IndraLab

Statements


EGFR increases the amount of EGFR. 10 / 162
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"The increased expression of EGFR in HPNE cells that expressed K-ras (GD12) was mediated by both stabilizing EGFR protein and by increasing EGFR transcription."

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"EGFR inhibition by gefitinib further decreased confluence-induced suppression of DcR3 mRNA expression, and, vice versa, knocking down DcR3 expression attenuated EGFR and EGFR ligand expression as well as EGFR activation."

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"The STAT3 activating kinase, JAK2, is activated in GBM cell lines and combined inhibition of JAK2 and EGFR and EGFRvIII abolishes STAT3 activation and synergistically suppresses the growth of EGFR- and EGFRvIII expressing cell lines of breast cancer [XREF_BIBR] and epidermoid carcinoma [XREF_BIBR, XREF_BIBR], and GBM [XREF_BIBR]."

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"2,3 Bladder and kidney tumor volume was analyzed by the unpaired Student 's t -test.In the first set of studies, we determined whether the in vitro exposure of human dermal endothelial cells to EGF or[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Through this interaction, CCN2 may be functioning as a regulator of EGFR signaling independent of EGFR or EGFR ligand expression."

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"Elevated levels of EGFR are usually induced by amplification of the EGFR gene and correlate with tumorigenicity and an unfavorable prognosis."

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"PKP2 induced phosphorylation of EGFR and subsequent ERK activation was entirely inhibited by the EGFR inhibitor lapatinib, which suggests that PKP2 exclusively mediates EGFR signal activation in EGFR expressing cancer cells."

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"The EGFR can induce cancer via at least three major mechanisms : overexpression of EGFR ligands, amplification of EGFR, and mutational activation of EGFR."

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"As shown in Figure 1 A, EGFR tyrosine kinase inhibitor, AEE788 (Traxler et al., 2004) (5.0 muM), did not decrease the expression of EGFR but did completely inhibit its phosphorylation."

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"We describe a clinically-applicable method to propagate and modify T cells to transiently express EGFR specific CAR to target EGFR expressing tumor cells that may be used to limit on-target, off-tissue toxicity to normal tissue."
Modified EGFR increases the amount of EGFR. 9 / 9
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"In this study we show that transient or stable overexpression of the EGFR predictably leads to ligand dependent apoptosis in a variety of cell lines suggesting that apoptosis may be a general outcome [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"EGFR surface expression increased 4-fold and 6-fold on BM KSL and SLAM + KSL cells, respectively, at 4 hours following 300 cGy irradiation, demonstrating induction of EGFR expression on HSCs following irradiation (XREF_FIG)."

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"Expression of EGFR (XREF_FIG), but not FSHR (XREF_FIG), after pre-IVM for 2 h was increased by the combination of dbcAMP and IBMX, but not by dbcAMP or IBMX alone (P < 0.05), suggesting a possible regulation of EGFR expression by cAMP."

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"Importantly, the ligand OSM regulates EGFR phosphorylation in wild type mouse astrocytes, and knockdown of OSMR in EGFRvIII expressing astrocytes reduces the phosphorylation and total levels of EGFRvIII."

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"However, further overexpression of EGFR on a background of Cbl-b overexpression can relieve Cbl-b-mediated EGFR degradation and restore EGFR expression, mesenchymal phenotype, and cell migration capacity in MDR gastric and breast cancer cells."

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"Transient expression of constitutively active EGFR (EGFR L858R) (Uchida et al., 2007) restored hBD3 mRNA expression 24 hr p.i., as did overexpression of WT EGFR."

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"In addition, the reduced levels of EGFR leads to decreased EGFR phosphorylation levels at Y992 and T1068, and decreased phosphorylation of EGFR also elicits reduction of several downstream kinase pathways."

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"Overexpression of EGFR on a background of Cbl-b overexpression restored EGFR expression and facilitated activation of EGFR and ERK and Akt compared with Cbl-b overexpression alone (XREF_FIG A)."

