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1 networks (GEMs) can assist in understanding cellular metabolism.
2 d various carbohydrate intermediates used in cellular metabolism.
3 a dynamic network, playing a central role in cellular metabolism.
4 or providing energy and carbon skeletons for cellular metabolism.
5 les served as the light harvester to sustain cellular metabolism.
6 y attributes, is significantly influenced by cellular metabolism.
7 onditions, suggesting its role in modulating cellular metabolism.
8 ed protein kinase (AMPKalpha), the sensor of cellular metabolism.
9 data suggest a novel role of GRP78-mediating cellular metabolism.
10 ens a new avenue for the characterization of cellular metabolism.
11 rules that govern organelle integration into cellular metabolism.
12 eraction of OTUB1 with proteins important in cellular metabolism.
13 nk the environmental signals with rhythms in cellular metabolism.
14 Mitochondria are central organelles for cellular metabolism.
15 d by a continuous energy supply derived from cellular metabolism.
16 olecules, providing clues for their roles in cellular metabolism.
17 tration states regulate different aspects of cellular metabolism.
18 y recognized as a physiological modulator of cellular metabolism.
19 s, we reveal that EVI1 overexpression alters cellular metabolism.
20 the critical connection between systemic and cellular metabolism.
21 e/threonine kinase, is a master regulator of cellular metabolism.
22 ria caused remarkable alterations in overall cellular metabolism.
23 ically showed mutations in genes involved in cellular metabolism.
24 es sustained mTORC1 activation and regulates cellular metabolism.
25 electrical signals in response to changes in cellular metabolism.
26 ions of cholesterogenic enzyme deficiency on cellular metabolism.
27 proteasome activity in CD8+ T cells affected cellular metabolism.
28 species (ROS/RNS) are natural byproducts of cellular metabolism.
29 owerful and versatile technique for studying cellular metabolism.
30 adian oscillations to integral properties of cellular metabolism.
31 these compounds readily during quenching of cellular metabolism.
32 bit PDH, highlighting SIRT4 as a guardian of cellular metabolism.
33 mitochondrial oxidative phosphorylation and cellular metabolism.
34 the metabolites was found as consequence of cellular metabolism.
35 inction, and could also potentially regulate cellular metabolism.
36 ge and often fail to take a holistic view of cellular metabolism.
37 Circadian rhythms are intimately linked to cellular metabolism.
38 onstrated that the epigenome is sensitive to cellular metabolism.
39 rtant signaling pathway to the regulation of cellular metabolism.
40 ed extensively to investigate alterations in cellular metabolism.
41 egulatory targets coupling energy storage to cellular metabolism.
42 ranscription does not restart to reestablish cellular metabolism.
43 ently sense and control vital points of core cellular metabolism.
44 at plays a central role in the regulation of cellular metabolism.
45 this energy is one of the central issues of cellular metabolism.
46 rvival of male germ cells via its effects on cellular metabolism.
47 at have profound and wide-ranging effects on cellular metabolism.
48 tochondrion is the primary energy source for cellular metabolism.
49 increasingly understood to be regulators of cellular metabolism.
50 of the apoplast has a profound influence on cellular metabolism.
51 e enzymes to form NADH is a key component of cellular metabolism.
52 ecycling, and generating molecules that fuel cellular metabolism.
53 or energy homeostasis and tightly coupled to cellular metabolism.
54 drawing a direct link between DNA repair and cellular metabolism.
55 ormation about the topology and operation of cellular metabolism.
56 ses mTORC1 activity, leading to dysregulated cellular metabolism.
57 naling cascade regulates multiple aspects of cellular metabolism.
58 er understand the burden of glycosylation on cellular metabolism.
59 ich hepatic autophagy monitors and regulates cellular metabolism.
60 monocytes and macrophages induces changes in cellular metabolism.
61 staining enzymes that are required for basic cellular metabolism.
65 y lymphoid tissues but necessary to regulate cellular metabolism and accumulation of CD103(+) DCs and
66 cin complex 1 (mTORC1) is a key regulator of cellular metabolism and also has fundamental roles in co
68 ies, is produced at low levels during normal cellular metabolism and at higher concentrations under p
70 , approved for type 2 diabetes therapy alter cellular metabolism and can heighten ROS production.
