ライフサイエンスコーパス: v-erbB

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1 of the transforming receptor tyrosine kinase v-erbB.

2 otein with tumorigenic activity analogous to v-erbB.

3 pproach to generate a selective inhibitor of v-erbB [a transforming allele of epidermal growth factor

4 gnal transduction events originating from S3-v-ErbB, a ligand-independent, oncogenic EGF receptor mut

5 moter to generate transgenic mice expressing v-erbB, a transforming allele of EGFR.

6 sis, we hypothesized that dual inhibition of v-erbB and phosphatidylinositol 3' (PI3) kinases could s

7 Inhibitors of v-erbB-as1 and of PI3 kinase showed enhanced efficacy in

8 Surprisingly, NaPP1-treated v-erbB-as1 cells failed to re-enter the cell cycle, show

9 nhanced efficacy in treating established 3T3:v-erbB-as1 tumor allografts.

10 ibroblasts by sensitized versions of v-erbB (v-erbB-as1) was blocked by 1-napthyl PP1 (NaPP1), a cell

11 When treated with NaPP1, v-erbB-as1-transformed fibroblasts showed cell-cycle arr

12 lso reversed morphological transformation by v-erbB-as1.

13 hat there is no apparent correlation between v-erbB dimerization and transformation of avian fibrobla

14 The avian erythroblastosis viral oncogene (v-erbB) encodes a receptor tyrosine kinase that possesse

15 Stimulation of v-ErbB:ER activity resulted in the activation of the pho

16 478 when the cells were grown in response to v-ErbB:ER as opposed to IL-3.

17 v-ErbB:ER conditionally transformed NIH-3T3 cells and ab

18 This novel v-ErbB:ER construct and these conditionally transformed

19 novel conditionally activated form of EGF-R, v-ErbB:ER, on the morphological transformation of NIH-3T

20 This construct, v-ErbB:ER, requires beta-estradiol or 4-OH tamoxifen for

21 , respectively, and induced apoptosis in the v-ErbB:ER-responsive cells.

22 sis when the cells were grown in response to v-ErbB:ER.

23 The v-ErbB ES-4 oncogene was fused to the hormone binding do

24 transforming and nontransforming mutants of v-erbB in fibroblasts to detect transformation-associate

25 Specifically, expression of S3-v-ErbB in primary fibroblasts results in anchorage-indep

26 revious studies showed that expression of S3-v-erbB in primary fibroblasts results in the tyrosine ph

27 ted mutant epidermal growth factor receptor (v-ErbB) induces the formation of a transformation-specif

28 S3-v-erbB is a retroviral oncogene that encodes a ligand-in

29 V-ErbB-mediated complex formation and transformation hav

30 Here we show that both v-ErbB-mediated phosphoprotein complex formation and tra

31 ates with actin stress fiber disassembly and v-erbB-mediated transformation.

32 further characterize this ligand-independent v-ErbB oncogenic signaling pathway.

33 l role of CaD tyrosine phosphorylation in S3-v-ErbB oncogenic signaling, we have generated a series o

34 fferent cell lines to examine the effects of v-erbB or EGFR inhibitors, in combination with PI3 kinas

35 e survival of mice allografted with S100beta-v-erbB/p53(-/-) glioma stem-like cells.

36 In this report, we demonstrate the v-erbB products can efficiently homodimerize in all thre

37 Furthermore, both oncogenic and nononcogenic v-erbB products can heterodimerize with the native c-erb

38 While oncogenic v-erbB products have been shown to be expressed on the c

39 Mutant v-erbB products of avian c-erbB1 have previously been us

40 ve carefully analyzed the ability of several v-erbB products to oligomerize in the three target cell

41 nal SH3 domain, in fibroblasts expressing S3-v-ErbB results in a reduction in phosphoprotein complex

42 ink4a/arf+/- animals transgenic for S100beta-v-erbB) showed a similar tumor-specific down-regulation

43 f the biochemical changes of myosin found in v-ErbB- transformed fibroblasts, thereby contributing to

44 the mutant, constitutively active oncogenic v-erbB tyrosine kinase, which induces avian erythroblast

45 rodent fibroblasts by sensitized versions of v-erbB (v-erbB-as1) was blocked by 1-napthyl PP1 (NaPP1)

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