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1  role in regulating mitochondrial fusion and cell metabolism.
2 hrough poorly defined mechanisms to modulate cell metabolism.
3 d hierarchical organization of breast cancer cell metabolism.
4 his occurs through alteration of endothelial cell metabolism.
5 repair, cell migration and invasiveness, and cell metabolism.
6 ver previously unexplored roles of TDP-43 in cell metabolism.
7 collagen-derived proline contributes to PDAC cell metabolism.
8 tabolic pathways with an influence on cancer cell metabolism.
9  to monitor the effect of therapy on myeloma-cell metabolism.
10  in live cells and gaining new insights into cell metabolism.
11 phorylation, signaling, gene regulation, and cell metabolism.
12 as long been considered a hallmark of cancer cell metabolism.
13 for HPV-associated malignancies by targeting cell metabolism.
14 rtunity to discover drugs that target cancer cell metabolism.
15 ignificant alteration of pathways related to cell metabolism.
16 tions including phagocytosis, autophagy, and cell metabolism.
17 in to assess the effects of 380 compounds on cell metabolism.
18 ents that specifically interfere with cancer cell metabolism.
19 tores, increases autophagy and restores beta-cell metabolism.
20 inositol biosynthesis, with broad effects on cell metabolism.
21 ce due to specific changes in energy and fat cell metabolism.
22 nes likely to be involved in rewiring cancer cell metabolism.
23 ld represent a new role for Wnt signaling in cell metabolism.
24 sregulated pathway that is critical for TNBC cell metabolism.
25 ed whether mitochondrial dynamics controls T cell metabolism.
26 ramming, naive/primed pluripotency, and stem cell metabolism.
27  are implicated in the regulation of RNA and cell metabolism.
28 ion and acts as critical regulator of tumour cell metabolism.
29 agy as a salvage pathway supporting leukemia cell metabolism.
30  by the DNA damage that arises during normal cell metabolism.
31 , were predicted to be dispensable in normal cell metabolism.
32 1-alpha degradation and takes control of Tr1 cell metabolism.
33 iciency, acts as central metabolic switch in cell metabolism.
34 nt demands of cancer cannot be met by normal cell metabolism.
35 sis, cytokine secretion, gene expression and cell metabolism.
36 ols mitochondrial Ca(2+) entry and regulates cell metabolism.
37 administered medications by targeting cancer cell metabolism.
38 glucose (2DG), a pharmaceutical that targets cell metabolism.
39 ng how C. trachomatis is able to hijack host cell metabolism.
40  factors play a major role in shaping cancer cell metabolism.
41  and how diet and nutrition influence cancer cell metabolism.
42  (also called LKB1) regulates stem cells and cell metabolism.
43 ery which dynamically and actively regulates cell metabolism.
44 rs for tumor suppression by targeting cancer cell metabolism.
45 deadly lymphoma in chickens and hijacks host cell metabolism.
46 al processes important for cancer, including cell metabolism.
47 rged as key components in determining cancer cell metabolism.
48  and 19 downregulated proteins with roles in cell metabolism.
49 he emerging functions of the complosome in T cell metabolism.
50 al of adoptive cell therapies by enhancing T cell metabolism.
51  media could revolutionize the monitoring of cell-metabolism.
52 lishes miR-22 as a novel regulator of tumour cell metabolism, a function that could contribute to the
53 synthetic demands of activated cells, immune cell metabolism also has direct roles in controlling the
54                             Thus, changes in cell metabolism alter Hh signalling through their effect
55                         In a recent paper in Cell Metabolism, Altman et al. (2015) report that MYC di
56 sophila to investigate the interplay between cell metabolism and a key developmental regulator-the He
57 is as a regulator of resting CD8(+) memory T cell metabolism and activity in humans.
58 s-2 signaling preferentially regulates tumor cell metabolism and adds to our understanding of how thi
59 regulates biological activities, involved in cell metabolism and aging.
60 y receptors present in the TME can inhibit T cell metabolism and alter T cell signaling both directly
61 ated protein kinase is a master regulator of cell metabolism and an attractive drug target for cancer
62  ligase Peli1 as an important regulator of T cell metabolism and antitumor immunity.
