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1 We asked if a biological membrane could employ kinetic energy
2 We asked if changes in the Ubl domain, a conserved domain adj
3 We asked if clusterin, known to be regulated by wnt, is part
4 We asked if cover values or patch-size metrics could predict
5 We asked if decreasing metabolism in the mutant superoxide di
6 We asked if functional muscle ischemia would be eliminated an
7 We asked if genes with a strong effect on survival and fitnes
8 We asked if individual lipid monolayers of the bilayer embody
9 We asked if large exons contain specific sequences that promo
10 We asked if leptin and its cognate receptor were present in n
11 We asked if proteoglycans play a role in this tight cell-cell
12 We asked if retinal tumors can arise from an undifferentiated
13 We asked if Rpe65 or perhaps another nearby gene is mutated a
14 We asked if Sirt1 governs endothelial Cav1 and endothelial fu
15 We asked if SLC7A14 (solute carrier family 7 member A14), an
16 We asked if sleep deprivation affects advice taking.
17 We asked if the type of carotid body (CB) chemoreceptor stimu
18 We asked if two resources: 1) free text, and 2) structured da
19 We asked if, during B cell activation, AID also induces DNA b
20 occur as a result of inappropriate PI3K pathway activation, we asked if loss of the PI3K pathway regulator, phosphatase a
21 expressed in many tissues and cells during development and we asked if Pias proteins regulated the pituitary homeobox 2
22 a serum response factor/MRTF cis-element (CC(A/T)6GG box), we asked if MRTF (and thus cytoskeleton organization) could r
23 ytic activation of Epstein-Barr virus (EBV)-infected cells, we asked if STAT3 contributes similarly to the life cycle of
25 Because c-Src is key to organizing the cell's cytoskeleton, we asked if the tyrosine kinase also mediates RANKL-stimulate
26 iller T (NKT) cells have been implicated in these diseases, we asked if these cells were affected by DOCK8 deficiency.
27 To test principles governing retention of ancient function, we asked if prokaryotic genes could replace their essential e
35 Because these CTFs are highly hydrophobic, we asked if they themselves aggregated and, if so, what param
36 ce of studies have focused on the role of soluble mitogens, we asked if the valve tissue microenvironment contributed to
37 e each cancer type has its own molecular signaling network, we asked if there are "signatures" embedded in these networks
38 use pancreas, while gene depletion of PAK5 or PAK6 did not, we asked if PAK4 might have a functional role in pancreas dev
39 K1/2/3) have been shown to modulate Ras-driven oncogenesis, we asked if these enzymes might regulate signaling in MPNSTs.
40 As some behaviours are easier to learn than others, we asked if some neural activity patterns are easier to gener
43 en shown to be functionally associated with ErbB receptors, we asked if this pathway could mediate P-Rex1/Rac1 activation
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