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1 lls and that it interacts with the 3'-UTR of Tiam1.
2 1 and its guanine nucleotide exchange factor Tiam1.
3 recruiting, phosphorylating, and activating Tiam1.
4 the Rac1 guanine nucleotide exchange factor Tiam1.
5 naling through the G protein exchange factor Tiam1.
6 moter by Src were also potently increased by Tiam1.
7 of Tiam1 in the membranes versus whole cell Tiam1.
8 ive and require CD44s binding to the Rac GEF TIAM1.
9 is involved in the membrane translocation of Tiam1.
10 ing (K(d) = approximately 0.13 nM) to intact Tiam1.
11 RT1 or 2 has not been previously linked with TIAM1.
12 tion is required for the mitotic function of Tiam1.
13 and demonstrate that they act downstream of Tiam1.
14 nockdown resulted in enhanced acetylation of TIAM1.
15 protein-protein interaction between Rac1 and Tiam1.
16 junctional recruitment of the Rac1 activator Tiam1.
17 plexes to stimulate Rac activity via the GEF Tiam1.
18 attenuated HGF-induced recruitment of c-Met, Tiam1 (a Rac1 exchange factor), cortactin (an actin cyto
20 f T-cell lymphoma invasion and metastasis 1 (TIAM1), a Rac guanine nucleotide exchange factor (GEF).
21 invasion and metastasis-inducing protein 1 (TIAM1)-a Rac guanine exchange factor-from the plasma mem
23 lls, probably through microtubule-associated Tiam1, a guanine nucleotide exchange factor for Rac.
26 osomes during prophase and prometaphase, and Tiam1, acting through Rac, ordinarily retards centrosome
28 er, these findings suggest that HRG regulate Tiam1 activation and lymphoid enhancer factor/beta-caten
29 with a fragment of Tiam1 blocks OGD-induced Tiam1 activation but has no effect on the deactivation o
30 Certain phosphoinositides also stimulated Tiam1 activity but were less potent than ascorbyl steara
31 lin-binding peptide (CBP)-tagged recombinant Tiam1 (amino acids 393-728) fragment that contains the a
32 d a specific binding interaction between the Tiam1 (amino acids 393-738) fragment and ankyrin in vitr
33 brane translocation of the Rac1-specific GEF Tiam1 and activation of Rac1-dependent peripheral cytosk
34 acted in a protein complex with the Rac1 GEF TIAM1 and colocalized with actin at the platelet lamelli
35 promotes the plasma membrane localization of Tiam1 and enhances the ability of Tiam1 to activate p70
37 tor essential for centrosome separation, and Tiam1 and its substrate Rac antagonize Eg5-dependent cen
39 haracterized mechanism for the activation of Tiam1 and of a role for this effector in neurotrophin-me
41 the Rac1 guanine nucleotide exchange factor Tiam1 and phosphorylation of caveolin-1, indicative of s
49 decan1 is a physiological binding partner of Tiam1 and that the PDZ domain has a function in cell-mat
50 ates with NMDA receptors (NMDARs) along with Tiam1 and that this protein complex is more abundant in
51 tation and immunoblot analyses indicate that Tiam1 and the cytoskeletal protein, ankyrin, are physica
56 the Rac guanine nucleotide exchange factors Tiam1 and Vav1 in unstimulated peripheral blood CLL cell
57 a regulatory complex composed of a Rac-GEF (Tiam1) and a Rac-GAP (Bcr) that cooperate to control exc
58 ignated as PHn-CC-Ex, amino acids 393-738 of Tiam1) and an in vitro binding assay, we have detected a
59 otic (Raf, phosphatidylinositol 3-kinase and Tiam1) and apoptotic (Nore1 and RASSF1) actions of oncog
60 ion of T lymphoma invasion and metastasis 1 (Tiam1) and its upstream activator Ras in a phosphoinosit
62 myloid beta (A4) precursor protein (APP) and TIAM1, and between immediate early gene (IEG) proteins a
63 show the guanine nucleotide exchange factor, Tiam1, and its cognate Rho-family G protein, Rac1, regul
