL-4 production via distinct mechani

89 Coordination of cell metabolism and immune signals is crucial for lympho

90 er cell biology, particularly altered cancer cell metabolism and impaired DNA repair processes, is pr

91 ups reduce the perturbations caused by GO on cell metabolism and increase biocompatibility.

92 laying critical roles in the control of host cell metabolism and inflammatory response.

93 pamycin (mTOR) regulates stem and progenitor cell metabolism and is frequently dysregulated in human

94 The complex cell metabolism and its link to oncogenic signaling path

95 cells-nanofibers interactions were tested by cell metabolism and migration assays.

96 Cancer cell metabolism and mitochondria provide unexplored targ

97 quantitative characterization of changes in cell metabolism and morphology as a response to toxin ex

98 droplet dynamics with implications in cancer cell metabolism and obesity.

99 arboxylate transporters (MCT) modulate tumor cell metabolism and offer promising therapeutic targets

100 gy is demonstrated here in the analysis of T cell metabolism and other large-scale metabolomic studie

101 g this loss of secretion are defects in beta-cell metabolism and perturbed mitochondrial structure.

102 ious consequences for the colonic epithelial cell metabolism and physiology in terms of mitochondrial

103 e inhibition of malic enzymes, p53 regulates cell metabolism and proliferation.

104 For example, HIV-induced changes in immune cell metabolism and redox state are associated with CD4(

105 ith increased expression of genes related to cell metabolism and respiration.

106 cing agents, which are currently involved in cell metabolism and signaling pathways, can regulate fas

107 all inositol compounds, has pivotal roles in cell metabolism and signaling pathways.

108 al structural as well as regulatory roles in cell metabolism and signaling.

109 mineral for both prokaryotic and eukaryotic cell metabolism and structure.

110 encing both cardiac contractile function and cell metabolism and survival and contributing to HF inde

111 As BAFF increases murine B-cell metabolism and survival and maintains autoreactive

112 a mitochondrial flavoprotein that regulates cell metabolism and survival in many tissues.

113 rcuits highlight pathways involved in immune cell metabolism and the cell cycle, including mTOR signa

114 The ubiquity of this natural product of cell metabolism and the complexity of its biochemistry p

115 sNAG fibers stimulated cell metabolism and the in vitro migratory activity of e

116 dependent NAD(+) biosynthesis contributes to cell metabolism and to the DNA repair process in a subse

117 of the YRO, which is an ultradian rhythm of cell metabolism and transcription.

118 (PKM), which plays a critical role in cancer cell metabolism and tumor growth.

119 hosphate pathway (PPP) is crucial for cancer cell metabolism and tumor growth.

120 rein), in Myc-mediated alterations in cancer cell metabolism and tumorigenesis.

121 sting a sophisticated interplay between host cell metabolism and virus replication.

122 t vector titres due to biological effects on cell metabolism and/or on the vector virion itself.

123 developing principles in the regulation of T cell metabolism, and discuss how these processes are aff

124 ysis ((13)C-MFA), offer direct insights into cell metabolism, and have been widely used to characteri

125 We further discuss how oncogenic signaling, cell metabolism, and histone modifications are interconn

126 energetics, and redox homeostasis in immune cell metabolism, and how these factors are reflected in

127 long been considered a "waste" by-product of cell metabolism, and it accumulates at sites of inflamma

128 ase (AMPK) is an energy sensor that controls cell metabolism, and it has been related to apoptosis an

129 roteostasis in mitochondria regulates tumour cell metabolism, and may provide a tractable target for

130 ancer-related signaling networks, intestinal cell metabolism, and physiology in a three-dimensional e

131 me implicated in development, transcription, cell metabolism, and signal transduction, are differenti

132 ffles, is critical for antigen presentation, cell metabolism, and signaling.

133 s, cell growth and proliferation, autophagy, cell metabolism, and stress responses, whereas mTORC2 se

134 s recently discovered roles in regulation of cell metabolism, and the potential for products of micro

135 PSC and cancer cell metabolism are overtly similar, with metabolite lev

136 ts that activate autophagy and reprogram PDA cell metabolism are unknown.

137 which is provided by the cytoskeleton, using cell metabolism as its energy source, and the dynamic in

138 of (18)F-FAC PET for the assessment of glial cell metabolism associated with neuroinflammation.

139 d postembryonic development and critical for cell metabolism at all stages of life.