72 arise from rare stochastic imperfections of cellular metabolism and deficiencies in maintenance gene
73 TOR1 complex inhibits TORC1 activity to slow cellular metabolism and drive the mitotic/meiotic transi
74 etabolic sensor LKB1 is critical to maintain cellular metabolism and energy homeostasis in Tregs.
75 he unfolded protein response, autophagy, and cellular metabolism and exploit these pathways to their
77 eal a previously hidden relationship between cellular metabolism and genome evolution and provide new
78 compounds that support, or are products of, cellular metabolism and growth) is entirely controlled b
83 onent of pathways involved in the control of cellular metabolism and has a role in regulating immune
89 tography tandem mass spectrometry, we mapped cellular metabolism and identified spatially defined met
90 roles of class I PI3Ks in the regulation of cellular metabolism and in immune system functions, two
91 hat miR-181 is a nonredundant determinant of cellular metabolism and is essential for supporting the
92 a pervasive model organism for investigating cellular metabolism and its regulation by signaling proc
93 e of N-acetylmannosamine, is found to endure cellular metabolism and label the surface of a mammalian
94 ntly alters several diagnostic parameters of cellular metabolism and leaf gas exchange in Arabidopsis
96 contribute in multiple ways to regulation of cellular metabolism and may have direct and indirect eff
97 increasing recognition of the importance of cellular metabolism and metabolic substrates for the fun
98 ng activated primarily genes associated with cellular metabolism and mitochondrial activation (e.g.,
99 a rapid autophagic flux to promptly restore cellular metabolism and mitochondrial fusion in keeping
100 K), a central stress-responsive regulator of cellular metabolism and mTOR signaling, which is known t
102 trand breaks (DSBs) are byproducts of normal cellular metabolism and obligate intermediates in antige
103 protein folding, turnover and transport, on cellular metabolism and on DNA and RNA synthesis and rep
110 epair DNA damage that is generated by normal cellular metabolism and stress from the environment.
113 channels provide a significant link between cellular metabolism and the antiviral immune response in
115 roles of mTOR signaling in the regulation of cellular metabolism and the pathogenesis of cancer.
116 articular the integration of complement with cellular metabolism and the potential implications in in
117 metal complexes can lead to major changes in cellular metabolism and to potent complexes with novel m
119 onths of life correspond with differences in cellular metabolism and transcriptomic profiles at birth
120 other metabolites, and thus is critical for cellular metabolism and various growth and developmental
122 .Sle3 lupus mice and patients present a high cellular metabolism, and a treatment combining 2-deoxy-D
125 glutamine are the major nutrients that fuel cellular metabolism, and the pathways utilizing these nu
126 lvement in many biological processes such as cellular metabolism, apoptosis, aging and inflammation.
127 ondria play an important role in controlling cellular metabolism, apoptosis, and innate immunity.
128 he past decades owing to its pivotal role in cellular metabolism, apoptosis, and neurotransmission.
129 receptor (Ryr2) Ca(2+) release channels and cellular metabolism are both disrupted in heart disease.
130 ecent studies have suggested that changes in cellular metabolism are important to these processes.
134 g free radicals, generated as by-products of cellular metabolism, are a major contributor to this dam
135 ion of ssb is a key component of both normal cellular metabolism as well as pathways responsible for
137 ccur in several types of cancer, and altered cellular metabolism associated with IDH1 mutations prese
138 ripts related to primary cell wall and basic cellular metabolism at the base to those involved in pho
139 tocin did not affect the glutathione-related cellular metabolism before OGD, oxytocin modulated the e
141 er, little is known regarding how changes in cellular metabolism, both within the cancer cell and the
142 ology to make great strides in interrogating cellular metabolism but does not provide sufficient insi
144 in that they spatially segregate aspects of cellular metabolism, but they do so by building not a li
145 lcNAc modification of their EGF repeats, and cellular metabolism by affecting pyrimidine synthesis an
147 erve as a crucial interaction hub in primary cellular metabolism by communicating transiently between
148 However, the overabundant lysosomes derange cellular metabolism by consuming the key glycolytic enzy
150 rrant immune responses and that manipulating cellular metabolism can beneficially enhance or temper i
152 the relationship between exogenous cysteine, cellular metabolism, cellular localization, and Hg(II) c
153 ceptor-dependent pathway, induced changes in cellular metabolism characterized by increased fatty aci
156 common lesion spontaneously generated during cellular metabolism, decreases the efficiency of human A
159 ave emerged for characterizing transients in cellular metabolism, dynamic metabolic flux analysis (DM
161 erting nicotinamide to NAD(+), essential for cellular metabolism, energy production, and DNA repair.