64 Rac guanine nucleotide-exchange factor (GEF) TIAM1, and spatially restricting it to dendritic spines.
65 c were affected only in cells with exogenous Tiam1, and were primarily increased in the membrane frac
67 n levels in cancer cells, and DVL along with TIAM1 are known to augment Rac activation; however, SIRT
68 ssed Rac1 guanine nucleotide exchange factor Tiam1 are phosphorylated in tyrosine residues in cells t
72 n betagamma subunits, Src kinase and the GEF Tiam1 as upstream modulators of S1P-mediated Rac1 activa
73 -Ex cDNA and Tiam1 cDNA effectively inhibits Tiam1 association with CD44 and efficiently blocks tumor
74 fection of SP1 cells with Tiam1cDNA promotes Tiam1 association with CD44v3 and up-regulates Rac1 sign
75 inhibition (LY294002) attenuated S1P-induced Tiam1 association with S1P1, Tiam1/Rac1 activation, alph
82 e Tiam1-NMDAR interaction with a fragment of Tiam1 blocks OGD-induced Tiam1 activation but has no eff
83 h required the activity of Rac1 and its GEF, Tiam1, both of which show suppressed activity in the pre
84 blood CLL cells with almost complete loss of Tiam1 but increased transcription of the potential Rac a
88 B, directly binds and specifically activates Tiam1 by phosphorylating Tyr-829, leading to Rac1 activa
91 ding of HA to CD44v3 of SP1 cells stimulates Tiam1-catalyzed Rac1 signaling and cytoskeleton-mediated
92 fection of SP1 cells with PHn-CC-Ex cDNA and Tiam1 cDNA effectively inhibits Tiam1 association with C
96 However, the mechanisms that restrict Par-Tiam1 complex activity to the leading edge to maintain c
97 diated nucleotide exchange based on the Rac1-Tiam1 complex structure, with SopE/E2 flexibility, parti
98 te that Bcr is an integral member of the Par-Tiam1 complex that controls polarized cell migration by
103 t T-cell lymphoma invasion and metastasis 1 (TIAM1) contains a conserved EEVIWVRRE peptide that was a
106 e results demonstrate that overexpression of Tiam1 contributes to the metastatic phenotype of colon c
107 have shown previously that the N terminus of Tiam1 contributes to the signaling specificity of its do
108 at the SCF(betaTrCP)-mediated degradation of Tiam1 controls the duration of the mTOR-S6K signaling pa
111 the guanine nucleotide exchange factor (GEF) Tiam1, dependent on its ability to activate the GTPase R
112 inally, IRSp53 depletion from cells prevents Tiam1-dependent lamellipodia induced by Tiam1 overexpres
118 ng a close correlation between the status of Tiam1 expression and invasiveness of human breast tumor
119 ense oligonucleotide, that miR-10b represses Tiam1 expression in breast carcinoma cells and that it i
121 , correlations between TRalpha1, miR-21, and TIAM1 expression patterns in animal models paralleled th
125 li-derived calmodulin-binding peptide-tagged Tiam1 fragment (i.e. the NH(2)-terminal pleckstrin homol
127 wn of Tiam1 protein by RNAi or inhibition of Tiam1 function with a dominant-negative Tiam1 mutant blo
129 for Rac1 GTP loading, whereas, surprisingly, Tiam1 functions as an adaptor in a VE-cadherin-p67phox-P
130 , we show that the PHn-CC-Ex domain inhibits Tiam1 GEF activity by directly interacting with the cata
131 ighlight the role of the PHn-CC-Ex domain in Tiam1 GEF regulation and suggest a combinatorial model f
134 d activation by the Rac-specific GEF Trio or Tiam1 in a dose-dependent manner without interfering wit
138 and Rac-specific nucleotide exchange factor Tiam1 in the mechanisms of EC barrier protection by HGF.
