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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
16 aneously function as a dominant negative and dominant positive for different pathways implies that ef
17 tested by transfecting arrestin3-(R170E), a dominant positive form of arrestin that does not require
18 owever, transfection of arrestin3-(R170E) (a dominant positive form of arrestin that does not require
20 activated by nSREBPs (-1a, -1c, and -2) or a dominant positive form of the SREBP cleavage-activating
21 se a model in which FLT3(ITD/-) represents a dominant positive, gain-of-function mutation providing A
22 discharge of the LTP probe, He(2)(+) is the dominant positive ion when helium is used as the plasma
23 xpression of Munc18b wild-type and, more so, dominant-positive K314L/R315L mutant promoted the assemb
24 es overexpressing LdRab5a, LdRab5b, or their dominant-positive (LdRab5a:Q93L and LdRab5b:Q80L) or dom
26 o(y)Mn(1-x-y)O(2) (0 < x, y < 1, NCM) is the dominant positive material for the state-of-the-art lith
28 Rab1:WT, GFP-LdRab1:Q67L (a GTPase-deficient dominant positive mutant of Rab1), and GFP-LdRab1:S22N (
29 aR truncated at position Pro(379) acted as a dominant positive mutant that down-modulated surface exp
30 role of TR in metamorphosis by developing a dominant positive mutant thyroid hormone receptor (dpTR)
31 sistent with these findings, expression of a dominant-positive mutant of AtRac1 blocked the ABA-media
32 ic pathways is suggested by the facts that a dominant-positive mutant of PAK3 does not alone cause ne
34 duced transgenic mice whose livers express a dominant positive NH2-terminal fragment of sterol regula
36 struct with a variety of plasmids expressing dominant positive or dominant negative mutant proteins i
38 cal microscopy and functionally exhibited a "dominant-positive" phenotype, implying positive cooperat
41 ts are largely without unique effect, except dominant positive Rac1-Q61L, and rapidly cycling Rac1-F2
46 Src activation was observed in KSHV-infected dominant-positive RhoA cells compared to wild-type cells
48 trate that aberrant AEG-1 expression plays a dominant positive role in regulating oncogenic transform
51 contrast with previously reported effects of dominant-positive SREBP-1a, which activated fatty acid s
52 We produced transgenic mice that express a dominant-positive truncated form of sterol regulatory el
53 ed in livers of transgenic mice that express dominant-positive versions of all three isoforms of SREB