166 or the differentiation of HSCs, reprogrammed cellular metabolism from mitochondrial aerobic metabolis
167 These results reveal a connection between cellular metabolism, gene regulation, and neural plastic
169 ycin (mTOR) pathway plays a critical role in cellular metabolism, growth, and proliferation and has b
172 nsitive intracellular processes that mediate cellular metabolism, growth, proliferation, and/or tissu
173 ell responses, it is now becoming clear that cellular metabolism has direct roles in regulating immun
174 minance of phosphorylation as a regulator of cellular metabolism has fostered the development of pept
178 olves global reprogramming of transcription, cellular metabolism, hormone signalling and chromatin mo
179 een successfully used to assess and engineer cellular metabolism; however, GEMs of phototrophic metab
181 particular focus on how host, commensal, and cellular metabolism impinge upon Treg homeostasis and fu
184 tion in matrix bioenergetics would influence cellular metabolism in glycolytic cells that do not requ
185 thod that allows for real-time assessment of cellular metabolism in isolated, intact long skeletal mu
189 dition to its well-known role in stimulating cellular metabolism in response to nutrients, TOR also p
190 The accuracy of these models to represent cellular metabolism in specific conditions has been impr
191 x of K(+), and thus membrane potential, with cellular metabolism in various cell types including insu
194 b5, for a range of biochemical reactions in cellular metabolism, including for fatty acid desaturati
195 clic AMP (cAMP) is essential for controlling cellular metabolism, including glucose and lipid homeost
196 traditional media, had widespread effects on cellular metabolism, including on the metabolome, redox
197 the c-MET tyrosine kinase pathway; shifts in cellular metabolism, including up-regulation of hypoxia
211 Elucidating signaling pathways that regulate cellular metabolism is essential for a better understand
213 unction of Bax, a pro-apoptotic regulator of cellular metabolism is implicated in neurodegenerative d
215 As such, the regulation of whole-body and cellular metabolism is intimately integrated with immune
219 ic fluxes (i.e. the rate of each reaction in cellular metabolism) is of particular interest for metab
220 ial to understanding a fundamental aspect of cellular metabolism leading to compounds that are not on
221 activation of glycolysis, and alterations in cellular metabolism may be a broadly applicable mechanis
222 oliferator-activated receptor-alpha-mediated cellular metabolism may play an important role in sepsis
223 the main interface between mitochondrial and cellular metabolisms, mediates the passage of a variety
224 most solid tumors and often lead to altered cellular metabolism, metastasis, and drug resistance.
225 the GOF activities, including alterations in cellular metabolism, might vary between the different p5
227 ting from inflammatory responses, changes in cellular metabolism, nuclear architecture, and epigenome
228 Dysregulation of vascular stiffness and cellular metabolism occurs early in pulmonary hypertensi
229 environment due to several factors including cellular metabolism of compounds, protein-protein intera
230 rganize subcellular membranes and rewire the cellular metabolism of host cells to achieve viral repli
231 or parasite-derived LBs and PGF2alpha in the cellular metabolism of Leishmania and its evasion of the
232 rimental method of choice to investigate the cellular metabolism of microbes, cell cultures and plant
234 eral decades of research investigations, the cellular metabolism of rice remains largely unclear.
