IndraLab
Statements
reach
"Because the PI3K and Akt signaling pathway plays a vital role in EGF induced migration by activating Rac1 and Cdc42, that are important for lamellipodia and filopodia formation respectively, and found upregulated in metastatic lesions, we further examined the activation status of Rac1 and Cdc42 in the absence or presence of EGF by G-LISA."
sparser
"We previously found that the EGF-induced biphasic activation of Rac1 and the second-wave Rac1 activation require the upregulation of Tiam1, a member of the Rac GEF family. xref We also demonstrated that CysLT1 signaling played an important role in Tiam1 upregulation required for the second EGF-induced wave of Rac1 activation."
reach
"In order to understand role for Rac1 in IMC-C225 mediated inhibition of cell invasion, pull-down assays using the PBD of PAK were performed to measure Rac1 activation in MDA-MB468 cells treated with either EGF or with IMC-C225 for the same time points as studied for RhoA activation."
reach
"In the present study, we demonstrate that MEK activation by EGF increased Rac1 activation, dissociation of intercellular contacts, and migration in both control and polyamine depleted cells, while U0126, a specific inhibitor of MEK1, prevented disruption of junctions as well as EGF induced Rac1 activation."
sparser
"Further investigation suggested involvement of the Eps8/Abi1/Sos1 tricomplex; we found up‐regulated expression of the Rac1 guanine nucleotide exchange factor, Sos1, in PDAC tissue and cell lines (supplementary material, Figure xref A, B), and Sos1 siRNA knockdown suppressed EGF‐induced Rac1 activation (supplementary material, Figure xref C)."
reach
"Pretreatment of VSMC by EGF receptor specific tyrosine kinase inhibitor AG1478 and non specific tyrosine kinase inhibitor genistein inhibited EGF induced activation of Rac1, PAK and JNK, whereas tyrosine kinase inhibitors specific for Src (PP1) and specific for platelet derived growth factor (AG1296) had no effect."
reach
"Further investigation suggested involvement of the Eps8/Abi1/Sos1 tricomplex; we found up-regulated expression of the Rac1 guanine nucleotide exchange factor, Sos1, in PDAC tissue and cell lines (supplementary material, Figure XREF_SUPPLEMENTARY A, B), and Sos1 siRNA knockdown suppressed EGF induced Rac1 activation (supplementary material, Figure XREF_SUPPLEMENTARY C)."
sparser
"Inhibition of ERK activity by U0126 or suppression of Rac1 activity by ectopic expression of inactive mutant form of Rac1 (Rac1-T17N) significantly prevents EGF-induced cell migration, suggesting that EGF-induced ERK and Rac1 activation was responsible for the migration of these cancer cells."
reach
"The results demonstrated that CHAG treatment efficiently blocked the phosphorylation and activation of EGFR, integrin and VEGFR, inhibited the EGF induced signaling of MAPK and ERK, PI3K and Akt and Rac1 mediated pathways, and diminished the EGF induced expression of proliferation and migration related proteins."
reach
"Indeed, we found that centrosome amplification induced a consistent ~ 1.5-fold Rac1 activation using a biochemical pull-down assay to measure GTP liganded Rac1 in multiple cell lines [Note : maximal Rac1 activity induced by EGF in MCF10A cells is ~ 2-fold (XREF_FIG and XREF_SUPPLEMENTARY)]."
sparser
"Recently, Arnst et al ( xref ) demonstrated two new compounds, referred in their publication as #1 and #6, that were design to target the nucleotide-binding site of Rac1 although, were able to block active Rac1 from binding to its effector PAK1, following EGF-induced Rac1 activation in a dose-dependent manner, they showed no inhibition of Cdc42 or RhoA."
sparser
"In the present study, we demonstrate that MEK activation by EGF increased Rac1 activation, dissociation of intercellular contacts, and migration in both control and polyamine-depleted cells, while U0126, a specific inhibitor of MEK1, prevented disruption of junctions as well as EGF-induced Rac1 activation."
reach
"Recently, Arnst et al demonstrated two new compounds, referred in their publication as # 1 and # 6, that were design to target the nucleotide binding site of Rac1 although, were able to block active Rac1 from binding to its effector PAK1, following EGF induced Rac1 activation in a dose dependent manner, they showed no inhibition of Cdc42 or RhoA."
sparser
"Pretreatment of VSMC by EGF receptor specific tyrosine kinase inhibitor AG1478 and non-specific tyrosine kinase inhibitor genistein inhibited EGF-induced activation of Rac1, PAK and JNK, whereas tyrosine kinase inhibitors specific for Src (PP1) and specific for platelet-derived growth factor (AG1296) had no effect."
reach
"Additionally, the activation of the planar cell polarity proteins PTK7 (protein tyrosine kinase 7), CELSR (Cadherin EGF LAG seven-pass G-type receptor), and VANG (Van Gogh like) by Wnts or Fzd receptors may support PCP GTPase signaling by recruiting the Rac1 and Cdc42 GEF PAK, the Rac1 GEF ARHGEF7, and the ARF GAP GIT1 [XREF_BIBR, XREF_BIBR]."