140 bolism are intimately linked, and changes in cell metabolism at both the cell and system levels have

141 balance model capturing the main features of cell metabolism at different nutrient uptakes and macrom

142 rial dysfunction, methods for studying brain cell metabolism at high spatial resolution are needed to

143 hagy actively suppresses haematopoietic stem-cell metabolism by clearing active, healthy mitochondria

144 y be generated endogenously in the course of cell metabolism by cytochrome P450, by oxidative stress

145 contributed to dysfunction, as a rescue of T cell metabolism by genetically increasing Akt/mTORC1 sig

146 Photosynthetic organisms support cell metabolism by harvesting sunlight to fuel the photo

147 article centers on the manipulation of host cell metabolism by human cytomegalovirus (HCMV).

148 Changes in cancer cell metabolism can directly impact epigenetic regulatio

149 These findings identify a mechanism by which cell metabolism can influence coupling between NMDA rece

150 le applications including dynamic control of cell metabolism, cell biology and synthetic gene circuit

151 riptional factor FoxO1 is a key regulator of cell metabolism, cell cycle and cell death.

152 egulates many cellular processes, especially cell metabolism, cell survival, and apoptosis.

153 permeability, subcellular distribution, and cell metabolism characteristics that are important for u

154 h inspire a novel top-down approach to study cell metabolism, combining mass balance and proteomic co

155 Reprogramming of tumour cell metabolism contributes to disease progression and r

156 t that programmed differences in infant stem cell metabolism correspond with differences in body comp

157 dependent N-reductive detoxication of HAP in cell metabolism could be demonstrated.

158 Beyond their role in cell metabolism, development, and reproduction, hormones

159 However, although the roles of glucose in T cell metabolism, diabetes and obesity are well character

160 Importantly, impaired T cell metabolism directly contributed to dysfunction, as

161 MCJ also adapted effector CD8(+) T cell metabolism during the contraction phase.

162 Monitoring cell metabolism during treatment is extremely valuable t

163 iological processes such as abnormalities in cell metabolism, energy production and oxidative stress

164 nd 80% naturally labeled glucose medium, the cell metabolism favored light isotopes and the measured

165 Engineering cell metabolism for bioproduction not only consumes buil

166 Modulation of cerebral cell metabolism for improving the outcome of hypoxia-isc

167 d RNA virus, dengue virus relies on the host cell metabolism for its translation, replication, and eg

168 g evidence also highlights the importance of cell metabolism for the activation of innate immunity up

169 ogenic signaling contribute to switch cancer cell metabolism from oxidative phosphorylation to aerobi

170 domains, and the minimal effects observed on cell metabolism, further studies are warranted to assess

171 ork and functional information for over 2000 cell metabolism genes in more than 30 cancer types.

172 Thus, a systematic annotation of cancer cell metabolism genes is imperative.

173 transcription initiation, mRNA splicing, and cell metabolism; genes involved in cell signaling and ce

174 both complexes may be critical regulators of cell metabolism, growth and proliferation.

175 ine to glutamate, plays a key role in cancer cell metabolism, growth, and proliferation.

176 are critical for their localized function in cell metabolism, growth, and survival.

177 T cell metabolism has a central role in supporting and sha

178 The role of metabolites produced from stem cell metabolism has been emerged as signaling molecules

179 ge between oncogenic mutated EGFR and cancer cell metabolism has not yet been clearly elucidated.

180 Research on tumor cell metabolism has provided valuable insight into metab

181 Immune cell metabolism has therefore become an attractive targe

182 Contemporary analyses of cell metabolism have called out three metabolites: ATP,

183 Studies on cancer cell metabolism have provided evidence that tumor-specif

184 Besides its effects on cell metabolism, HO-1 is also capable of modulating host

185 etter understanding of metabolic syndrome, T-cell metabolism, hormones, and microbiota may lead to ne

186 BTN1A1 and BTN2A2 also inhibited T cell metabolism, IL-2, and IFN-gamma secretion.

187 ging and microfluidic devices to investigate cell metabolism in a limited amount of living tissue.

188 l screening of candidate compounds targeting cell metabolism in a microplate-reader-based assay, alon

189 compared the effect of these oncoproteins on cell metabolism in an isogenic background.

190 apshot analysis, allowing spatial mapping of cell metabolism in concert with cell phenotype.

191 and environmental parameters that influence cell metabolism in culture.

192 vident that genetic modifications can affect cell metabolism in HGG; however, it is currently unclear

193 ce of the mutual regulation of autophagy and cell metabolism in maintaining cell homeostasis.

