ライフサイエンスコーパス: cellular

1 ome 30 proteins involved in the synthesis of cellular [2Fe-2S] and [4Fe-4S] clusters and their incorp

2 g esters, suggesting that the high levels of cellular 2OG may preclude inhibition.

3 this disorder is complicated by the complex cellular abnormalities and challenges in achieving effec

4 on the nerves within the pancreas slice, CCK cellular actions directly affected human acinar cells.

5 provide a phospho-switch that regulates the cellular activity of ATG4B to control LC3 processing.Upo

6 ed in neurons and muscle where they modulate cellular activity.

7 Tissue regeneration requires dynamic cellular adaptation to the wound environment.

8 in-mediated adhesion is a central feature of cellular adhesion, locomotion, and endothelial cell mech

9 s is mediated by a complex interplay between cellular adhesions, actomyosin-driven contractility, and

10 epidermidis, and electron microscopy showed cellular aggregates connected by discrete surface linkag

11 We found that cellular albumin internalization was proportional to FcR

12 hybridization technology with morphokinetic cellular analysis to provide rapid species identificatio

13 cing selection of viral variants that escape cellular and antibody (Ab)-mediated immune pressure, yet

14 These experiments showed that alpha-cellular and beta-cellular clocks are oscillating with d

15 he koose inhibited radical-induced oxidative cellular and DNA damage.

16 To gain insight into the cellular and molecular interactions mediating the desmop

17 However, the cellular and molecular mechanisms by which dysfunction o

18 ch and inflammation are mediated by distinct cellular and molecular mechanisms in a mouse model of AC

19 e extent to which overlap exists between the cellular and molecular mechanisms triggered by these var

20 lar cardiomyopathy/dysplasia, although their cellular and molecular pathomechanisms are not precisely

21 in the human nervous system, as well as the cellular and molecular reorganization of its neural circ

22 of optobiological approaches in the study of cellular and organismal functions, discuss current chall

23 Cellular and secreted levels of OEA and PEA (P < 0.001-0

24 e find that Brevican simultaneously controls cellular and synaptic forms of plasticity in PV+ cells b

25 Herein, we review the factors within the cellular and the extracellular microenvironment regulati

26 cules even in densely labeled samples and in cellular and tissue environments.

27 re, we use genetic association of molecular, cellular, and human disease traits and experimental vali

28 F-E2-related factor 2, a key mediator of the cellular antioxidant response.

29 Broad cellular antiproliferative potency of 24 is supported by

30 the progression of lung fibrosis, attenuated cellular apoptosis (caspase-3/7) and lung deposition of

31 trast, homozygous deletion of Sirt1 triggers cellular apoptotic pathways, increases cell death, dimin

32 kdown of EmMBD2/3 expression disrupts normal cellular architecture and development of E. muelleri.

33 also had variable stimulatory effects in the cellular assay, but not in vitro Sequencing analyses fur

34 icrofluidic devices and permit the design of cellular assays, which can ultimately impact disparities

35 nstrates a novel role of FANCD2 in governing cellular ATP production, and advances our understanding

36 language dynamics based on the principles of cellular automata/agent-based modeling and combine it wi

37 Distinct cellular barriers that protect primary human blood cells

38 However, the cellular basis and pathogenic mechanism of the SLC25A46-

39 ctivity-dependent neuronal plasticity is the cellular basis for learning and memory, and it is crucia

40 widely used to investigate the molecular and cellular basis of angiogenic mechanisms.

41 evelopment, and fundamental understanding of cellular behavior during hypoxia.

42 The approach integrates cellular behaviors via agent-based modeling (ABM) and he

43 while utilizing both endogenous and ectopic cellular behaviours to dismantle the aberrant structures

44 pared to APP, APLP1 exhibits increased trans-cellular binding and elevated cell-surface levels due to

45 have an evolutionary relationship with other cellular biological entities that share the common funct

46 de a review of the ecology and molecular and cellular biology of New World arenaviruses, as well as a

47 functionally modulate effects of EFS-induced cellular calcium oscillations.

