ライフサイエンスコーパス: de-adhesion

1 timing of adhesion, traction generation, and de-adhesion.

2 the cytoskeleton that is critical for LFA-1 de-adhesion.

3 od, extreme uropod elongation, and defective de-adhesion.

4 egulation of integrin-dependent adhesion and de-adhesion.

5 ely regulate motility but may regulate LFA-1 de-adhesion.

6 egulation of integrin-dependent adhesion and de-adhesion.

7 ation of beta(1) integrin results in MM cell de-adhesion.

8 lasm prevented calpain activation as well as de-adhesion.

9 jor functions defined for SPARC in vitro are de-adhesion and antiproliferation.

10 endocytosis of CDH2, allowing for segmental de-adhesion and individualization of somites.

11 ivation in both BMEC and HSC/P, and in HSC/P de-adhesion and mobilization.

12 RhoA kinase inhibitor effects on de-adhesion and spreading were reversed by treatment wit

13 our knowledge, novel drivers of adhesion (or de-adhesion) and sort cell populations based on complex

14 Rearrangement of the actin cytoskeleton, de-adhesion, and an increase in cortical rigidity accomp

15 panied by changes in the actin cytoskeleton, de-adhesion, and an increase in cortical rigidity.

16 Cell adhesion, cell de-adhesion, and cell motility all appeared to be normal

17 sion mechanisms may have to be shed to allow de-adhesion, and this may contribute to TCR down-regulat

18 ll migration involves cycles of adhesion and de-adhesion, and we propose that the dynamic spatiotempo

19 Transcript profiling mapped a set of de-adhesion, angiogenesis, and wound healing regulators

20 ed inhibition of calpain activation and cell de-adhesion as described for interferon gamma inducible

21 astasis that requires integrins for adhesion/de-adhesion, as well as matrix metalloproteinases (MMPs)

22 pulling against those leading adhesions; and de-adhesion at the rear.

23 activation of RhoA kinase promotes leukocyte de-adhesion by inhibiting cytoskeletal-dependent spreadi

24 Because reduced de-adhesion could mimic augmentation of adhesion at late

25 how that LFA-1 can mediate both adhesion and de-adhesion, dependent on receptor clustering.

26 nt membrane, apical constriction, epithelial de-adhesion, directed motility, loss of apical-basal pol

27 is required for cortical retraction but not de-adhesion during mitotic cell rounding.

28 h the integrin can mediate both adhesion and de-adhesion events dependent on receptor cross-linking.

29 ike many other cellular processes, this cell de-adhesion exhibits a complex, time-dependent pattern.

30 OCK), which mediates nuclear contraction and de-adhesion from integrin ligands, significantly reduced

31 the mechanism that regulates efficient LFA-1 de-adhesion from intercellular adhesion molecule (ICAM)-

32 Epidermal growth factor (EGF)-induced cell de-adhesion has been implicated as a critical step of no

33 the ADMIDAS domain, in controlling integrin de-adhesion in mice (see the related article beginning o

34 Whether de-adhesion is an active process mediated by a distinct

35 and temporal regulation of cell adhesion and de-adhesion is critical for dynamic lymphocyte migration

36 ation and provides a mechanism by which cell de-adhesion is directed to the cell body and tail as pho

37 Cellular de-adhesion is induced by the highly regulated matricell

38 The process of cellular de-adhesion is potentially important for the ability of

39 CAL-101 caused CLL cell de-adhesion, leading to increased CLL cell priming.

40 ritical role in cell migration enabling rear de-adhesion of adherent cells by cleaving structural com

41 dversely affect cell migration by preventing de-adhesion of cells from the substrate.

42 sting that during inflammation ROCK mediates de-adhesion of DC-expressed integrins from lymphatic-exp

43 e colony-stimulating factor (G-CSF) requires de-adhesion of HSPCs from the niche.

44 n regulating integrin-dependent adhesion and de-adhesion of neutrophils during inflammation.

45 ance of a proper balance in the adhesion and de-adhesion of the alpha4beta7 integrin, both for lympho

46 Calpain activity is required for de-adhesion of the cell body and rear to enable producti

47 MAdCAM-1 substrates resulting from improper de-adhesion of the lymphocyte trailing edge.

48 ost notably, lack of ion transport inhibited de-adhesion, resulting in trailing edges that failed to

49 In accord with elimination of IP-9-induced de-adhesion, RNA interference-mediated depletion of calp

50 nhibitor I, limited EGF-induced motility and de-adhesion similarly to IP-10.

51 ime points, we developed an assay to measure de-adhesion specifically.

52 ciency in bone marrow cells impeded monocyte de-adhesion, thereby increasing vascular permeability an

53 coordinated, integrin-mediated adhesion and de-adhesion to substrates and blood vessel walls.

54 or C3 exoenzyme markedly reduced the rate of de-adhesion, while markedly increasing their spreading.

55 urements revealed an increase of the work of de-adhesion with temperature that was coupled to a gradu

56 B as the factor responsible for coordinating de-adhesion with the ability of cells to enter mitosis.