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1 d bilayer modulates channel gating, although it is not clear how.
2 during morphogenesis is tightly linked, but it is not clear how.
3 ation complex often alter cell width, though it is not clear how.
7 ow in many chemosensitive human cancers, and it is not clear how a drug that only kills dividing cell
8 ellular Ca2+ signaling instability; however, it is not clear how a high atrial rate and Ca2+ instabil
9 n, have been performed on 2D substrates, and it is not clear how a more realistic 3D environment infl
10 ssential for Metnase function in DNA repair, it is not clear how a protein with sequence-specific DNA
13 S1P distribution is controlled in vivo, and it is not clear how a ubiquitously made lipid functions
14 nd are implicated in postsynaptic functions, it is not clear how Abl kinases regulate dendritic morph
16 en shown to contribute to actin disassembly, it is not clear how activity of these locally acting pro
18 sing of AgrD to produce mature AIP; however, it is not clear how AgrD interacts with AgrB and how thi
22 polycystic liver disease in humans; however, it is not clear how altered SEC63 influences disease man
23 eplete their own tryptophan supply; however, it is not clear how amino acid depletion influences macr
24 -regulatory elements affect gene expression, it is not clear how amino-acid substitutions in transcri
26 hortcoming of Kurzban et al.'s model is that it is not clear how animals persist through subjectively
27 is orchestrated with diverse pheromones, but it is not clear how ants perceive these social signals.
30 tening conditions is not known, and, indeed, it is not clear how attended speech is internally repres
32 cterial sensor in dendritic cells (DCs), but it is not clear how bacterial recognition links with ant
34 ll established in high-income countries, but it is not clear how behavioural risk factors are distrib
36 osa cells in maintaining meiotic arrest, but it is not clear how binding of LH to receptors that are
40 is known to affect transcriptional activity, it is not clear how broadly patterns of changes in histo
48 isms of CPPs are still under discussion, and it is not clear how cells compensate the disturbances in
50 and aneuploidy are hallmarks of cancer, but it is not clear how changes in the chromosomal content o
51 as circulating indicators of adiposity, but it is not clear how changes in their levels are perceive
52 ical information on the system's components, it is not clear how chemoreceptor clusters are reliably
53 its functional significance remains unknown: it is not clear how connection strength relates to neuro
55 and biofilm formation of this bacterium, but it is not clear how covR expression is regulated in S. m
57 with cardiovascular complications; however, it is not clear how diabetes promotes cardiac dysfunctio
59 ha is present on several neural populations, it is not clear how different regions of the brain media
61 target proteins identified to date, however, it is not clear how distinct signaling outputs can be ge
62 isease (AD) and Down syndrome (DS); however, it is not clear how dysfunction in this pathway influenc
67 nd a more ubiquitous long form (L-WNK1), but it is not clear how either of these isoforms influence r
68 tic embryo divisions are highly regular, but it is not clear how embryo patterning is established in
69 perimental studies on treatment effects, but it is not clear how estimates based on these 2 approache
71 cs are commonly prescribed for children, but it is not clear how exposure to antibiotics early in lif
73 ical signal and activated TGF-beta; however, it is not clear how fibroblasts sense and transmit the m
74 yotrophic lateral sclerosis (FALS); however, it is not clear how FUS mutations cause neurodegeneratio
77 eptibility to autoimmune disorders; however, it is not clear how genetic variations in these loci con
87 athogenesis of Alzheimer's disease; however, it is not clear how individual amyloid-beta species accu
88 s) are thought to express autoreactive TCRs, it is not clear how individual TCRs influence Treg devel
90 wn determinant of overall life satisfaction, it is not clear how it affects moment-to-moment variatio
91 ined to short separations between sites, and it is not clear how it contributes to long-range DNA loo
92 in several neuropsychiatric conditions, yet it is not clear how it is maintained in the healthy huma
95 coronary artery disease in humans; however, it is not clear how its protein product tribbles-1 regul
100 es, the mechanisms that control it vary, and it is not clear how licensing is regulated in plants.
101 s SH2B3) are found in Ph-like ALLs; however, it is not clear how LNK regulates normal B cell developm
102 postnatal development and in adulthood, but it is not clear how long these plastic changes persist n
104 ts, two beta subunits and one gamma subunit, it is not clear how many alpha and beta subunits must ca
105 known to be important to maintain cohesion, it is not clear how many neighbors each individual can s
106 s are injected into the host blastocyst, but it is not clear how many of the injected cells contribut
107 ousand sites during early embryogenesis, but it is not clear how many of these binding events are fun
108 pulvinar and LGN on their way to cortex, but it is not clear how many synapses are required to comple
111 d in regulating cell proliferation in vitro, it is not clear how menin regulates cell cycle and wheth
112 l for mutagenesis by retrotransposition, but it is not clear how methylation of these elements is mai
117 an independent risk factor for diabetes, but it is not clear how much adding family history to other
118 populations against epidemics in nature, but it is not clear how much diversity is required to preven
121 lain a small proportion of the genetic risk, it is not clear how much of the heritability these SNPs
123 indle in female meiosis in many species, but it is not clear how multiple chromosomes form one shared
124 brogate WNK kinase degradation in cells, but it is not clear how mutant forms of CUL3 promote WNK sta
128 ain is essential for cognitive function, but it is not clear how neural circuits support reliable and
129 development of acute pancreatitis (AP), but it is not clear how neutrophil-induced tissue damage is
131 of fumarate hydratase (FH) inactivation, but it is not clear how NRF2 may be activated in sporadic fo
132 pancreatic ductal adenocarcinoma (PDAC), but it is not clear how obesity contributes to pancreatic ca
136 f angiogenesis in IBD is well characterized, it is not clear how or if increased lymphangiogenesis pr
137 isease progression in treated HIV infection, it is not clear how or whether inflammatory mediators co
138 iates RAS-driven tumor development: however, it is not clear how p110alpha/RAS-dependant signaling me
140 th behavioral and cognitive dysfunction, but it is not clear how Pb produces these behavioral changes
141 ns are involved in direction perception, but it is not clear how perceptual decisions are related to
149 ey intracellular mediators of Fas signaling, it is not clear how recruitment of these proteins to the
151 pagate into axons, given their unusual shape it is not clear how reliably these bursts reach nerve te
155 an pass through the channel to engage Rrp44, it is not clear how RNA is directed to Rrp6 or whether R
156 sites for the same transcription factor, and it is not clear how robust enhancers can evolve loss of
157 d musculoskeletal injuries in nursing staff, it is not clear how safe these new programs are for pati
158 and lower urinary tract symptoms (LUTS), and it is not clear how sex steroid hormones contribute to t
162 ing TGF-beta functions in hepatic cells, but it is not clear how STATs are activated under these circ
175 h TGF-beta activation in podocytes; however, it is not clear how TGF-beta signaling promotes disease.