63  and downstream mTORC1-mediated actions on T cell metabolism and antitumor immunity.
64 himeric antigen receptor (CAR) can control T cell metabolism and balance the response toward long-liv
65          Because our understanding of immune cell metabolism and cancer metabolism has grown signific
66 , including intracellular Ca(2+) signalling, cell metabolism and cell death.
67  of adoptive cell therapy by reprogramming T-cell metabolism and cytokine expression.
68 t of organic acids plays a key role in plant cell metabolism and demonstrate that AtQUAC1 reduce diff
69 erstanding miRNA signaling underlying cancer cell metabolism and development of new strategies for th
70 WNT signaling in the reprogramming of cancer cell metabolism and examines the role of these signaling
71  function, the mechanisms that regulate Treg cell metabolism and function remain unclear.
72 ever, how nutrient availability influences T cell metabolism and function remains poorly understood.
73 te P2Y11 receptor stimulation that impairs T cell metabolism and functions.
74 iological networks including cell signaling, cell metabolism and gene regulation.
75    The lysosomal Ragulator complex regulates cell metabolism and growth by coordinating the activitie
76 oles in normal cells (including coordinating cell metabolism and growth), highlighting the features o
77  a pleiotropic role in the control of cancer cell metabolism and has been associated with a good prog
78 enes important for general functions such as cell metabolism and homeostasis.
79 tions between oncogenic signaling and cancer cell metabolism and how these links may be exploited for
80                        Ndfip1 restricts Treg cell metabolism and IL-4 production via distinct mechani
81 ng able to unravel the interaction of cancer cell metabolism and immune metabolism in therapeutically
82 e microbial pathogenesis as well as the host cell metabolism and immune responses.
83 er cell biology, particularly altered cancer cell metabolism and impaired DNA repair processes, is pr
84 ups reduce the perturbations caused by GO on cell metabolism and increase biocompatibility.
85 pamycin (mTOR) regulates stem and progenitor cell metabolism and is frequently dysregulated in human
86                                  The complex cell metabolism and its link to oncogenic signaling path
87  repressor Zbtb20 negatively regulates CD8 T cell metabolism and memory differentiation in mice.
88 ls were enriched in proteins associated with cell metabolism and MFM223 cells enriched in proteins as
89 arboxylate transporters (MCT) modulate tumor cell metabolism and offer promising therapeutic targets
90 gy is demonstrated here in the analysis of T cell metabolism and other large-scale metabolomic studie
91 g this loss of secretion are defects in beta-cell metabolism and perturbed mitochondrial structure.
92 ious consequences for the colonic epithelial cell metabolism and physiology in terms of mitochondrial
93 gnificant correlations between measures of T cell metabolism and plasma cytokine abundance that diffe
94                                   Changes in cell metabolism and plasma membrane potential have been
95 ctivation of an immune response, a switch in cell metabolism and processes related to muscle contract
96  support a novel role for Itch in limiting B cell metabolism and proliferation to suppress antigen-dr
97   For example, HIV-induced changes in immune cell metabolism and redox state are associated with CD4(
98 ith increased expression of genes related to cell metabolism and respiration.
99 oints towards its overall effect in lowering cell metabolism and RNA processing and modification.
100 cing agents, which are currently involved in cell metabolism and signaling pathways, can regulate fas
101 all inositol compounds, has pivotal roles in cell metabolism and signaling pathways.
102  mineral for both prokaryotic and eukaryotic cell metabolism and structure.
103 encing both cardiac contractile function and cell metabolism and survival and contributing to HF inde
104 rcuits highlight pathways involved in immune cell metabolism and the cell cycle, including mTOR signa
105                A causal relationship between cell metabolism and the fate of pluripotent stem cells t
106 dependent NAD(+) biosynthesis contributes to cell metabolism and to the DNA repair process in a subse
107 (PKM), which plays a critical role in cancer cell metabolism and tumor growth.
108 hosphate pathway (PPP) is crucial for cancer cell metabolism and tumor growth.
109 rein), in Myc-mediated alterations in cancer cell metabolism and tumorigenesis.