194 Akt can control cell metabolism in many cell types but whether this role

195 The revival of interest in cancer cell metabolism in recent years has prompted the need fo

196 Overall, our findings extend the role of T cell metabolism in regulating T cell function.

197 disease (GVHD), yet little is known about T cell metabolism in response to alloantigens after hemato

198 Here we report plasticity in effector T cell metabolism in response to changing nutrient availab

199 (18)F-FAC as a specific PET tracer of glial cell metabolism in rodent models of glioblastoma, stroke

200 reveal how MEK1/2 inhibition affects cancer cell metabolism in the context of BRAF oncogene addictio

201 Our study provides novel insight into cancer cell metabolism in the context of the endothelial microe

202 f research have sought to characterize tumor cell metabolism in the hope that tumor-specific activiti

203 osis of T cells, little is known regarding T cell metabolism in the progression of human type 1 diabe

204 e effects on flagellar sterol enrichment and cell metabolism in the two life cycle stages.

205 nderstanding of the role of inflammation and cell metabolism in tissue-regenerative responses, highli

206 rgence of interest in the regulatory role of cell metabolism in tumor biology and immunology.

207 pact of the MCT1 inhibitor AZD3965 on cancer cell metabolism in vitro and in vivo Exposing human lymp

208 development and survival and can regulate T cell metabolism in vitro, we hypothesized it may be esse

209 ecies and other toxic mediators that disrupt cell metabolism, induce apoptosis, and exacerbate ischem

210 many oncogenes impart a common alteration in cell metabolism, inhibition of the M2 isoform might be o

211 f insulin that parallel oscillations in beta-cell metabolism, intracellular Ca(2+) concentration, and

212 ia telangiectasia mutated), those within the cell metabolism (IR-alpha, IR-beta, and AMP-activated pr

213 Cell metabolism is adaptive to extrinsic demands; howeve

214 ermodynamic modeling, we show that the plant cell metabolism is affected predominantly by hydroxo-spe

215 This LKB1-dependent reprogramming of cell metabolism is dependent on the hypoxia-inducible fa

216 Immune cell metabolism is dynamically regulated in parallel wit

217 his study, we demonstrate that altered tumor cell metabolism is essential for the regulation of drug

218 Strict regulation of stem cell metabolism is essential for tissue functions and tu

219 Regulation of cell metabolism is essential to support the demands of l

220 rent cell types suggests that control of the cell metabolism is feasible through manipulation of the

221 It is now apparent that T cell metabolism is highly dynamic and has a tremendous i

222 t of different mutant p53 proteins on cancer cell metabolism is largely unknown.

223 T cell metabolism is normally held under tight regulation

224 the interplay between PD-1 inhibition and T cell metabolism is not well studied.

225 As a result of these findings, cell metabolism is now appreciated as a key regulator of

226 Thus, whereas in normal aging cell metabolism is reduced, in the diabetic mice a compe

227 ytical tools for the investigation of living cell metabolism is still a challenge to be faced.

228 inhibitor protein of F1F0-ATPase) in cancer cell metabolism is still uncertain.

229 of cancer-specific regulatory mechanisms of cell metabolism is still very limited.

230 t to be a mere consequence of the state of a cell, metabolism is now known to play a pivotal role in

231 In Cell Metabolism, Jin et al. (2014) show that this proces

232 Recently in Cell Metabolism, Logan et al. (2016) exploit membrane po

233 Cell metabolism may be central to this cell death pathwa

234 standing the impact of MCT blockade on tumor cell metabolism may help develop combination strategies

235 to drugs, genetic variation of patients and cell metabolism may help managing side effects by person

236 Altered beta-cell metabolism may underlie both the progressive impair

237 late multiple pathways of cancer or parasite cell metabolism, might lead to more effective treatments

238 een TET and two critical enzymes involved in cell metabolism: O-linked beta-N-acetylglucosamine trans

239 the profound (anoikis-independent) impact of cell metabolism on the viability of ECM-detached cells.

240 cer development, the emerging role of p53 in cell metabolism, oxidative responses, and ferroptotic ce

241 ; however, recent findings suggest that stem cell metabolism plays an important role in the regulatio

242 Given that the integrins regulate cell metabolism, proliferation, and migration, we sugges

243 in (CREB) plays key transcriptional roles in cell metabolism, proliferation, and survival.

244 assumptions in enzymology, biochemistry and cell metabolism regarding the fate of transiently genera

245 l understood, whereas our knowledge of guard cell metabolism remains limited, despite several decades

246 ic signals activate LDH-A to regulate cancer cell metabolism remains unclear.