142 thways in epithelial tumor cells and lack of Tiam1 in tumor cells retards tumor growth in Tiam1 knock
151 the Rac1 guanine nucleotide exchange factor Tiam1 interacts with the EphB2 receptor in a kinase-depe
153 the implantation of clones that overexpress Tiam1 into the cecum of athymic mice resulted in tumor g
157 Enzyme kinetics experiments suggested that Tiam1 is auto-inhibited through occlusion of the catalyt
158 ere, we report that in response to mitogens, Tiam1 is degraded by the ubiquitin-proteasome system via
162 ac1 provided by various extended portions of Tiam1 is not influenced by (a) soluble phosphoinositide
168 n CD44v3 isoform and the PHn-CC-EX domain of Tiam1 is required for HA stimulated Rac1 signaling and c
169 Indeed in LIM 1863 cells, suppression of TIAM1 is required for miR-21/miR-31 to enhance cell migr
172 T-cell lymphoma invasion and metastasis 1 (Tiam1) is a Dbl-family guanine nucleotide exchange facto
173 ell lymphoma invasion and metastasis gene 1 (Tiam1) is a guanine exchange factor (GEF) for the Rho-fa
180 al delivery of short hairpin RNA to suppress Tiam1 levels in three different experimental models.
182 ac1 guanine nucleotide exchange factor (GEF) Tiam1 markedly enhanced Rac1 activity, whereas a dominan
183 ogether, these results suggest that Vav2 and Tiam1 may act as downstream effectors of Src, thereby re
186 ta provide a mechanism for the regulation of Tiam1-mediated Rac activation in breast cancer cells and
188 The Rac1 guanine nucleotide exchange factor Tiam1 mediates an OGD-induced increase in Rac1 activity
189 t interfering mutants of Tiam1 suggests that Tiam1 mediates effects of the NMDA receptor on dendritic
191 n of Tiam1 function with a dominant-negative Tiam1 mutant blocks dendritic spine formation induced by
192 d Rac1 activity, whereas a dominant negative Tiam1 mutant significantly attenuated S1P-mediated Rac1
197 duced phosphorylation of membrane-associated Tiam1 occurred more rapidly than that of the total Tiam1
201 IB2/JIP2 in cells potentiates the ability of Tiam1 or Ras-GRF1 to activate the p38 MAP kinase cascade
206 ents Tiam1-dependent lamellipodia induced by Tiam1 overexpression or platelet-derived growth factor s
207 data report on a physiological role for the Tiam1 PDZ domain and establish a novel link between two
209 We determined the crystal structures of the Tiam1 PDZ domain free and in complex with a "model" pept
211 two regions (S(0) and S(-2) pockets) of the Tiam1 PDZ domain that are important determinants of liga
212 synthetic peptide capable of binding to the Tiam1 PDZ domain, but little is known about its ligand s
216 perturbation experiments indicated that the Tiam1 PDZ/Syndecan1 and PDZ/Caspr4 complexes were struct
219 interaction between the small GTPase Ras and Tiam1 plays an essential role in the activation of Rac1.
220 occurred more rapidly than that of the total Tiam1 pool, and CaMK II, but not PKC, played a significa
223 (Tiam1) to specialized cellular sites, where Tiam1 promotes local Rac1 activation and cytoskeletal re
224 ndicate that both the CD44v3 isoform and the Tiam1 protein are expressed in SP1 cells and that these
226 was transfected with a plasmid encoding the Tiam1 protein, and single cell clones were established.
227 T-lymphoma invasion and metastasis factor 1 (Tiam1) protein in complex with its cognate Rho family G
228 ting both guanine nucleotide association and Tiam1 Rac guanine nucleotide exchange factor-stimulated
230 st that mutant B-RAF signaling downregulates Tiam1/Rac activity resulting in an increase in N-cadheri
231 st that mutant B-RAF signaling downregulates Tiam1/Rac activity resulting in an increase in N-cadheri
232 n where SIRT1/2 positively modulates the DVL/TIAM1/Rac axis and promotes sustained pathway activation
233 knockdown using siRNA or treatment with the Tiam1/Rac inhibitor NSC-23766 attenuated c-Myc transcrip
238 gents that have been reported to disrupt the Tiam1-Rac1 interaction or to prevent phosphorylation of
239 al permeability requires the activation of a Tiam1-Rac1 signaling module, suggesting a novel therapeu
241 inhibits cell migration by blocking the Ras-Tiam1-Rac1-Pak1 signaling pathway in endothelial cells.