110 sting a sophisticated interplay between host cell metabolism and virus replication.
111 t vector titres due to biological effects on cell metabolism and/or on the vector virion itself.
112 developing principles in the regulation of T cell metabolism, and discuss how these processes are aff
113 ysis ((13)C-MFA), offer direct insights into cell metabolism, and have been widely used to characteri
114  energetics, and redox homeostasis in immune cell metabolism, and how these factors are reflected in
115 is reduced lipid storage, reprogrammed tumor cell metabolism, and inhibited invasive migration in vit
116 long been considered a "waste" by-product of cell metabolism, and it accumulates at sites of inflamma
117 ancer-related signaling networks, intestinal cell metabolism, and physiology in a three-dimensional e
118 ffles, is critical for antigen presentation, cell metabolism, and signaling.
119 s, cell growth and proliferation, autophagy, cell metabolism, and stress responses, whereas mTORC2 se
120 used in the care of patients with SLE affect cell metabolism, and the development of novel therapeuti
121              Obesity-associated changes in T-cell metabolism are associated with impaired T-cell resp
122           Given that coordinated shifts in T cell metabolism are essential for T cell responses to nu
123 ts that activate autophagy and reprogram PDA cell metabolism are unknown.
124 nd activation, but recent findings highlight cell metabolism as a crucial regulator of these processe
125 rently, the effect of HCMV infection on host cell metabolism as an increase in glycolysis during infe
126 which is provided by the cytoskeleton, using cell metabolism as its energy source, and the dynamic in
127 d postembryonic development and critical for cell metabolism at all stages of life.
128 rial dysfunction, methods for studying brain cell metabolism at high spatial resolution are needed to
129 hagy actively suppresses haematopoietic stem-cell metabolism by clearing active, healthy mitochondria
130 y be generated endogenously in the course of cell metabolism by cytochrome P450, by oxidative stress
131 contributed to dysfunction, as a rescue of T cell metabolism by genetically increasing Akt/mTORC1 sig
132             Photosynthetic organisms support cell metabolism by harvesting sunlight to fuel the photo
133  article centers on the manipulation of host cell metabolism by human cytomegalovirus (HCMV).
134                  A recent study published in Cell Metabolism by Wu et al. (2019) shows that DR repres
135       Emerging evidence suggests that cancer cell metabolism can be regulated by cancer-associated fi
136 ccumulation impacts longevity, and how aging cell metabolism can be rewired to modulate lipid accumul
137                            Changes in cancer cell metabolism can directly impact epigenetic regulatio
138             Oncogene-driven changes in tumor cell metabolism can impact the TME to limit immune respo
139 le applications including dynamic control of cell metabolism, cell biology and synthetic gene circuit
140 technology that provides direct insight into cell metabolism, cell dynamics and protein activity.
141 h inspire a novel top-down approach to study cell metabolism, combining mass balance and proteomic co
142  data indicate that patients have impaired T cell metabolism consistent with ongoing immune alteratio
143                                   Eukaryotic cell metabolism consists of processes that generate avai
144 t that programmed differences in infant stem cell metabolism correspond with differences in body comp
145 dependent N-reductive detoxication of HAP in cell metabolism could be demonstrated.
146         Here, we investigated whether cancer cell metabolism defines its susceptibility to OV and if
147                         Beyond their role in cell metabolism, development, and reproduction, hormones
148  However, although the roles of glucose in T cell metabolism, diabetes and obesity are well character
149 mary role of LIN28A and LIN28B in modulating cell metabolism, differentiation, and invasion, we hypot
150                      Importantly, impaired T cell metabolism directly contributed to dysfunction, as
151 or immunity, suggest that TGF-beta targets T cell metabolism directly, thus diminishing T cell functi
152 k is a systemic inflammation associated with cell metabolism disorders and cardiovascular dysfunction
153           MCJ also adapted effector CD8(+) T cell metabolism during the contraction phase.
154  a pivotal role in biological events such as cell metabolism, early stage apoptosis, and cell differe
155 odulated gradients of cell proliferation and cell metabolism emerging in response to fluid convection
156 iological processes such as abnormalities in cell metabolism, energy production and oxidative stress
157 actor (HIF) transcription factors to control cell metabolism, erythrogenesis, and angiogenesis.
