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1 ariation on enzyme activity and steady-state cellular abundance with a large, well-curated clinical c
2 ption of genes, including those that lead to cellular accumulation of protective organic osmolytes.
6 Hyperreflective foci and HRS are markers of cellular activity associated with visual dysfunction, es
7 molecular pathways that are the backbone of cellular activity drive the cell to certain outcomes and
8 onist bicuculline methiodide while recording cellular activity in PFC of male rhesus monkeys performi
11 heir biological function, in terms of, e.g., cellular adhesion, endo/exocytosis, cellular uptake, and
16 le of reversibly inducing transient NPC-like cellular and biochemical phenotypes, constitute plausibl
17 sesses an impressive diversity of molecular, cellular and circuit mechanisms, embedded in a dynamic,
18 ve shown that MAGE proteins regulate diverse cellular and developmental pathways, implicating them in
19 nelles for egress provides insights into the cellular and immunological abnormalities observed in pat
21 fundamental split, our current knowledge of cellular and molecular mechanism driving root developmen
23 gs and explore mechanistic links between the cellular and network properties of, and the computations
26 iously reported enzyme kinetic parameters of cellular and viral DNA and RNA polymerases with respect
31 nd primed pluripotency and harbor molecular, cellular, and phenotypic features characteristic of form
33 ion and their heterogeneity, and enabled the cellular architecture of breast cancer tissue to be char
34 cond messenger," may be linked to changes in cellular architecture that favor pathogen-host interacti
36 le showcases distinctive features, including cellular asymmetry and differentiation during the cell c
48 orrelated with a protection from TAC-induced cellular Ca(2+) signaling alterations (increased SOCE, d
51 between the plasma membrane (PM), where most cellular cholesterol resides, and the endoplasmic reticu
52 lexoform, it remains unclear how and whether cellular circuits control the distribution of a complexo
53 cellular trophic relationships and shifts in cellular communication after angiotensin II treatment th
54 on interfacial protein action, ranging from cellular communication to immune responses and the prote
56 nd disassembly of many molecules in multiple cellular compartments and their transport among compartm
57 , the molecular connection between these two cellular compartments has not been clearly elucidated.
59 mphasize the potential prominent role of the cellular component of the immune system in the developme
62 ls to the higher strain rate imposed by xDC, cellular components other than the actin cytoskeleton do
67 ion is formed from the Fenton reaction under cellular conditions and from decomposition of nitrosoper
68 notypes are strongly modulated by changes in cellular conditions or genetic context, the latter deter
69 ce helps bridge the gap between high-density cellular connectivity studies in rodents and imaging-bas
74 cay rate, lower SR Ca(2+) load and depressed cellular contractility) and SERCA2a downregulation in ve
75 Hepatic stellate cells (HSC) are the major cellular contributors to excess extracellular matrix dep
81 ear conditions, despite obvious decrement of cellular deformation at moderate-to-higher shear stresse
83 Phosphorylation makes cyclin L2 amenable to cellular degradation, leading to restriction of HIV repl
85 a lesser degree UBR4, were down-regulated as cellular demand for antibody expression increased in CHO
86 ases SOD2 activity as an early adaptation to cellular detachment, which is followed by SIRT3-dependen
91 how therapy-induced adaptation of the multi-cellular ecosystem of metastatic cancer shapes clinical
92 Brain tumors (gliomas) are heterogeneous cellular ecosystems, where non-neoplastic monocytic cell
93 uate over the course of the day, observed at cellular (eg, transcription, translation, and signaling)
94 e electron transport chain that functions in cellular energy metabolism and as a membrane antioxidant
96 discernible trends in the data suggest that cellular environment is a major factor dictating stabili
98 of BrdU lead to the activation of apoptotic cellular events as evidenced by both terminal deoxynucle
100 e of the Arf-activating proteins, GBF1, is a cellular factor required for enterovirus replication.