48 t as a transporter of mitochondria and other cellular cargoes by attaching them to dynamic microtubul

49 eriments showed that alpha-cellular and beta-cellular clocks are oscillating with distinct phases in

50 ced cellular uptake, and distribution across cellular compartments.

51 suggesting that VEGF inhibition could reduce cellular complement regulatory capacity.

52 The partitioning of cellular components between the nucleus and cytoplasm is

53 mmation, pancreatic islet morphometry, islet cellular composition, and inflammation.

54 The cellular content of pancreatic cyst fluid aspirate is of

55 The sign of the effect depends on cellular context, implying that some of the emerging phe

56 mic infection in a physiologically relevant, cellular context.

57 GRP78 and that both proteins interact in the cellular context.

58 nsights into the genetic, environmental, and cellular contributions to islet (dys)function and T2DM p

59 ing interest in utilizing antibody-dependent cellular cytotoxicity (ADCC) to eliminate infected cells

60 We also observed a congruent pattern of cellular damage with tissue-specific expression of APOL1

61 endrocyte progenitor cells (OPCs) it induces cellular death.

62 The bacterial condensin MukB and the cellular decatenating enzyme topoisomerase IV interact.

63 Thus, cellular defects due to this ACTA2 mutation in both aort

64 ity from the otherwise inhibitory effects of cellular depolarization imposed by elevating extracellul

65 amino acids, converting the lysosome into a cellular depot for them.

66 ver, little is known about the molecular and cellular determinants in mPFC for stress-associated ment

67 and serve as useful models for investigating cellular differentiation and human embryogenesis.

68 The first cellular differentiation event in mouse development lead

69 Notch inhibitor dibenzazepine (DBZ) to drive cellular differentiation into secretory cell lineages, w

70 cell competition arising from differences in cellular differentiation status, thus providing a physio

71 2 and H3K27me3, which are involved in stable cellular differentiation, specifically in cardiomyocytes

72 , which may in turn influence the outcome of cellular differentiation.

73 Regional differences in the cellular distribution of aromatase (estrogen synthase) i

74 ded DNA nature of the adenovirus genome, the cellular DNA damage response (DDR) is considered a barri

75 nute virus of mice (MVM) induces a sustained cellular DNA damage response (DDR) which the virus explo

76 triphosphohydrolase activity by reducing the cellular dNTP pool to a level that cannot support produc

77 nd responses of immune cells produce diverse cellular ecosystems composed of multiple cell types, acc

78 by vaccines, can trigger antibody-dependent cellular effector functions, through engagement of their

79 nduced transmembrane protein 3 (IFITM3) is a cellular endosome- and lysosome-localized protein that r

80 d ER membrane (MAM) plays a critical role in cellular energetics and calcium homeostasis; however, ho

81 ions of histones have been shown to regulate cellular energy metabolism, but their role in white adip

82 luable tool and has formed the foundation of cellular engineering for adoptive cell therapy in cancer

83 s contained viral glycoproteins required for cellular entry, as well as tegument proteins involved in

84 e pH switching that occurs between different cellular environments could control beta-synuclein (beta

85 llows them to function and adapt to changing cellular environments.

86 lls, and must therefore be modified to allow cellular expansion.

87 Therefore, we have used cellular expression profiling tools to define the distin

88 ly reiteratively signals to direct disparate cellular fates throughout embryogenesis.

89 egion of FUS is sufficient to retain ASOs in cellular foci.

90 to reflect the capacity of the host-encoded cellular form of the prion protein (PrP(C)) to selective

91 s predicted to result in an elevation of the cellular fraction of active eEF-2K.

92 ically disordered proteins are important for cellular function and common in all organisms.

93 gest that replication in macrophages affects cellular function and plays an important role in pathoge

94 nvironment to epigenetic gene regulation and cellular function, and their actions may be relevant to

95 Proteins have evolved to perform diverse cellular functions, from serving as reaction catalysts t

96 th proteins that serve as hubs for essential cellular functions.

97 an proteome play important roles in numerous cellular functions.

98 to visualize molecular signals or manipulate cellular functions.