158 ng device to evaluate the cell viability and cell metabolism for a healthy cell line (Human Dermal Fi
159                                  Engineering cell metabolism for bioproduction not only consumes buil
160 , but little is understood about the role of cell metabolism for natural killer T (NKT) cell survival
161 ueled anaplerosis that reverses basal Muller cell metabolism from production to consumption of glutam
162 n to boost FAO in other tissues, on CD8(+) T-cell metabolism, function, and efficacy in a murine ACT
163 domains, and the minimal effects observed on cell metabolism, further studies are warranted to assess
164 ork and functional information for over 2000 cell metabolism genes in more than 30 cancer types.
165      Thus, a systematic annotation of cancer cell metabolism genes is imperative.
166 some of the osmoregulatory pathways in guard cell metabolism, genes and signals that determine stomat
167 ine to glutamate, plays a key role in cancer cell metabolism, growth, and proliferation.
168 signals and serves as a central regulator of cell metabolism, growth, survival, and stress responses.
169                                            T cell metabolism has a central role in supporting and sha
170   The role of metabolites produced from stem cell metabolism has been emerged as signaling molecules
171 e tumor microenvironment dysregulated immune cell metabolism has emerged as a key mechanism of tumor
172                                       Immune cell metabolism has therefore become an attractive targe
173                     Contemporary analyses of cell metabolism have called out three metabolites: ATP,
174                       Besides its effects on cell metabolism, HO-1 is also capable of modulating host
175 l screening of candidate compounds targeting cell metabolism in a microplate-reader-based assay, alon
176 apshot analysis, allowing spatial mapping of cell metabolism in concert with cell phenotype.
177  and environmental parameters that influence cell metabolism in culture.
178 vident that genetic modifications can affect cell metabolism in HGG; however, it is currently unclear
179 ce of the mutual regulation of autophagy and cell metabolism in maintaining cell homeostasis.
180  disease (GVHD), yet little is known about T cell metabolism in response to alloantigens after hemato
181      Here we report plasticity in effector T cell metabolism in response to changing nutrient availab
182 Our study provides novel insight into cancer cell metabolism in the context of the endothelial microe
183 osis of T cells, little is known regarding T cell metabolism in the progression of human type 1 diabe
184 e effects on flagellar sterol enrichment and cell metabolism in the two life cycle stages.
185 nderstanding of the role of inflammation and cell metabolism in tissue-regenerative responses, highli
186 pact of the MCT1 inhibitor AZD3965 on cancer cell metabolism in vitro and in vivo Exposing human lymp
187  ULBP2 expression was linked to altered host cell metabolism, including increased cytoplasmic (iso)ci
188  whereby stromal fibroblasts regulate cancer cell metabolism independent of genetic mutations in canc
189 ecies and other toxic mediators that disrupt cell metabolism, induce apoptosis, and exacerbate ischem
190                                       Immune cells' metabolism influences their differentiation and f
191 f insulin that parallel oscillations in beta-cell metabolism, intracellular Ca(2+) concentration, and
192 ia telangiectasia mutated), those within the cell metabolism (IR-alpha, IR-beta, and AMP-activated pr
193                                       Cancer cell metabolism is a targetable vulnerability; however,
194                                              Cell metabolism is adaptive to extrinsic demands; howeve
195 ermodynamic modeling, we show that the plant cell metabolism is affected predominantly by hydroxo-spe
196 it remains unclear how lymphatic endothelial cell metabolism is altered in the tumor microenvironment
197                    It now becomes clear that cell metabolism is an integral part of the complex lands
198                                       Immune cell metabolism is dynamically regulated in parallel wit
199 his study, we demonstrate that altered tumor cell metabolism is essential for the regulation of drug
200                    Strict regulation of stem cell metabolism is essential for tissue functions and tu
201 e mechanisms of how autophagy supports tumor cell metabolism is essential.
202                                       Cancer cell metabolism is heavily influenced by microenvironmen
203 nce fumaric acid esters are metabolites, and cell metabolism is highly intertwined with the epigeneti
204 t of different mutant p53 proteins on cancer cell metabolism is largely unknown.
