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A common polymorphism in the EGFR promoter was associated with altered promoter activity and gene expression both in vitro and in vivo. A common polymorphism in the EGFR promoter was associated with altered promoter activity and gene expression both in vitro and in vivo. A significantly higher frequency of EGFR expression occurred in PC than in AC glottic cancer. A subgroup of patients with non-small-cell lung cancer have specific mutations in the EGFR gene, which correlate with clinical responsiveness to the tyrosine kinase inhibitor gefitinib. A truncated form of the hEGFR ectodomain comprising residues 1-501, unlike the full-length hEGFR ectodomain (residues 1-621), binds hEGF and hTGF-alpha with high affinity and is a competitive inhibitor of EGF-stimulated mitogenesis. Activated epidermal growth factor receptor-Stat-3 signaling promotes tumor survival in non-small cell lung cancer. Active mutation of the EGFR kinase domain was strongly associated with response to gefitinib. An inhibitor of this and of the mTOR pathwway inhibits growth of glioma in a xenograft mousse model. Analysis with phospho-specific antibodies indicates that 3 kinases generate a signal-specific, combinatorial phosphorylation profile of the Hrs-STAM complex, with the potential of diversifying tyrosine kinase receptor signalling through a common element. Antisense epidermal growth factor receptor RNA transfection in human glioblastoma cells down-regulates telomerase activity and telomere length. Approximately 6% of breast carcinomas show EGFR amplification with EGFR protein overexpression and may be candidates for trials of EGFR-targeted antibodies or small inhibitory molecules. Breast carcinomas with squamous differentiation are a distinct subgroup of breast tumors with a very high frequency of EGFR expression. CaM co-immunoprecipitates with EGF-activated and non-activated receptors. Calmodulin binds to the EGFR. Carbon black causes oxidative stress-mediated proliferation of airway epithelium, involving activation of EGF-R. Cbl-CIN85-endophilin complex mediates ligand-induced downregulation of EGF receptors. Cbl-directed monoubiquitination of CIN85 is involved in regulation of ligand-induced degradation of EGF receptors. Cell proliferation, nuclear ploidy, and EGFr and HER2/neu tyrosine kinase oncoproteins in infiltrating ductal breast carcinoma. Cell surface expression of EGFR is associated with osteosarcoma pathogenesis. Characterization and expression of novel 60-kDa and 110-kDa EGFR isoforms in human placenta. Chemical/biological model for EGFR activation. Chromogenic in situ hybridization analysis and morphology identified 22 small cell (SCGBM) and 22 non-small cell glioblastoma (NSCGBM), and 12 cases of a mixed phenotype. Comparative study in the expression of p53, EGFR, TGF-alpha, and cyclin D1 in verrucous carcinoma, verrucous hyperplasia, and squamous cell carcinoma of head and neck region. Cpd 5-caused ERK phosphorylation is probably regulated by both EGFR-dependent and EGFR-independent pathways. Crystal structure of a truncated epidermal growth factor receptor extracellular domain bound to transforming growth factor alpha. Crystal structure of the complex of human epidermal growth factor and receptor extracellular domains. CsA affects EGF-r metabolism in gingival keratinocytes resulting in an increased number of cell surface receptors. Data demonstrate that at least four different sets of endogenously expressed gangliosides, including GD3, did not have a significant effect on epidermal growth factor receptor distribution in the plasma membrane. Data demonstrate that the alpha-hemolysin elevates the activity of receptor-like protein tyrosine phosphatase sigma (rPTPsigma). Data indicate that phospholipase A2 downregulates the EGF receptor-mediated intracellular signal transduction that may be mediated by arachidonic acid and/or ceramide. Data report that antagonism of the type 1 insulin-like growth factor receptor in combination with inhibitors of the epidermal growth factor receptor synergistically sensitizes human malignant glioma cells to CD95L-induced apoptosis. Data show that activation of ADAM-17 results in discrete cellular responses, while G protein-coupled receptor agonists promote activation of the Ras/MAPK pathway and cell proliferation via the epidermal growth factor receptor. Data show that blockade of epidermal growth factor receptor import into the nucleus also blocks radiation-induced activation of DNA-PK, inhibits DNA repair, and increases radiosensitivity of treated cells. Data show that by using RNA interference , the expression of endogenous erbB1 can be specifically and extensively suppressed in A431 human epidermoid carcinoma cells. Data show that detachment-induced expression of Bim requires a