235 ethers and their oxidized derivatives on the cellular metabolism of WEHI-164 and HEK-293T cell lines
238 d OXPHOS, depleted cellular ATP, and altered cellular metabolism pathways that compromise their survi
241 transcription factors are key regulators of cellular metabolism, proliferation, and stress resistanc
242 of rapamycin (mTOR) is a major regulator of cellular metabolism, proliferation, and survival that is
243 cted roles of cytosine methylation in global cellular metabolism providing evidence for a 'core' m5C
244 ndrial citric acid cycle is a central hub of cellular metabolism, providing intermediates for biosynt
245 accinia virus (VACV) infection alters global cellular metabolism, providing the first metabolomic ana
246 s dominated by DO concentration (affected by cellular metabolism), rather than potential nucleation s
251 ate through metabolic reprogramming, whereby cellular metabolism shifts from oxidative phosphorylatio
252 d quantitative analysis of these markers for cellular metabolism show in response to doxorubicin, NAD
253 f temperature compensation as fV , M O2, and cellular metabolism significantly decreased following th
254 ry effectors of cellular function, including cellular metabolism, structural dynamics, and informatio
255 intracellular vesicles to protect the normal cellular metabolism, structure, and function of podocyte
256 transport processes, energy production, and cellular metabolism, suggesting a major change in cell p
258 of naive T cells induces dramatic changes in cellular metabolism that are essential for cell growth,
259 ndrial respiration is a crucial component of cellular metabolism that can become dysregulated in canc
260 ation, gene regulation, and other aspects of cellular metabolism that reinforce thermostable polymera
261 ystems-biology computational method to study cellular metabolisms that are assumed to be in a steady
263 ounced changes in cell cycle progression and cellular metabolism, thereby highlighting its putative r
264 process that mends DNA lesions formed during cellular metabolism; these lesions include double-strand
265 ion of cytoprotective genes, which reprogram cellular metabolism through activation of the integrated
266 hotosynthetic apparatus and other changes in cellular metabolism through extensive changes in transcr
267 tochondria and suggests that it may regulate cellular metabolism through modulating the interaction b
268 that metabolic alterations in cancer rewire cellular metabolism through unconventional pathways.
269 ute of phosphatidic acid utilization rewires cellular metabolism to adopt a triacylglycerol-rich life
272 biology is that oncogenes actively reprogram cellular metabolism to enable tumors to survive and prol
274 eciated that oncogenic transformation alters cellular metabolism to facilitate cell proliferation, bu
275 randial blood glucose, an enforced change in cellular metabolism to maintain glucose homeostasis.
276 ability of cardiomyocytes, using a model for cellular metabolism to predict the levels of ATP followi
279 cer cells undergo a multifaceted rewiring of cellular metabolism to support their biosynthetic needs.
280 In addition, they convey oscillations in cellular metabolism to the membrane by sensing adenine n
281 ., acetylation versus crotonylation) couples cellular metabolism to the regulation of gene expression
282 ation of stem cell, cell survival/death, and cellular metabolism under both physiological and patholo
283 nt in HIF signalling to reveal its effect on cellular metabolism under normal oxygen conditions as we
285 ed protein kinase (AMPK), a key regulator of cellular metabolism, using primary mouse and human hepat
287 ecause both IDH1 and p53 are known to affect cellular metabolism, we compared the requirements for gl
289 d monocytes primarily use glucose to support cellular metabolism, we hypothesized that chronic monocy
290 s, e.g. genes related to cell wall and basic cellular metabolism were highly expressed in immature le
291 Metabolites are small molecules involved in cellular metabolism, which can be detected in biological
292 luoro-2-deoxy-D-glucose can be used to image cellular metabolism, which during lung inflammation main
293 an interplay between oxygen availability and cellular metabolism, which in turn has significant effec
294 luoro-2-deoxy-D-glucose can be used to image cellular metabolism, which, during lung inflammatory pro
296 Despite considerable research connecting cellular metabolism with differentiation decisions, the
298 nalling network integrates transcriptome and cellular metabolism with shoot-root coordination and dev
299 This leads to a functional heterogeneity of cellular metabolism within WAT that has potential impact
300 resently, agents that target angiogenesis or cellular metabolism would be reasonable therapeutic appr
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