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"Expression of wild-type EGFR and mutant EGFR receptors increased p-EGFR levels compared with vector control or mutant K-ras retrovirus infected cells."
Mutated EGFR increases the amount of EGFR. 4 / 4
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"Human EGFR (EGFR; HER-1) is over-expressed in 40%-60% of primary GBM tumours and mostly occurs in the classical subtype (XREF_FIG) [XREF_BIBR], but EGFR mutation which leads to EGFRvIII expression (XREF_FIG) present in 20%-30% of primary GBM [XREF_BIBR]."

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"Therefore, the exact mechanism remains unclear whether EGFR mutation is the major contributor to EGFR overexpression."

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"It is also possible that EGFR is able to override DOK2 mediated inhibition via mechanisms such as increased expression of EGFR driven by amplification of the mutant EGFR allele."

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"One type of EGFR mutation in primary gliomas results in overexpression of an aberrant EGFR messenger RNA (mRNA) that lacks sequences of exons II through VI of the human EGFR gene."
Kinase-active EGFR increases the amount of EGFR bound to GRB2. 3 / 3
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"In this study, we describe the specific interaction of PAK1 with the Grb2 adapter protein both in vitro and in vivo. We identify the site of this interaction as the second proline-rich SH3 binding domain of PAK1. Stimulation of the epidermal growth factor receptor (EGFR) in HaCaT cells enhances the level of EGFR-associated PAK1 and Grb2, although the PAK1-Grb2 association is itself independent of this stimulation. "

"The dimerization of two EGFR family molecules leads to phosphorylation of C-terminal tyrosine residues either by autophosphorylation or by a SRC-related kinase followed by binding of GRB2, a RAS adaptor protein, at the SH2 domain of the receptor; binding of the proline-rich C-terminus of SOS, a guanine nucleotide exchange factor, to the SH3 domain of the receptor; exchange of a GTP from the receptor complex for a GDP from the RAS protein to form activated RAS; activation of phosphatidylinositol-3-kinase (PI-3 kinase) to initiate signaling by the biochemical pathways that are triggered by diacylglycerol production and protein kinase C activation; and activation of the series of cytoplasmic serine and threonine kinases beginning with RAF to initiate signaling by the biochemical pathways that are triggered by members of the MAPK family (e.g. ERK 1 and 2). EGFR signaling also activates other pathways in the cell including the Janus kinase (JAK)/signal transduction activators of transcription (STAT) pathways [80, 81]."

"Epidermal growth factor (EGF) stimulates recruitment of RN-tre to the EGF receptor (EGFR) in a Grb2-dependent manner."
EGFR increases the amount of mutated EGFR. 2 / 2
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"An amplified EGFR gene may lead to expression of mutant EGFR (EGFRvIII) in high grade astrocytomas [XREF_BIBR], providing a possible target for immunotherapy [XREF_BIBR]."

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"Transient transfection of del (E746-A750) EGFR cDNA induced enhanced expression of activated mutant EGFR in PC9 and ER1 (XREF_FIG)."
Kinase-active EGFR increases the amount of EGFR bound to SHC1. 2 / 2
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"Shc products are phosphorylated on tyrosine by the activated epidermal growth factor receptor (EGFR) and become physically associated with EGFR via their SH2 domain. "