lack of beta(1)-integrin engagement, downregulation of EGF receptor (EGFR) expression and inhibition of Erk signalling. Data show that epidermal growth factor receptor dileucine motif 679-LL is an alpha-helical stabilizing motif that regulates a predominant step during lysosomal sorting, involving intracellular retention under both sub-saturating and saturating conditions. Data show that epidermal growth factor receptor signaling results in phosphorylation of CUG-BP1, and leads to increased binding of CUG-BP1 to CCAAT/enhancer binding protein beta (C/EBP beta) mRNA and elevated expression of the C/EBPbeta LIP isoform. Data show that expression of epidermal growth factor receptors (EGFR) in transgenic mouse Schwann cells elicited features of neurofibromas, supporting the relevance of EGFR to peripheral nerve tumor formation. Data show that human sprouty2 potentiates epidermal growth factor receptor signalling by specifically intercepting c-Cbl-mediated effects on receptor down-regulation. Data show that stimulation of epidermal growth factor receptors differentially regulates chemokine expression in keratinocytes. Data suggest the possibility of a mechanically activated epidermal growth factor receptor (EGFR) autocrine feedback loop involving selected EGFR ligands. Data support that EGFR and HER-2/neu play an important role in cell cycle control in ductal carcinoma in situ. Decorin causes EGFR internalization via caveolae. Dephosphorylation of the EGFR and the consequent suppression of EGFR signalling. Review. Detection of serum epidermal growth factor receptor in the diagnosis of proliferation of pituitary adenomas. Differential EGFR patterns by interphase cytogenetics in malignant peripheral nerve sheath tumor and morphologically similar spindle cell neoplasms. E-cadherin and epidermal growth factor receptor (EGFR) are associated in mammary epithelial cells and that E-cadherin engagement in these cells induces transient activation of EGFR, as previously seen in keratinocytes. EGF receptor down-regulation by UVA may play an important role in the execution of the cell suicide program by attenuating its anti-apoptotic function. EGF receptor expression was elevated in the prefrontal cortex in schizophrenic. EGF receptor is activated in a pathway that requires ARF4 to induce phospholipase D2. EGF receptor traffic is disrupted by farnesyltransferase inhibitors through modulation of the RhoB GTPase. EGF signalling amplification is induced by dynamic clustering of EGFR. EGFR and COX-2 cooperate to promote cervical neoplasm progression. EGFR and ErbB-2 have roles in ligand-dependent apoptosis that could be a natural mechanism to protect tissues from unrestricted proliferation. EGFR and c-Src-mediated Stat-3 activation is facilitated by Pyk2. EGFR antisense-odn can significantly inhibit proliferation of human hepatoma cells, indicating that EGFR may play important role in development of hepatoma and will be new target for its treatment. EGFR binds to c-src and has a role in oncogenesis. EGFR downregulation is inhibited by Sprouty2 targeting both the Cbl and CIN85 pathways. EGFR expression status in lung cancer correlates with its mutation. EGFR expression was associated with improved survival. EGFR gene 2073*T-related genotypes and allele are associated with higher susceptibilities to endometriosis and leiomyoma. EGFR gene expression is identified in recurrent glioblastoma multiforme. EGFR has a role in beta2 tyrosine phosphorylation of AP-2 by interacting at receptor 974YRAL and di-leucine motifs. EGFR has been detected in the nucleus and might function as a transcription factor to activate gene transcription. EGFR inhibition promotes desmosome assembly in oral squamous cell carcinoma cells, resulting in increased cell-cell adhesion. EGFR is a necessary component for HCMV-triggered signalling and viral entry. EGFR is an aldosterone-induced protein and is involved in the manifold (patho)biological actions of aldosterone. EGFR is increased by cAMP, a potent inducer of decidualization of the endometrial stroma. EGFR is often strongly expressed and is a potential therapeutic target in patients with malignant thymic tumors. EGFR microsatellite polymorphism is associated with autosomal dominant polycystic kidney disease. EGFR mutations were significantly related to histology and smoke exposure and were a strong predictive factor for gefitinib responsiveness in non-small cell lung cancers. EGFR overexpression is frequent in NSCLC, is most prominent in SCC, and correlates with increased gene copy number per cell. High gene copy numbers per cell showed a trend toward poor prognosis. EGFR physically interacts with signal transducers and activators of transcription 3 in the nucleus, leading to transcriptional activation of inducible nitric oxide synthase. EGFR regulation by