101 s important to identify and characterize the cellular factors that control HIV multiplication in thes
105 e have characterized the binding site of the cellular FHL1 protein in CHIKV HVD and defined the biolo
106 ce the sensitivity and spatial resolution of cellular force imaging, we developed a force-activatable
115 lear pore complexes (NPCs) are important for cellular functions beyond nucleocytoplasmic trafficking,
117 various protein complexes to confer distinct cellular functions, but how the multi-subunit complexes
118 necks, a process that is essential for many cellular functions, from cell division to lysosome degra
119 ls such as iron and copper are essential for cellular functions, others such as cadmium and arsenic a
120 ting death domain protein, regulates various cellular functions, such as vesicle trafficking, activit
122 s catalog, we characterize shared and unique cellular genes, proteins, and pathways targeted by parti
125 and integration (scAI) method to deconvolute cellular heterogeneity from parallel transcriptomic and
126 tophagy is a cellular process that preserves cellular homeostasis and promotes cellular survival duri
127 be boosted by light driven perturbations of cellular homeostasis and that this biosensing concept is
131 of the endoplasmic reticulum (ER), the main cellular hub of lipid biosynthesis and the entry site fo
134 Ebola VLP vaccine elicits strong humoral and cellular immune responses against pathogenic Ebola virus
136 into the basic biology of adjuvant-elicited cellular immunity and have clear implications for the sc
138 glioblastoma (GBM) is characterized by rapid cellular infiltration of brain tissue, raising the possi
139 s of type-2 immune activation, inflammation, cellular infiltration, tissue repair enzymes, pathways o
143 everal mesenchymal-like properties including cellular invasion and colony formation in vitro, as well
145 nt on their intracellular activation by host cellular kinases to yield ultimately the bioactive nucle
151 synergistic H3-tail binding causing distinct cellular localization and enhanced H3K9me3-nucleosome ub
155 a priori knowledge of tumor antigen, ex vivo cellular manipulation, or cellular manufacture, could dr
156 r antigen, ex vivo cellular manipulation, or cellular manufacture, could dramatically reduce costs an
160 types (e.g., hepatitis C) and add additional cellular mechanisms (tissue recovery and variable cell s
161 ings have implications for the molecular and cellular mechanisms of cerebral cavernous malformation p
163 cuit changes in several brain areas, but the cellular mechanisms that underlie these defects are not
165 itical insights into the phase separation of cellular membranes and, more generally, two-dimensional
166 ough the host endomembrane system, penetrate cellular membranes, and undergo capsid disassembly to re
169 ated with this novel scaffold that increased cellular metabolic rates in vitro using changes in oxyge
171 chondrogenesis, SOX9 acts as a regulator of cellular metabolism by suppressing oxidation of fatty ac
172 ydrolysis, reactive oxygen species, aberrant cellular metabolism or other perturbations that cause DN
173 hondrial morphology shifts rapidly to manage cellular metabolism, organelle integrity, and cell fate.
176 and characterized the first biochemical and cellular microgravity responsive device using an enginee
177 s, we have simulated numerically a confluent cellular monolayer spreading on an empty space and the c
178 dented approach to untangle the dysregulated cellular network in the vicinity of pathogenic hallmarks
179 nty in the allocation of proteins to new sub-cellular niches, as well as in the number of newly disco
181 ways, and distal alveoli, is a complex multi-cellular organ that intimately links with the cardiovasc
183 Phosphoinositides (PI) are key regulators of cellular organization in eukaryotes and genes that tune
184 that improves systems-level understanding of cellular organization in health and disease through inte
187 standing the mechanisms of HPgammaCD-induced cellular pathways could contribute to effective NPC ther
189 ligate parasites, all viruses exploit common cellular pathways, providing the possibility to develop
190 s support engraftment and maintenance of the cellular phenotype of injected tissue-resident macrophag
191 rotein stability changes that cause dramatic cellular phenotypes observed at nonpermissive temperatur
192 ponent of homologous recombination deficient cellular phenotypes, the image-based algorithm was studi
195 less, robust application of these methods in cellular populations without side effects has remained c
196 ctive representatives combined submicromolar cellular potency and nanomolar target affinity with bala
198 esign concepts, coupled with optimization of cellular potency, in vitro drug-target residence times,
202 l link between the Hofmeister series and the cellular process of neurotransmitter release via exocyto
204 to proteins and lipids, regulates nearly all cellular processes and is critical in the development an
205 om tissues to characterize physiological and cellular processes associated with venom production and
206 ity of genes undergo pre-mRNA splicing, most cellular processes depend on proper spliceosome function
207 stimulatory influences of electric fields on cellular processes in tissue and regenerative engineerin
208 ver, the role of such proteins in regulating cellular processes in vivo and development in metazoans
209 Through these interactions, RNAs mediate cellular processes such as the regulation of gene transc
210 e differential effects of YAP and TAZ on key cellular processes were also associated with differentia
211 atory cell polarization and controls dynamic cellular processes, such as focal adhesion formation and
212 s a critical signaling node for a variety of cellular processes, which are mediated by protein comple
216 that uses scRNA-seq to characterize dynamic cellular programs and their molecular drivers, and apply
217 sion, potency, and function, particularly in cellular proliferation and differentiation, as well as i
218 studies implicate Gal-9 in the regulation of cellular proliferation and epithelial restitution after
220 It can provide clonal-level insights into cellular proliferation, development, differentiation, mi
222 sensing motif and its capacity for providing cellular protection against oxidative stress while servi
223 In human papillomavirus (HPV) infection, the cellular protein complex known as retromer binds to the
224 is is the first study reporting the distinct cellular protein targets of mHAAs and mHAMs at the prote
226 antigen 6 family member E (LY6E), the three cellular proteins identified to function in interference
227 ool for the precise chemical modification of cellular proteins with spatial and temporal control.