247 , through its ability to link cell cycle and cell metabolism, represents a particularly powerful onco

248 w specific metabolic rates to altered cancer cell metabolism resulting from mutated enzymes or cancer

249 finding has been attributed to altered tumor cell metabolism resulting from these mutations and does

250 Environmental nutrient levels impact cancer cell metabolism, resulting in context-dependent gene ess

251 id, glutamine, exerts pleiotropic effects on cell metabolism, signalling and stress resistance.

252 hway and C3 being a driver and programmer of cell metabolism suggest that the complement system utili

253 Akt1 is implicated in cell metabolism, survival migration, and gene expression

254 Recently in Cell Metabolism, Szabat et al. (2015) present evidence t

255 tool to provide more detailed information on cell metabolism that are unprecedented in cell biology.

256 a label-free imaging method to monitor stem-cell metabolism that discriminates different states of s

257 o multiple processes and plasticity in guard cell metabolism that enable these cells to function effe

258 novel role for RhoC as a regulator of tumor cell metabolism that extends beyond its well known role

259 uman cancers and induces adaptive changes in cell metabolism that include a switch from oxidative pho

260 Despite their fundamental importance to cell metabolism, the mechanisms by which regions of the

261 A key transcriptional regulator of cell metabolism, the peroxisome proliferator-activated r

262 rties of these key metabolites power much of cell metabolism, the underlying molecular logic remains

263 glycolysis and consequently rescues leukemic cell metabolism, thereby abrogating the antileukemic eff

264 ating the integration of systemic and immune cell metabolism through in-depth analysis of immune cell

265 as a master regulator for the adaptation of cell metabolism to a transformed state.

266 In addition, loss of KEAP1 altered cell metabolism to allow cells to proliferate in the abs

267 where coordinated biochemical pathways allow cell metabolism to be characterized and potentially cont

268 ATP-sensitive K(+) (K(ATP)) channels couple cell metabolism to cell electrical activity.

269 tBP1 is a critical factor linking changes in cell metabolism to cell phenotype in hypoxic and other f

270 K(ATP) channels link cell metabolism to excitability in many cells.

271 pancreatic adenocarcinoma, modulates cancer cell metabolism to facilitate growth properties of cance

272 ssion of ERRgamma reprograms prostate cancer cell metabolism to favor mitochondrial activity and cell

273 exploring and potentially manipulating guard cell metabolism to improve plant water use and productiv

274 es mediate T cell signaling and coordinate T cell metabolism to meet the metabolic demands of partici

275 d checkpoint in linking immune signaling and cell metabolism to orchestrate memory CD8(+) T-cell deve

276 se effects is by sustaining sufficient basal cell metabolism to prevent cell atrophy.

277 Deregulated Myc transcriptionally reprograms cell metabolism to promote neoplasia.

278 cell activation leads to dramatic shifts in cell metabolism to protect against pathogens and to orch

279 Viruses require host cell metabolism to provide the necessary energy and bios

280 , these data demonstrate that induction of T cell metabolism upon activation is dependent on systemic

281 tive, high-resolution technique for studying cell metabolism via endogenous fluorescence of reduced n

282 nocytes were studied in vitro with regard to cell metabolism, viability, growth, gene expression sign

283 Ang1 promoted skin cell metabolism/viability, adhesion, and akt and MAPK(p4

284 For many years, stem cell metabolism was viewed as a byproduct of cell fate s

285 To investigate the effects of age on beta-cell metabolism, we established a novel assay to directl

286 tty acid into mitochondria to support cancer cell metabolism, we tested several clinically relevant i

287 activated by QseA, whereas genes involved in cell metabolism were repressed.

288 strumental function of Cdc25A in controlling cell metabolism, which is essential for EGFR-promoted tu

289 s suggest a more integrated view of vascular cell metabolism, which may open unique therapeutic prosp

290 (i.e. 20%) short wavelength light inhibited cell metabolism, while negligible effects were seen with

291 effects of HCMV, and other viruses, on host cell metabolism will provide new understanding of viral

292 regulator that connects changes in satellite cell metabolism with changes in the transcriptional mach

293 AMPK acts as an energy sensor to coordinate cell metabolism with environmental status in species fro

294 Targeting altered cancer cell metabolism with the glycolysis inhibitor, 2-deoxygl

295 ine determines many physiological aspects of cell metabolism, with a turnover that can be measured in

296 tanding of hypoxia-induced changes in cancer cell metabolism, with an initial focus on HIF-mediated e

297 wing attention has been directed toward stem cell metabolism, with the key observation that the plast

298 ducts such as lactate--emerge due to altered cell metabolism within poorly perfused tumors, creating

299 linical tools that measure changes in immune cell metabolism would improve the diagnosis and treatmen

300 Knowledge of single-cell metabolism would provide a powerful look into cell