205                                            T cell metabolism is normally held under tight regulation
206  the interplay between PD-1 inhibition and T cell metabolism is not well studied.
207 t or "passenger" of cell-fate determination, cell metabolism is now starting to take center stage as
208 ytical tools for the investigation of living cell metabolism is still a challenge to be faced.
209  inhibitor protein of F1F0-ATPase) in cancer cell metabolism is still uncertain.
210                                              Cell metabolism is strongly influenced by mechano-enviro
211                        It is recognized that cell metabolism is tightly connected to other cellular p
212          Inflammation-driven changes in host cell metabolism lead to the release of l-lactate and mol
213 increase our understanding of TSC2-deficient cell metabolism, leading to novel potential therapeutic
214                                       Cancer cell metabolism leads to a uniquely acidic microenvironm
215 rcadian clock and output pathways regulating cell metabolism (lipids and xenobiotics), extracellular
216                                  Recently in Cell Metabolism, Logan et al. (2016) exploit membrane po
217 standing the impact of MCT blockade on tumor cell metabolism may help develop combination strategies
218  to drugs, genetic variation of patients and cell metabolism may help managing side effects by person
219 ar nutrient signaling pathways regulate beta-cell metabolism may thus offer new targets to improve be
220                                 Altered beta-cell metabolism may underlie both the progressive impair
221 the CAR costimulatory domain can alter the T cell metabolism, memory differentiation, and influence l
222 late multiple pathways of cancer or parasite cell metabolism, might lead to more effective treatments
223 een TET and two critical enzymes involved in cell metabolism: O-linked beta-N-acetylglucosamine trans
224 the profound (anoikis-independent) impact of cell metabolism on the viability of ECM-detached cells.
225 flammatory effect, with itaconate connecting cell metabolism, oxidative and electrophilic stress resp
226 cer development, the emerging role of p53 in cell metabolism, oxidative responses, and ferroptotic ce
227 uniquely targeting a HIF1alpha/LEO1-mediated cell metabolism pathway.
228 ; however, recent findings suggest that stem cell metabolism plays an important role in the regulatio
229 e a powerful tool to noninvasively analyze T cell metabolism, possibly in vivo.
230 dent deacetylase Sirtuin 1 (SIRT1) regulates cell metabolism, proliferation, and DNA repair and acts
231 r-activated receptor delta (PPARD) regulates cell metabolism, proliferation, and inflammation and has
232 in (CREB) plays key transcriptional roles in cell metabolism, proliferation, and survival.
233 , EGFL9 regulates COX activity and modulates cell metabolism, promoting a Warburg-like metabolic phen
234  assumptions in enzymology, biochemistry and cell metabolism regarding the fate of transiently genera
235 ssed proteins were predominantly involved in cell metabolism, regulation of focal and intracellular c
236                           Our knowledge of T cell metabolism relies primarily on studies performed in
237 l understood, whereas our knowledge of guard cell metabolism remains limited, despite several decades
238 , through its ability to link cell cycle and cell metabolism, represents a particularly powerful onco
239 finding has been attributed to altered tumor cell metabolism resulting from these mutations and does
240  Environmental nutrient levels impact cancer cell metabolism, resulting in context-dependent gene ess
241 sphorylation (OXPHOS) and glycolytic rate in cell metabolism studies.
242 hway and C3 being a driver and programmer of cell metabolism suggest that the complement system utili
243                                  Recently in Cell Metabolism, Szabat et al. (2015) present evidence t
244 tool to provide more detailed information on cell metabolism that are unprecedented in cell biology.