243 o CEM fractions promotes PI3 kinase-mediated Tiam1/Rac1 activation required for alpha-actinin-1/4-reg
244 ted S1P-induced Tiam1 association with S1P1, Tiam1/Rac1 activation, alpha-actinin-1/4 recruitment, an
245 on through two parallel signaling units, Ras/Tiam1/Rac1 and Dbs/Cdc42, and that Schwann cell migratio
246 r findings highlight a regulatory pathway of Tiam1/Rac1 in Th17 cells and suggest that it may be a th
247 defects by activating a calcium/CamKinaseII/Tiam1/Rac1 pathway that substitutes for fibronectin-depe
249 receptor expression blocked OxPAPC-mediated Tiam1 recruitment to CEMs, Rac1 activation, and EC barri
252 reas a mutant that cannot interact with Par3/Tiam1 rescues neither spine defects nor Par3 localizatio
254 , simultaneous depletion of B-RAF and Rac or Tiam1 resulted in invasive capacity similar to that of c
255 ream pathways, and suggest that manipulating Tiam1-scaffold interactions can modulate Rac-dependent c
256 veral multiphosphorylated phosphoinositides, Tiam1 selectively interacts with phosphatidylinositol 3-
257 t Dbl family proteins, intersectin, Dbs, and Tiam1, selectively bind lipid vesicles only when phospho
259 RNA (siRNA) based depletion of either Rac or Tiam1 significantly attenuated HGF-induced peripheral tr
262 of mammary epithelial cells and fibroblasts, Tiam1 silencing in fibroblasts led to increased epitheli
264 inase activation in cells, suggesting that a Tiam1/spinophilin complex contributes to p70 S6 kinase r
265 us studies indicate that larger fragments of Tiam1, such as the region encompassing the N-terminal to
266 ith RNAi and dominant interfering mutants of Tiam1 suggests that Tiam1 mediates effects of the NMDA r
267 ly, a mutant spinophilin that cannot bind to Tiam1 suppresses serum-induced p70 S6 kinase activation
269 Together, our findings suggest that in CRC TIAM1 suppresses tumor progression by regulating YAP/TAZ
270 at miR-21 stimulation by T(3) and subsequent TIAM1 suppression promotes hepatoma cell migration and i
271 ysis of potential miR-10b targets identified Tiam1 (T lymphoma invasion and metastasis 1), a guanidin
272 specific guanine nucleotide exchange factor, Tiam1 (T lymphoma invasion and metastasis 1), in transdu
274 cal analysis revealed that the Rac activator Tiam1 (T-cell lymphoma invasion and metastasis 1) is ove
275 t2 (epithelial cell transforming squence 2), Tiam1 (T-cell lymphoma invasion and metastasis 1), Vav a
278 hus, Par3 coordinates the action of PI3K and Tiam1 to define membrane identity, revealing a signaling
279 tyrosine phosphorylation and recruitment of Tiam1 to EphB complexes containing NMDA-type glutamate r
280 the Rac1-guanine nucleotide exchange factor Tiam1 to spines, the polarity protein Par3 promotes syna
281 , and that simultaneously targeting PI3K and Tiam1 to the apical membrane has a synergistic effect on
282 itogenic stimulation triggers the binding of Tiam1 to the F-box protein betaTrCP via its degron seque
283 hosphatidic acid induce the translocation of Tiam1 to the membrane fraction of NIH 3T3 fibroblasts in
285 ed the phosphorylation and redistribution of Tiam1 to the membrane ruffles and the loosening of inter
286 vely active PI3K stimulated translocation of Tiam1 to the membrane, increased Rac1 activity, and incr
287 factor T-lymphoma invasion and metastasis 1 (Tiam1) to specialized cellular sites, where Tiam1 promot
288 cell adhesion or migration, including SS18, TIAM1, TSTA3 and LDB2, which warrant further investigati
293 , T-cell lymphoma invasion and metastasis 1 (TIAM1), was identified as a miR-21 target additionally d
295 1 and its guanine nucleotide exchange factor Tiam1 were found associated with a membrane fraction fro
296 Tiam1 and Trio siRNAs and dominant-negative Tiam1 were used to determine which Rac1-specific guanine
297 d SIRT2 resulted in increased acetylation of TIAM1, whereas chronic SIRT2 knockdown resulted in enhan
299 are known to phosphorylate the Rac activator Tiam1, which has recently been shown to be Abeta-respons
300 CD44 binding site in the PHn-CC-Ex domain of Tiam1 with an apparent dissociation constant (K(d)) of 0
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