99 r cells undergo determination and eventually cellular fusion.

100 ensive EBV regulome encompassing 1,992 viral/cellular genes and enhancers.

101 y responses.Several metabolic factors affect cellular glucose metabolism as well as the innate inflam

102 identify a mechanism by which alterations in cellular glucose metabolism can influence cellular infla

103 pecifically to GODZ (also known as DHHC3), a cellular Golgi apparatus-specific Asp-His-His-Cys (DHHC)

104 a vital role in transcriptional regulation, cellular growth control, and cell-cycle progression.

105 roteins are enriched in pathways involved in cellular growth, cellular trafficking and transmembrane

106 could be of significant value for dissecting cellular heterogeneity in tumors and analyzing single ci

107 espective effects of age, sex, genetics, and cellular heterogeneity on the interindividual variabilit

108 at potential to improve our understanding of cellular heterogeneity through discovering novel quality

109 ng provides unparalleled resolution to study cellular heterogeneity.

110 tric control of genetic programs involved in cellular homeostasis and the associated diseases.

111 nger E3 ubiquitin ligase associated with the cellular hypoxic response, to be the ubiquitin E3 ligase

112 ions ranging from in vitro sensing assays to cellular imaging are separated and discussed in more det

113 Cellular imaging using a phospho-specific p-T153/Y155 an

114 e case of weakly interacting biomolecules or cellular imaging.

115 ed breadth and magnitude of MHC-B-restricted cellular immune responses in HIV-infected individuals.

116 Adaptive cellular immunity is initiated by antigen-specific inter

117 accine is more effective than the humoral or cellular immunization alone.

118 Despite the broad cellular impact of SCF enzymes, important questions rema

119 elds, including point-of-care diagnostics or cellular in vivo biosensing when using ultrathin fiber o

120 in key processes related to fatty liver and cellular inflammation associated with atherosclerosis an

121 in cellular glucose metabolism can influence cellular inflammatory responses.Several metabolic factor

122 Cellular injury markers lactate dehydrogenase and aspart

123 ess similar potencies but different rates of cellular intoxication and pathology in a mouse model of

124 l-based model of MMP-dependent breast cancer cellular invasiveness, this N-TIMP2 mutant acted as a fu

125 Sub-cellular investigations reveal that the plasma membrane

126 Hence, the cellular iron balance must be tightly controlled.

127 pression, which in turn results in decreased cellular iron export.

128 combined with these chelators, ELT enhanced cellular iron mobilization more than additive (synergist

129 ical and in vivo MRI assessments of non-heme cellular iron revealed that preclinical prostate tumor m

130 ntly unclear how this is orchestrated at the cellular level and how cell fate is affected by severe t

131 s scales such that patterned disorder at the cellular level leads to the emergence of organism-level

132 were investigated by RNA studies and on the cellular level using immunofluorescence and microscopy.

133 Here, we describe functional units, at a cellular level, of a compound eye from the base of the C

134 rk for the development of E/I balance at the cellular level.

135 tissue engineered constructs to control the cellular-level damage and cell-cell distance in individu

136 In vitro techniques at the molecular and cellular levels were now applied to assess their functio

137 nd the formation of micronuclei by targeting cellular ligases through a sT domain that also inhibits

138 a decade, the equally important functions of cellular lipids in virus replication have been gaining f

139 Together, our results show that cellular localization of Clusterin leads to divergent ef

140 Defining the kinetics, dynamics, and cellular location of uncoating of virions leading to inf

141 chnine, are synthesized in several different cellular locations.

142 ecies and how these interact with the cancer cellular machinery.

143 ication, influencing cell wall formation and cellular mechanics.

144 iding information on cell culture viability, cellular mechanisms and multicellular movements.

145 dinated regulation of KCNQ and VGSCs and the cellular mechanisms governing KCNQ trafficking to the AI

146 To facilitate the study of cellular mechanisms in human cells, we established sever

147 However, some cellular mechanisms involved in HSV infection in rodents

148 s on neutrophil functions and the underlying cellular mechanisms involved.