"Finally, ErbB-1 activated by all EGF-related peptides (EGF, HB-EGF, BTC and NDF) couples to SHC, whereas only ErbB-1 activated by its own ligands associates with and phosphorylates Cbl."
EGFR increases the amount of phosphorylated EGFR. 1 / 1
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"The constitutive activation of these downstream EGFR signaling proteins agrees with the observed enhanced level of total and phosphorylated EGFR in the absence of the TRPV1."
EGFR bound to EGFR_ligand increases the amount of EGFR bound to ERBB2. 1 / 1
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"The first group includes EGF, amphiregulin (AR), and transforming growth factor-alpha (TGF-alpha), which bind specifically to ErbB1; the second group betacellulin (BTC), heparin-binding EGF (HB-EGF), and epiregulin (EPR), which exhibit dual specificity in that they bind ErbB1 and ErbB4. The third group is composed of the neuregulins (NRG) and forms two subgroups based upon their capacity to bind ErbB3 and ErbB4 (NRG-1 and NRG-2) or only ErbB4 (NRG-3 and NRG-4). ErbB2 has no direct ligand and needs a heterodimerization partner to acquire signaling potential ErbB3...has impaired kinase activity."
Kinase-active EGFR increases the amount of EGFR bound to PAK1. 1 / 1
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"In this study, we describe the specific interaction of PAK1 with the Grb2 adapter protein both in vitro and in vivo. We identify the site of this interaction as the second proline-rich SH3 binding domain of PAK1. Stimulation of the epidermal growth factor receptor (EGFR) in HaCaT cells enhances the level of EGFR-associated PAK1 and Grb2, although the PAK1-Grb2 association is itself independent of this stimulation. "
Modified mutated EGFR increases the amount of EGFR. 1 / 1
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"Expression of wild-type EGFR and mutant EGFR receptors increased p-EGFR levels compared with vector control or mutant K-ras retrovirus infected cells."
Kinase-active EGFR increases the amount of EGFR bound to TNK2. 1 / 1
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"The interaction of ACK1 with EGFR was dependent on the kinase activity or tyrosine phosphorylation of EGFR. "
Phosphorylated EGFR increases the amount of EGFR. 1 / 1
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"Cell line and human tumor models show that the CQ mediated impairment of maturation from endosome to lysosome results in decreased intralysosomal degradation of phosphorylated EGFR, which in turn causes over-expression of activated EGFR."
EGFR bound to TGFA increases the amount of EGFR. 1 / 1
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"Renal cancer produced a transforming growth factor-alpha (TGF-alpha), which bound to epidermal growth factor receptor (EGFR) and upregulated the expression of EGFR and TGF-alpha."
Kinase-active EGFR increases the amount of EGFR bound to SOS. 1 / 1
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"The dimerization of two EGFR family molecules leads to phosphorylation of C-terminal tyrosine residues either by autophosphorylation or by a SRC-related kinase followed by binding of GRB2, a RAS adaptor protein, at the SH2 domain of the receptor; binding of the proline-rich C-terminus of SOS, a guanine nucleotide exchange factor, to the SH3 domain of the receptor; exchange of a GTP from the receptor complex for a GDP from the RAS protein to form activated RAS; activation of phosphatidylinositol-3-kinase (PI-3 kinase) to initiate signaling by the biochemical pathways that are triggered by diacylglycerol production and protein kinase C activation; and activation of the series of cytoplasmic serine and threonine kinases beginning with RAF to initiate signaling by the biochemical pathways that are triggered by members of the MAPK family (e.g. ERK 1 and 2). EGFR signaling also activates other pathways in the cell including the Janus kinase (JAK)/signal transduction activators of transcription (STAT) pathways [80, 81]."
EGFR bound to EGF increases the amount of EGFR. 1 / 1
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"EGF binding to EGFR in PC3-AR cells exposed to 5alpha-DHT was increased, suggesting an upregulation of EGFR expression by androgens (XREF_FIG)."
Kinase-active EGFR increases the amount of EGFR bound to IRS1. 1 / 1
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"Significantly, challenge of Tam-R cells with the EGFR-selective tyrosine kinase inhibitor gefitinib, for 7 days, reduces IRS-1/EGFR association"
EGFR bound to Sigma-2 receptor increases the amount of EGFR. 1 / 1
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"Sigma-2 receptor associates with EGFR, increases plasma membrane EGFR levels and promotes invasion."