180 nelles themselves are inherently active, and it is not clear how the active, energy-consuming process
183 improve future housing interventions, though it is not clear how the built environment and occupant b
185 ernal Ca(2+) store depletion in these cells, it is not clear how the cells decode individual Ca(2+) s
187 s critical for drug seeking and relapse, but it is not clear how the circuitry centred on hypocretin-
190 ates the expression of enterocyte genes, but it is not clear how the concomitant silencing of stem ce
195 repression of transposable elements (TE) but it is not clear how the extensive loss of DNA methylatio
197 of language processing in natural contexts: it is not clear how the human brain processes linguistic
203 to splicing is often explored and utilized, it is not clear how the intein navigates through the rea
204 dorsolateral prefrontal cortex (dlPFC), but it is not clear how the interactions among these regions
208 this lipid at the plasma membrane, although it is not clear how the localisation of these kinases is
211 nked to changes in gene expression; however, it is not clear how the multiple remodeling enzymes foun
215 these patients become thrombocytopenic, and it is not clear how the proteasome influences platelet p
218 ies of a TCR to the peptide and the MHC, but it is not clear how the specificity to both components d
223 However, at an environmental response level, it is not clear how the two organelles intersect in prog
224 creased ER-mediated protein degradation, but it is not clear how the UPR is involved in the postprand
225 factors and function as obligate dimers, but it is not clear how the various dimer combinations contr
227 igen within the respiratory endothelium, but it is not clear how the virus can traverse the respirato
231 e involved in the perception of objects, but it is not clear how these areas interact with first tier
232 AG1), which encodes a Notch ligand, although it is not clear how these contribute to disease developm
237 ownstream target genes including MMACHC, but it is not clear how these HCFC1 targets play a role in t
239 on feedback from antennal mechanosensors but it is not clear how these inputs combine to elicit fligh
240 to be important in olfactory processing, but it is not clear how these interactions shape the odour r
242 PKD1 mutations are missense variants, though it is not clear how these mutations promote disease.
247 o and iron-regulatory proteins in fungi, but it is not clear how these proteins function in mammalian
248 ssociated with an increase in these repeats, it is not clear how these proteins might have directed a
249 ndrial connexin 43 (Cx43) in cytoprotection, it is not clear how these signaling modules are linked m
254 Its expression levels vary in humans, and it is not clear how these variations affect lipid metabo
255 mportant target for neutralizing antibodies, it is not clear how these viruses avoid cross-neutraliza
256 into the initiating events of HTRs; however, it is not clear how they are modulated and how they comb
257 t a query about the logic of forward models: It is not clear how they are supposed to work, nor why t
259 ine ignores such technological developments, it is not clear how they would fit within her framework.
263 BIR domain interactions are well understood, it is not clear how this binding event influences the ac
264 precedes the stable flipped-out complex, but it is not clear how this complex differs from nonspecifi
265 high in glioblastoma-type brain tumors, but it is not clear how this contributes to tumor growth.
266 pear to activate pDCs through their TLRs and it is not clear how this difference affects IFN-alpha/be
272 s in calcium (Ca(2+) responses) in glia, but it is not clear how this process affects intestinal func
273 ny positive regulators have been identified, it is not clear how this process is inhibited at transcr
274 orming a complex with the SECIS element, but it is not clear how this regulates eEFSec during Sec inc
276 erved in postpartum breast cancers; however, it is not clear how this remodeling process promotes met
277 tical regulator of tissue growth in animals, it is not clear how this signaling pathway controls cell
278 and sometimes coexisting conformations, and it is not clear how this three-dimensional structure aff
279 ost common alterations in human cancers, yet it is not clear how this transcription factor acts to pr
280 d ability to obtain a feeding territory, but it is not clear how this translates into performance in
296 ulted in highly diverse viral sequences, and it is not clear how viral proteins such as Tat, which pl
297 oss-species pathogen transmissions; however, it is not clear how viruses adapt to productively infect
299 ty, and rad51 mutations cause lethality, but it is not clear how widely these functions are conserved
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