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1 in BCR/ABL-transformed cells is reduction of hypermotility.
2 ed expression of the fliA and fliC genes and hypermotility.
3 rlie withdrawal-induced hyperalgesia and gut hypermotility.
4 rocaine did not, however, produce subsequent hypermotility.
5 5-10 micrograms amphetamine into VP produced hypermotility.
6 re it binds Ena/VASP), and this mediates the hypermotility.
7 ing on control surfaces with TGFbeta induced hypermotility after a 1-day lag time and growth arrest b
8 nuated ADR-elicited cytoskeleton disruption, hypermotility and apoptosis, associated with restored in
9                                Additionally, hypermotility and flagellar gene over- and underexpressi
10 d the lipopolysaccharide elicited apoptosis, hypermotility and impairment of filtration barrier funct
11 X. fastidiosa exhibited reduced cell length, hypermotility (and subsequent lack of biofilm formation)
12 d-effect relationships among laminin 5, p16, hypermotility, and growth arrest.
13 roduction of extracellular proteins/enzymes, hypermotility, and hypervirulence.
14 accumulation of mitochondria and progressive hypermotility as cells increase size.
15 nin 5 (LN5') immediately induced directional hypermotility at approximately 125 microm/hour, followed
16 ans infected with Giardia exhibit intestinal hypermotility, but the underlying mechanisms and functio
17 loss of GABA VTA neurons was associated with hypermotility, further supporting their important regula
18 ide over agar surfaces (referred to here as "hypermotility"), greater resistance to phage infection a
19                                              Hypermotility in yenI mutants was also suppressed by mut
20 l of nNOS inhibition, and in the PCP-induced hypermotility model in the rat.
21 e models of giardiasis that small-intestinal hypermotility occurs in a delayed fashion relative to pe
22 del explaining the principles underlying the hypermotility phenotype is presented.
23              To identify the cause(s) of the hypermotility phenotype, the genome sequences of normal
24 n I triggered a TGFbetaRI kinase-independent hypermotility unaccompanied by smad translocation or gro
25     Overexpression of TblncRNA-23 results in hypermotility, whereas KO compromises this capacity, sug