149 ls of atherosclerosis, and the molecular and cellular mechanisms involved.

150 ducted to examine the neural connections and cellular mechanisms of GLP-1R signaling on PVT-to-nucleu

151 t progress in understanding the systemic and cellular mechanisms that underlie the regulation of iron

152 Here, we explore the underlying cellular mechanisms.

153 easurements showed decreased hypoxia-induced cellular membrane depolarization in Cox4i2(-/-) PASMCs c

154 een positive-strand RNA [(+)RNA] viruses and cellular membranes that contribute to the biogenesis of

155 emical GTPases involved in the remodeling of cellular membranes.

156 hat function to slowly degrade molecular and cellular memory traces.

157 Cellular metabolism in mammalian cells represents a chal

158 ses, such as HDAC3, have been shown to alter cellular metabolism in various tissues.

159 ation of stem cell, cell survival/death, and cellular metabolism under both physiological and patholo

160 networks (GEMs) can assist in understanding cellular metabolism.

161 vitro, have aggregate-clearing activity in a cellular model of Huntington's disease, and induce autop

162 Functional analysis with miRNA mimics in cellular models confirmed these findings.

163 increased calls for advanced in vitro multi-cellular models that provide reliable and valuable tools

164 neral terms, prompts the use of iPSC-derived cellular models to study epigenetic mechanisms impacting

165 experience introduces precise molecular and cellular modifications in PV+ cells that are required fo

166 this toxicity and the associated changes in cellular morphology are related to the putative interact

167 mage patches from brightfield microscopy and cellular movement.

168 at these enzymes are important in regulating cellular NEIL1 steady state protein levels.

169 nteract with other macromolecules in complex cellular networks for signal transduction and biological

170 here are no studies that have determined the cellular or enzymatic function of UBE3B.

171 This coupled cellular oscillator architecture permits stable and repl

172 ency were analyzed for G6PD enzyme activity, cellular oxidized nicotinamide adenine dinucleotide phos

173 xic phenotype is linked to severe cerebellar cellular pathology, characterized by nuclear degeneratio

174 us tactic responses are mediated by the same cellular pathway, but sensing of physical stimuli remain

175 ferent gene mutations induce DCM via diverse cellular pathways.

176 which circulating anti-PE antibodies access cellular PE remains unknown.

177 ions between chirality, protease resistance, cellular penetration, and intracellular activity that ma

178 poration, which investigate ablation-induced cellular permeability.

179 e BER activity in a gene promoter and impact cellular phenotype ascribes an epigenetic role to OG.

180 erity of growth retardation and the in vitro cellular phenotype.

181 huntingtin markedly accelerates all of these cellular phenotypes in a dose- and age-dependent manner

182 suggest links between energy metabolism and cellular physiology, morphology, and symbiotic interacti

183 njection have been developed to overcome the cellular plasma membrane, but they all result in reduced

184 re extremely poor prognosis, may result from cellular plasticity.

185 d in the regulation of membrane composition, cellular polarity and trafficking, and the organization

186 ng vascular system of the brain, and altered cellular positioning.

187 ukaryotic cells because they function as the cellular power plant and play a central role in the earl

188 Cellular prion protein (PrP(C)) is a mammalian glycoprot

189 rvival protein FPV039 promiscuously binds to cellular proapoptotic Bcl-2 and engages all major proapo

190 quitin (Ub), regulates virtually every known cellular process in eukaryotes.

191 Despite its fundamental importance in cellular processes and abundant use in biotechnology, we

192 circuits embedded in host cells compete with cellular processes for limited intracellular resources.

193 transferred to recipient cells and regulate cellular processes in an autocrine or paracrine manner.

194 by oxidative phosphorylation and mediate key cellular processes such as apoptosis.

195 lexes are orchestrated by several fine-tuned cellular processes that encompass (a) synthesis of the s

196 creen in near-haploid human cells to uncover cellular processes that regulate HIF1alpha.

