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1 egulation of protein-protein interactions of pp60c-src.
2  Ras protein cascade via the tyrosine kinase pp60c-src.
3 -vis the c-src protooncogene-encoded product pp60c-src.
4 tyrosine residues that are phosphorylated by pp60(c-)src.
5 xamined their effectiveness as inhibitors of pp60(c-)src.
6 and Tyr-527, the negative regulatory site in pp60(c-src).
7 avian c-src DNA and functional expression of pp60(c-src).
8 se respective protein products pp60v-src and pp60c-src(527) show a different spectrum of amino acid s
9 nse based on recognition of self peptides of pp60c-src(527).
10                                              pp60(c-)src, a tyrosine kinase that promotes neurite gro
11 ergic receptor kinase1 overexpressing cells, pp60(c-src) activation was inhibited, and in normal cell
12                                              pp60(c-src) activity is frequently increased in breast t
13  protein kinase, and protein-tyrosine kinase pp60(c-)(src), also label annexin 7 with high efficiency
14                    Cortactin, a substrate of pp60(c-)src and a potent filamentous actin binding and c
15                                The activated pp60(c-Src) and Fyn co-immunoprecipitated with caveolin-
16 osphorylated the Src family tyrosine kinases pp60(c-Src) and Fyn.
17 e T mutant was defective in association with pp60(c-src) and in transformation.
18 eta(3) model peptides by the tyrosine kinase pp60(c-src) and we found that the presence of a phosphat
19 2) domain of the nonreceptor tyrosine kinase pp60c-src and beta-lactamase, both inserted into E. coli
20  a link between tyrosine phosphorylation via pp60c-src and membrane traffic.
21 receptor tyrosine kinases of the Src family, pp60c-src and pp62c-yes, respectively.
22 e activator of the cytosolic tyrosine kinase pp60c-src, and bath application of 5 microM insulin, whi
23 gyrin are tyrosine phosphorylated in vivo by pp60c-src, and experiments with recombinant proteins sho
24 mes including phosphatidylinositol 3-kinase, pp60c-Src, and protein kinase C had no effect on insulin
25 sal potential (about +10 mV) of the Na3VO4-, pp60c-src- and insulin-induced currents were similar to
26 tion was inhibited, and in normal cells anti-pp60(c-src) antibody inhibited Ang II-stimulated PLD act
27                                         Anti-pp60c-src antibody also blocked angiotensin II-stimulate
28                      Electroporation of anti-pp60c-src antibody into cultured, adherent smooth muscle
29                                 Mice lacking pp60c-src are resistant to VEGF-induced VP and show decr
30                 This study identified c-Src (pp60(c-Src)) as one such common signaling intermediate a
31 ential in cis in MT complexes for subsequent pp60(c-src) association.
32               This effect may be mediated by pp60(c-src), because in beta-adrenergic receptor kinase1
33  (MaxiK, BK) and the cellular proto-oncogene pp60(c-Src) (c-Src) are abundant proteins in vascular sm
34 tic mice to form ruffled membranes indicates pp60(c-src) (c-src) is essential to osteoclast polarizat
35  This study presents the first evidence that pp60(c-src) can directly regulate the activity of its su
36 bservations suggest that a host tolerance to pp60c-src can be broken so as to permit a tumor immune r
37 is necessary for subsequent association with pp60(c-src), catalytically inactive C subunits were exam
38 nt with late calpain-mediated events such as pp60(c-src) cleavage, but not early events such as prote
39                We found that tyrosine kinase pp60(c-src) coisolates with acid-transporting osteoclast
40 (v)beta5 complex is significantly reduced in pp60c-src-deficient mice.
41 eceptor coupling to tonic PLD activation via pp60(c-src)-dependent mechanisms, and that RhoA is invol
42 tigen species, N-terminal myristylation from pp60c-src did not.
43 ity of, several cellular proteins, including pp60(c-src) family kinases.
44 ession with FAK leads to a redistribution of pp60(c-src) from a diffuse cellular location to focal ad
45 eously derived transforming mutants of avian pp60(c-src) from a Syrian hamster embryo-derived cell li
46 er, the DNA sequence of the coding region of pp60(c-src) from a third line, E2T, was completely wild
47 gen bromide cleavage analyses of the altered pp60(c-src) from lines 4AT and 4BT showed that Tyr-527,
48                              After training, pp60c-src from hippocampus showed enhanced interactions
49 n kinase, cGMP-dependent protein kinase, and pp60(c-)(src), have been shown to label the protein with
50                             We characterized pp60(c-src) in detail from three of the tumor-derived li
51 r their ability to form complexes containing pp60(c-src) in MT-expressing cells.
