ライフサイエンスコーパス: anchorage dependence

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1 te, suppress contact inhibition, or suppress anchorage dependence.

2 s that is presumably achieved by controlling anchorage dependence.

3 ell-matrix interactions, a phenomenon called anchorage dependence.

4 M construct also lost contact inhibition and anchorage dependence.

5 med phenotype was characterized by a loss of anchorage dependence and hallmarks of epithelial to mese

6 s had a robust impact on mitogen dependence, anchorage dependence and overall survival, which was sig

7 on in low serum, increases invasion, reduces anchorage dependence and promotes the progression into t

8 e define a mechanism by which RalA regulates anchorage dependence and provide a new link between inte

9 th rate, lower plating efficiency, increased anchorage dependence, and morphological differences.

10 ing changes in growth factor requirements or anchorage dependence for proliferation.

11 ncluding growth factor independence, loss of anchorage dependence, loss of contact inhibition, and tu

12 Anchorage dependence of cell growth is a key metastasis-

13 Anchorage dependence of cell growth, which is mediated b

14 important implications for understanding the anchorage dependence of cell growth.

15 cyclin E-CDK2 activity may thus underlie the anchorage dependence of cell growth.

16 PEA-15 bypasses the anchorage dependence of ERK activation.

17 This cooperation may contribute to anchorage dependence of mitogenic cell cycle progression

18 adhesion, an effect that contributes to the anchorage dependence of normal cell growth.

19 form of c-Cbl increases neither adhesion nor anchorage dependence of v-Abl-transformed fibroblasts.

20 d interaction with Nck may contribute to the anchorage-dependence of PAK activation as well as to the

21 Furthermore, the anchorage-dependence phenotype and tumor-forming capacit

22 In addition, sensitivity to anchorage dependence was restored partially in ZR-75-1 c

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