197 d in a wide range of molecular functions and cellular processes, and showed diverse subcellular local

198 GTP is a major regulator of multiple cellular processes, but tools for quantitative evaluatio

199 ESCRT proteins are implicated in myriad cellular processes, including endosome formation, fusion

200 from yeast to man and regulate a variety of cellular processes, including proliferation and differen

201 re determination, to cover the full scale of cellular processes.

202 spatial and temporal elements of fundamental cellular processes.

203 r the versatility of CCPs to control diverse cellular processes.

204 ar RNAs and chemical modifications to RNA in cellular processes.

205 ifier (SUMO) modification regulates numerous cellular processes.

206 ovel explanations regarding how pH may drive cellular processes; how plants may respond to, and perha

207 ions in the expression of well characterized cellular proliferation and apoptosis guards (NF-kappaB,

208 pathway, an essential event for uncontrolled cellular proliferation and transformation.

209 ed for HIV infection yet are dispensable for cellular proliferation and viability.

210 erving as reaction catalysts to coordinating cellular propagation and development.

211 ilability, a mechanism that critically links cellular properties of T-type Ca(2+) channels to their p

212 was reflected in increased amounts of total cellular protein and several free amino acids.

213 for protein AMPylation in the regulation of cellular protein homeostasis beyond the endoplasmic reti

214 Hsp70 molecular chaperones play key roles in cellular protein homeostasis by binding to exposed hydro

215 Cellular protein homeostasis depends on heat shock prote

216 ow an EV71 IRES structure adapts to hijack a cellular protein, and it suggests that the SLII domain i

217 on and xplanation of m ulti- oc alization of cellular proteins in multiple organisms.

218 Cellular proteins regulating and targeting lentiviral an

219 posttranslational reversible modification of cellular proteins through the conjugation of small ubiqu

220 versible, post-translational modification of cellular proteins with the small modifier, ubiquitin (Ub

221 We identify profound rearrangement in cellular proteostasis occurring very early on after loss

222 regulates the localization of some mRNAs at cellular protrusions but the underlying mechanisms and f

223 Numerous RNAs are enriched within cellular protrusions, but the underlying mechanisms are

224 dard practice for laboratories to assess the cellular quality of expectorated sputum specimens to che

225 Mitophagy is a cellular quality-control pathway, which is essential for

226 highly abundant viral and host siRNAs by the cellular RdRPs.

227 recording techniques and high-density multi-cellular recording methods with poor anatomical correlat

228 direct targets encoding proteins involved in cellular redox balance and DNA replication, including th

229 ement for the assembly factor depends on the cellular redox environment.

230 amine Biosynthesis Pathway (HBP), as well as cellular redox homeostasis, resulting in global changes

231 rs has seen an expansion in knowledge of new cellular regulators and roles of CRTCs beyond CREB.

232 eveloped a strategy to rewire the endogenous cellular regulatory network of yeast to enhance compatib

233 ated with antibody mediated rejection, acute cellular rejection, and bronchiolitis obliterans syndrom

234 A), antibody-mediated rejection (AMR), acute cellular rejection, and graft status.

235 increase Mical-mediated F-actin disassembly, cellular remodeling, and repulsive axon guidance.

236 htly synchronized diel coupling of viral and cellular replication cycles in both photoautotrophic and

237 We describe a cellular reporter to directly monitor the phenotypic swi

238 Because cellular resistance to viral replication is marked by ex

239 es of gap junctions in a complex behavior at cellular resolution and provide a tool for similar explo

240 Calcium imaging with cellular resolution typically requires an animal to be t

241 f a tissue in response to a known force with cellular resolution.

242 er, our results suggest that manipulation of cellular resource allocation is a key control parameter

243 regulators and pathways that orchestrate the cellular response to ssUVR.

244 CAN channels are involved in cellular responses such as neuronal bursting activity an

245 s of this assembly machinery trigger complex cellular responses that prevent aggregation of unassembl

246 aled that in vitro SLC16A5-silencing altered cellular responses to cisplatin treatment, supporting a

247 Viral replication and cellular responses were measured using quantitative real

248 llenge the resident genome and must overcome cellular responses, including the DDR.