52 tion of Tyr-416 correlate with activation of pp60(c-src) in the tumor-derived lines 4AT and 4BT, resp
53     However, in line E2T, the high levels of pp60(c-src), in combination with a partial activation of
54                        Combined ALK and SRC (pp60c-src) inhibition was effective in several ALK-drive
55                                              pp60(c-src) is a prototypical nonreceptor tyrosine kinas
56              The negative regulatory site of pp60(c-src) is hypophosphorylated when in complex with F
57      Here, we report that the mRNA signal of pp60c-src is widely distributed in the rat brain with pa
58                 The protein tyrosine kinase, pp60(c-)(src), is involved in cellular signaling and is
59         Cortactin, a prominent substrate for pp60(c-src), is a filamentous actin (F-actin) binding pr
60 ectly stimulates tyrosine kinases, including pp60(c-src) kinase (c-Src), focal adhesion kinase (FAK),
61 t regulate osteoclast function by activating pp60(c-Src) kinase and alpha(v)beta3 integrin.
62                                Activation of pp60(c-Src) kinase and phosphorylation of ERK were obser
63 lso formed complexes that included an active pp60(c-src) kinase, demonstrating that PP2A activity is
64                                 In addition, pp60(c-src) moderately inhibits the F-actin binding acti
65  that simultaneous overexpression of FAK and pp60(c-src) or p59(fyn) results in the enhancement of th
66 al adhesion targeting fail to cooperate with pp60(c-src) or p59(fyn) to induce paxillin phosphorylati
67 ting these results, mice deficient in either pp60c-src or integrin beta5, but not integrin beta3, hav
68 howed normal angiogenesis, mice deficient in pp60c-src or pp62c-yes showed no VEGF-induced vascular p
69 25FAK, which fails to bind the SH2 domain of pp60c-Src, or a mutant that fails to bind paxillin did n
70       These results suggest, therefore, that pp60c-src participates in the regulation of hippocampal
71                                 Furthermore, pp60(c-src) phosphorylates cortactin in vitro, resulting
72 iments with recombinant proteins showed that pp60c-src phosphorylates the cytoplasmic tails of these
73 combination with a partial activation of the pp60(c-src) protein as indicated by phosphorylation of T
74 ampus, which was accompanied by increases in pp60c-src protein in hippocampal synaptosomal preparatio
75   In contrast, expression of pp41/43FRNK and pp60c-Src reconstituted cell spreading and tyrosine phos
76         This study supports a model in which pp60(c-src) regulates dynamin-mediated endocytosis of L1
77 st tumors; however, the mechanisms governing pp60(c-src) regulation of the cell cycle in breast epith
78  display enhanced inhibitory activity toward pp60(c-)src relative to the corresponding phenylalanine-
79 osine retained some binding affinity for the pp60(c-src) SH2 domain but caused local structural pertu
80 pplied to a series of peptide ligands of the pp60(c-src) SH2 domain in an attempt to understand the c
81 on of dipeptide analogues as ligands for the pp60c-src SH2 domain are described.
82 Thr203 in MT has no affect on the binding of pp60c-src, showing that these sites interact with src-ki
83           The Src homology 3 (SH3) domain of pp60(c-src) (Src) plays dual roles in signal transductio
84 ted tyrosine phosphorylation of the specific pp60(c-src) substrate p120 and c-Src association with EG
85 essed an electrophoretically altered form of pp60(c-src), suggesting mutations in src.
86  not effectively induce the translocation of pp60(c-src) to focal adhesions.
87 s the aggregation-dependent translocation of pp60(c-src) to the cytoskeleton.
88 acts as a "switchable adaptor" that recruits pp60c-Src to phosphorylate paxillin, promoting cell spre
89 The kinetic mechanisms for the inhibition of pp60(c-src) tyrosine kinase (Src TK) by 4-anilinoquinazo
90 4 caused a time-dependent activation of Src (pp60c-src) tyrosine kinase and Src tyrosine kinase inhib
91                           Rapid digestion of pp60c-src tyrosine kinase (src TK) in combination with e
92  calcitonin and vitronectin receptors and of pp60c-src tyrosine kinase.
93                  Tyrosine phosphorylation by pp60(c-)src up-regulates the activity of calpain toward
94              The nonreceptor tyrosine kinase pp60(c-src) was required for L1-triggered MAPK phosphory
95                               In the case of pp60(c-)(src), we note that this kinase, if anything, mo
96                           The association of pp60c-src with insulin receptor in the synaptic membrane