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1 ed on fluorescence-activated cell sorting or dominant positive and negative drug selection, and appro
2 nists and antagonists of RhoA activation and dominant positive and negative plasmid constructs demons
3 mary hepatocytes, primary liver macrophages, dominant positive and negative transgenic mice of the C/
4 utinin-tagged plasmids expressing wild-type, dominant-positive, and dominant-negative forms of RhoA i
5 h between these alternatives, we expressed a dominant positive arrestin, arr2(R169E), that desensitiz
8 found that overexpression of a constitutive dominant positive Cdc42 itself was sufficient to produce
9 HD, approximately 320 amino acids long with dominant positive charge, and its interaction with sulfa
10 ilar to that of mice expressing an E protein dominant-positive construct, ET2, suggesting that the ba
11 h mannose/hybrid N-glycans functioned like a dominant positive displaying increased interaction with
12 e previously shown that an iron-insensitive, dominant-positive dtxR(E175K) mutant allele from Coryneb
13 ests of chimeric molecules revealed that the dominant-positive effect of SynCAM on synaptic function
15 aneously function as a dominant negative and dominant positive for different pathways implies that ef
16 tested by transfecting arrestin3-(R170E), a dominant positive form of arrestin that does not require
17 owever, transfection of arrestin3-(R170E) (a dominant positive form of arrestin that does not require
19 activated by nSREBPs (-1a, -1c, and -2) or a dominant positive form of the SREBP cleavage-activating
20 se a model in which FLT3(ITD/-) represents a dominant positive, gain-of-function mutation providing A
21 discharge of the LTP probe, He(2)(+) is the dominant positive ion when helium is used as the plasma
22 xpression of Munc18b wild-type and, more so, dominant-positive K314L/R315L mutant promoted the assemb
23 es overexpressing LdRab5a, LdRab5b, or their dominant-positive (LdRab5a:Q93L and LdRab5b:Q80L) or dom
26 Rab1:WT, GFP-LdRab1:Q67L (a GTPase-deficient dominant positive mutant of Rab1), and GFP-LdRab1:S22N (
27 aR truncated at position Pro(379) acted as a dominant positive mutant that down-modulated surface exp
28 role of TR in metamorphosis by developing a dominant positive mutant thyroid hormone receptor (dpTR)
29 sistent with these findings, expression of a dominant-positive mutant of AtRac1 blocked the ABA-media
30 ic pathways is suggested by the facts that a dominant-positive mutant of PAK3 does not alone cause ne
32 duced transgenic mice whose livers express a dominant positive NH2-terminal fragment of sterol regula
34 struct with a variety of plasmids expressing dominant positive or dominant negative mutant proteins i
36 cal microscopy and functionally exhibited a "dominant-positive" phenotype, implying positive cooperat
39 ts are largely without unique effect, except dominant positive Rac1-Q61L, and rapidly cycling Rac1-F2
43 Src activation was observed in KSHV-infected dominant-positive RhoA cells compared to wild-type cells
45 trate that aberrant AEG-1 expression plays a dominant positive role in regulating oncogenic transform
47 contrast with previously reported effects of dominant-positive SREBP-1a, which activated fatty acid s
48 We produced transgenic mice that express a dominant-positive truncated form of sterol regulatory el
49 ed in livers of transgenic mice that express dominant-positive versions of all three isoforms of SREB
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