249 Cellular-scale imaging of the mechanical properties of t

250 d to reveal the origins of disease; however, cellular-scale resolution is not readily achievable in i

251 and regeneration as two distinct aspects of cellular self-repair by examining a few model organisms

252 h blocked their tumorigenic capacity through cellular senescence and apoptosis.

253 r is tempered by the activation of premature cellular senescence in an NF1-deficient background.

254 lication and oxidative stresses in mediating cellular senescence in cancer cells treated with RSV.

255 Further analysis revealed the induction of cellular senescence in zebrafish embryos overexpressing

256 Cellular senescence markers are detectable within IPF lu

257 ely impaired EGFR signaling and the onset of cellular senescence.

258 , reduced DNA repair responses, and elevated cellular senescence.

259 liver, and endocrine systems, by influencing cellular signaling pathways and sulfhydration of target

260 embranes are naturally curved at each of the cellular sites believed to engage in autophagosome forma

261 including the sizes of vascular and lacunar (cellular) spaces, provide useful indicators of RBC size

262 Cellular specificity of dmd-3 action is ensured by its c

263 says to gain higher-confidence insights into cellular states.

264 ly across different species, cell types, and cellular states.

265 lar mechanism of transcription regulation on cellular stress and reveal functional similarities to th

266 Celastrol is known to elicit a cellular stress response resembling the response to heat

267 1 and TORC2 signaling pathways to coordinate cellular stress responses with sterol homeostasis.

268 Cellular stress, including oxidative stress, results in

269 y regulate specific protein abundance during cellular stress.

270 atures and expression patterns indicative of cellular stress.

271 drastic morphological changes as a result of cellular stress.

272 Many cellular stresses activate senescence, a persistent hypo

273 p53 tumor suppressor responds to various cellular stresses and regulates cell fate.

274 to obtain the spatiotemporal distribution of cellular stresses from measured traction forces in motil

275 gene encodes SGCA, which is involved in the cellular structure of muscle fibers and, along with DMD,

276 ork dynamics, but the temporal evolution and cellular substrates of the neuronal activity patterns as

277 gions expressed BMI1 protein, which promoted cellular survival under stress due to downregulation of

278 our findings support the emerging view that cellular systems have evolved the use of pH signals as a

279 Only 1 cellular target HLA antigen for the serum was expressed

280 It is believed to be the cellular target of several antimycobacterial compounds;

281 ted that tubulin and/or microtubules are the cellular targets of the L-acetate fraction.

282 ered neural circuits and their molecular and cellular targets offer a biological underpinning for dev

283 ive for fractionating blood for transfusion, cellular therapy and blood-based diagnostics, and could

284 We hypothesize that the cellular toxicity and vasoconstrictive effects of depola

285 ts causes constitutive activation and severe cellular toxicity.

286 c protein (GFAP) promoter is used to express cellular toxins that eliminate glia in mice, intestinal

287 significantly and irreversibly remodelled by cellular traction forces and by macroscopic strains.

288 hed in pathways involved in cellular growth, cellular trafficking and transmembrane transport.

289 y by sensing lipophilic ligands and adapting cellular transcription appropriately.

290 1 expression by increasing expression of two cellular transcription factors (KLF4 and BLIMP1) which c

291 ly showed that the differentiation-dependent cellular transcription factors KLF4 and BLIMP1 induce ly

292 s type 16 (HPV16) oncoproteins contribute to cellular transformation in vitro.

293 As the non-cellular transmission of mycoviruses is rare, the foundi

294 eolae-mediated pathway significantly reduced cellular uptake of MOFs.

295 provides high colloidal stability, enhanced cellular uptake, and distribution across cellular compar

296 o molecules to CPPs invariably reduces their cellular uptake.

297 mprehensive analyses of release profiles and cellular-uptake and cell viability studies.

298 NO-induced reduction of cellular viability was demonstrated by in-cell NO detect

299 ICANCE STATEMENT Effective disposal of brain cellular waste products via CSF has been demonstrated re

300 es in the fatty acid selectivity profiles of cellular zDHHC enzymes and mapped molecular determinants