228 oading reduces non-specific encapsulation of cellular proteins, particularly nucleic-acid-binding pro
230 unds (ouabain and CdCl(2)) demonstrates that cellular reactivity can be boosted by light driven pertu
231 te noisy morphogen signaling and large-scale cellular rearrangements during morphogenesis and growth.
236 Levels of glutathione, a key regulator of cellular redox status, are reduced in the medial prefron
239 bleweed, and Pebble are all used during this cellular repair, each has a unique localization pattern
242 of PD-L1 positive tumor cells and CTLs with cellular resolution by non-invasive NIR-IIb light sheet
243 tor of INterferon Genes) mediates protective cellular response to microbial infection and tissue dama
247 ess and autophagy plays an important role in cellular responses to a wide variety of physiological an
253 ostulated that increases in cAMP, a critical cellular "second messenger," may be linked to changes in
256 tion of MC(1) is a viable strategy to induce cellular senescence, affording a distinct way to control
257 ole for skeletal muscle lamin A/C to prevent cellular senescence, IL-6 expression, hyperosteoclastoge
261 r demonstrated that SOX9 knockdown increases cellular sensitivity to cisplatin, whereas its overexpre
262 y to study TNFR1 assembly directly in native cellular settings and at physiological cell surface abun
264 l histopathology; (ii) Renal function; (iii) Cellular signaling changes; (iv) Oxidative stress and in
265 via pattern recognition receptors, internal cellular signaling pathways are induced to ultimately fe
266 e show that beta-HPV E6 more broadly impairs cellular signaling, indicating that the viral protein dy
268 ted with immunoregulation and were the major cellular source of IL-22 binding protein (IL-22BP) at st
269 ss the potential causes of inflammaging, the cellular source of the inflammatory mediators, and the m
271 by caAKT1 and c-Myc and reveals an impact of cellular status on initiation of lineage plasticity.
273 physiologically associated with significant cellular stress but, paradoxically, it favors tumor prog
274 gy responds to a variety of intra- and extra-cellular stress conditions including, but not limited to
277 ic) triggered by multiple factors, including cellular stress, DNA damage and immune surveillance.
287 RNA polymerase as well as a broader range of cellular target pathways controlled by (pp)pGpp, includi
289 au with low nanomolar affinity, and inhibits cellular Tau aggregate propagation similarly to standard
290 oach to engender endogenous patient-specific cellular therapy, without the need for a priori knowledg
291 es with orthogonal orientation suggests that cellular transition rates depend on the cell polarizatio
292 Furthermore, we identify genes involved in cellular transport, including calcium transporters and c
294 t transcriptional heterogeneity arising from cellular types, spatio-temporal contexts and environment
295 values were high enough to explain observed cellular uptake by passive diffusion with no need to pos
296 d that plasma membrane depolarization blocks cellular uptake of N-acylethanolamides-lipoprotein-borne
297 distinguish between those that measure total cellular uptake of RNA therapeutics, which includes both
298 apitulates full-length Abeta stereoselective cellular uptake, allowing us to decouple aggregation fro