245 o multiple processes and plasticity in guard cell metabolism that enable these cells to function effe
246  novel role for RhoC as a regulator of tumor cell metabolism that extends beyond its well known role
247 to insufficient vascular exchange and cancer cell metabolism that leads to hypoxia, depletion of nutr
248 ablishes a link between nutrition and tumour cell metabolism that may allow for tumour-specific metab
249      Despite their fundamental importance to cell metabolism, the mechanisms by which regions of the
250           A key transcriptional regulator of cell metabolism, the peroxisome proliferator-activated r
251 rties of these key metabolites power much of cell metabolism, the underlying molecular logic remains
252 glycolysis and consequently rescues leukemic cell metabolism, thereby abrogating the antileukemic eff
253 ating the integration of systemic and immune cell metabolism through in-depth analysis of immune cell
254 se phosphate pathway (oxiPPP) contributes to cell metabolism through not only the production of metab
255    Here we show that CAFs regulate malignant cell metabolism through pathways under the control of FA
256 nscription factor HIF1alpha and reprogrammed cell metabolism to a glycolytic state.
257           In addition, loss of KEAP1 altered cell metabolism to allow cells to proliferate in the abs
258 stabilized under energy shortage and reshape cell metabolism to allow energy regeneration, we propose
259 tBP1 is a critical factor linking changes in cell metabolism to cell phenotype in hypoxic and other f
260        Here we find that p53 remodels cancer-cell metabolism to enforce changes in chromatin and gene
261 ic structure that mediates the adaptation of cell metabolism to environmental cues.
262 ssion of ERRgamma reprograms prostate cancer cell metabolism to favor mitochondrial activity and cell
263 activity, and ATP production and also shifts cell metabolism to higher glycolytic activity.
264 exploring and potentially manipulating guard cell metabolism to improve plant water use and productiv
265  manipulation can specifically affect tumour-cell metabolism to mediate broad aspects of cancer outco
266 nd to various diets, how diet impacts cancer cell metabolism to mediate these responses and whether d
267 anner how viral oncoproteins hijack the host cell metabolism to meet their own energy demands and how
268 d checkpoint in linking immune signaling and cell metabolism to orchestrate memory CD8(+) T-cell deve
269 explore current strategies that shift immune cell metabolism to pro-inflammatory states in the TME an
270 Deregulated Myc transcriptionally reprograms cell metabolism to promote neoplasia.
271 whether PPARbeta/delta modulates endothelial cell metabolism to support the dynamic phenotype remains
272 f the actomyosin cytoskeleton, thus coupling cell metabolism to the mechanical properties of the surr
273                           Finally, skewing T cell metabolism toward aerobic glycolysis by deleting mi
274 ppaB activation, leading to reprogramming of cell metabolism towards glycolysis and lactate dehydroge
275 king PKM2 in NK cells showed no defect in NK cell metabolism, transcription or antiviral responses to
276 stinct pathways such as hypoxia, glycolysis, cell metabolism, translation initiation, cell cycle, and
277                   We present a study of beta-cell metabolism under increased fuel pressure using a st
278 , these data demonstrate that induction of T cell metabolism upon activation is dependent on systemic
279 tive, high-resolution technique for studying cell metabolism via endogenous fluorescence of reduced n
280 nocytes were studied in vitro with regard to cell metabolism, viability, growth, gene expression sign
281                                           NK cell metabolism was maintained due to compensatory PKM1
282 mpaired memory T-cell response nor altered T-cell metabolism was reversed with weight loss.
283                         For many years, stem cell metabolism was viewed as a byproduct of cell fate s
284    To investigate the effects of age on beta-cell metabolism, we established a novel assay to directl
285 tty acid into mitochondria to support cancer cell metabolism, we tested several clinically relevant i
286 nsity and dispersion, free water, myelin and cell metabolism were assessed with Neurite Orientation D
287 luenza PR8, and memory T-cell function and T-cell metabolism were measured.
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 nges in droplet volume being used to measure cell metabolism, while simultaneously imaging the cells
292 on of a STAT3/c-Myc pathway and increased NK cell metabolism with a shift towards aerobic glycolysis.
293 regulator that connects changes in satellite cell metabolism with changes in the transcriptional mach
294  showed increased UCP1 protein abundance and cell metabolism with enhanced oxygen consumption and pro
295  AMPK acts as an energy sensor to coordinate cell metabolism with environmental status in species fro
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 y cholesterol and its derivatives, in cancer cell metabolism within intrinsically harsh tumor microen
299                          Knowledge of single-cell metabolism would provide a powerful look into cell
300                         In a recent issue of Cell Metabolism, Ying et al. (2018) report that two subp

 
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