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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  form of cell death in response to substrate de-adhesion.
10 jor functions defined for SPARC in vitro are de-adhesion and antiproliferation.
11  endocytosis of CDH2, allowing for segmental de-adhesion and individualization of somites.
12 ivation in both BMEC and HSC/P, and in HSC/P de-adhesion and mobilization.
13             RhoA kinase inhibitor effects on de-adhesion and spreading were reversed by treatment wit
14 our knowledge, novel drivers of adhesion (or de-adhesion) and sort cell populations based on complex
15     Rearrangement of the actin cytoskeleton, de-adhesion, and an increase in cortical rigidity accomp
16 panied by changes in the actin cytoskeleton, de-adhesion, and an increase in cortical rigidity.
17                          Cell adhesion, cell de-adhesion, and cell motility all appeared to be normal
18 sion mechanisms may have to be shed to allow de-adhesion, and this may contribute to TCR down-regulat
19 ll migration involves cycles of adhesion and de-adhesion, and we propose that the dynamic spatiotempo
20         Transcript profiling mapped a set of de-adhesion, angiogenesis, and wound healing regulators
21 ed inhibition of calpain activation and cell de-adhesion as described for interferon gamma inducible
22 astasis that requires integrins for adhesion/de-adhesion, as well as matrix metalloproteinases (MMPs)
23 pulling against those leading adhesions; and de-adhesion at the rear.
24 activation of RhoA kinase promotes leukocyte de-adhesion by inhibiting cytoskeletal-dependent spreadi
25                              Because reduced de-adhesion could mimic augmentation of adhesion at late
26 how that LFA-1 can mediate both adhesion and de-adhesion, dependent on receptor clustering.
27 nt membrane, apical constriction, epithelial de-adhesion, directed motility, loss of apical-basal pol
28  is required for cortical retraction but not de-adhesion during mitotic cell rounding.
29 h the integrin can mediate both adhesion and de-adhesion events dependent on receptor cross-linking.
30 ike many other cellular processes, this cell de-adhesion exhibits a complex, time-dependent pattern.
31 OCK), which mediates nuclear contraction and de-adhesion from integrin ligands, significantly reduced
32 the mechanism that regulates efficient LFA-1 de-adhesion from intercellular adhesion molecule (ICAM)-
33   Epidermal growth factor (EGF)-induced cell de-adhesion has been implicated as a critical step of no
34  the ADMIDAS domain, in controlling integrin de-adhesion in mice (see the related article beginning o
35                                      Whether de-adhesion is an active process mediated by a distinct
36 and temporal regulation of cell adhesion and de-adhesion is critical for dynamic lymphocyte migration
37 ation and provides a mechanism by which cell de-adhesion is directed to the cell body and tail as pho
38                                     Cellular de-adhesion is induced by the highly regulated matricell
39                      The process of cellular de-adhesion is potentially important for the ability of
40                      CAL-101 caused CLL cell de-adhesion, leading to increased CLL cell priming.
41 ritical role in cell migration enabling rear de-adhesion of adherent cells by cleaving structural com
42 dversely affect cell migration by preventing de-adhesion of cells from the substrate.
43 sting that during inflammation ROCK mediates de-adhesion of DC-expressed integrins from lymphatic-exp
44 e colony-stimulating factor (G-CSF) requires de-adhesion of HSPCs from the niche.
45            Surprisingly, classic schizogeny (de-adhesion of neighboring cells) is relatively infreque
46 n regulating integrin-dependent adhesion and de-adhesion of neutrophils during inflammation.
47 ance of a proper balance in the adhesion and de-adhesion of the alpha4beta7 integrin, both for lympho
48             Calpain activity is required for de-adhesion of the cell body and rear to enable producti
49  MAdCAM-1 substrates resulting from improper de-adhesion of the lymphocyte trailing edge.
50 ost notably, lack of ion transport inhibited de-adhesion, resulting in trailing edges that failed to
51   In accord with elimination of IP-9-induced de-adhesion, RNA interference-mediated depletion of calp
52 nhibitor I, limited EGF-induced motility and de-adhesion similarly to IP-10.
53 ime points, we developed an assay to measure de-adhesion specifically.
54 ciency in bone marrow cells impeded monocyte de-adhesion, thereby increasing vascular permeability an
55  coordinated, integrin-mediated adhesion and de-adhesion to substrates and blood vessel walls.
56  Strikingly, the activation of INF2 promotes de-adhesion, which in turn facilitates migration across
57 or C3 exoenzyme markedly reduced the rate of de-adhesion, while markedly increasing their spreading.
58 urements revealed an increase of the work of de-adhesion with temperature that was coupled to a gradu
59 B as the factor responsible for coordinating de-adhesion with the ability of cells to enter mitosis.