E-cadherin was associated with complex formation between EGFR and E-cadherin that depended on the extracellular domain of E-cadherin but was independent of beta-catenin binding or p120-catenin binding. EGFR signaling has a role in regulating host defense and immune response by tightly controlling TLR2 induction during bacterial infections. EGFR signaling involves reinforcing altered gene expression of uPAR,thus further inducing cell motility. EGFR, DI, and the diploid are valuable targets for judging metastasis and recurrence of gastric cancer before and after operation. EGFR, PYK2, Yes, and SHP-2 are involved in transduction of the TF/FVIIa signal possibly via transactivation of the EGF receptor. EGFR, c-erbB-2, VEGF and MMP-2 and MMP-9 play an important role in tumor growth, invasion and metastasis in squamous cell carcinoma of the head and neck. EGFR-related protein (ERRP) is a 53 to 55 kDa protein that is a natural inhibitor of EGFRs in human but not in mouse or rat cells. EGFR/HER2 heterodimers traffic as single entities; levels of HER2 in normal cells are barely at the threshold necessary to drive efficient heterodimerization. EGFRvIII expressed in human tumors is phosphorylated and hence activated; sustained activation of EGFRvIII is implicated in the pathogenesis of non-small cell lung cancers. ERBB1 is overexpressed and may play a role in high-grade diffusely infiltrative pediatric brain stem glioma. Effects of pharmacologic antagonists of epidermal growth factor receptor, PI3K and MEK signal kinases on NF-kappaB and AP-1 activation and IL-8 and VEGF expression in human head and neck squamous cell carcinoma lines. Egfr Wa5 is a novel ENU-induced antimorphic allele caused by a kinase-dead receptor acting as a dominant negative. Endocytosis is regulated by Grb2-mediated recruitment of the Rab5 GTPase-activating protein RN-tre. Endothelial cell vessel assembly requires EGFR signaling transduction pathways. Epidermal growth factor and ionizing radiation up-regulate the DNA repair genes XRCC1 & ERCC1 in DU145 & LNCaP prostate carcinoma through MAPK signaling indicating a capacity of the EGFR-ERK signaling to modulate DNA repair in cancer cells. Epidermal growth factor receptor (a potential therapeutic target) and SALL2 stained most cases of synovial sarcoma; staining was significantly less common among other tested sarcomas. Epidermal growth factor receptor gene polymorphisms have higher risk of pelvic recurrence in patients with rectal cancer treated with chemoradiation. Epidermal growth factor receptor negatively regulates intracellular kinase activation in the absence of ligand. Epidermal growth factor receptor-independent constitutive activation of STAT3 in head and neck squamous cell carcinoma is mediated by the autocrine/paracrine stimulation of the interleukin 6/gp130 cytokine system. ErbB1 and ErbB2 employ different mechanisms of plasma membrane targeting during keratinocyte differentiation; cytoskeletal association may facilitate the coupling of activated ErbB1 and ERK. Existence of unidirectional IGF-IR/EGFR cross-talk mechanism whereby IGF-II, acting through IGF-IR, regulates basal and ligand-activated EGFR signaling and cell proliferation in a c-SRC-dependent manner in tamoxifen-resistant breast cancer. Exogenous OPN increased EGFR mRNA expression, as well as EGFR kinase activity. Inhibition of EGFR significantly impaired the cell migration response to OPN. Expression of EGF and EGFR is involved in the gallbladder carcinogenesis, and is related to high activity of cell proliferation. Expression of EGFR seems to play an important role in metastasis, especially liver metastasis and recurrence of pancreatic cancer. Expression of nuclear EGFR correlated positively with increased levels of cyclin D1 and Ki-67, both are indicators for cell proliferation for prognosis of breast cancer. Expression of the invasive phenotype in breast epithelial cells requires increased EGF receptor signaling, involving both PI 3-kinase and Erk 1,2 activities, which leads to enhanced secretion of MMP-9 and transcription of invasion-related genes. Expression of this molecule and its correlation with prognostic markers in patients with head and neck tumors. Findings provide evidence that STAT 3 signal activity in head and neck carcinomas, which is partially responsible for proliferative activity, can be controlled via the EGFR. Findings suggest that a distinct minority of colorectal adenocarcinomas exhibit somatic mutations of EGFR, and these tumors may be susceptible to gefitinib treatment. Five autophosphorylation sites in the extra-kinase C-terminal domain of EGFR are not required for the ability of EGFR to induce morphological differentiation of PC12 cells. For genotype of EGFR gene Bsr I polymorphism, there was statistically significant differences between systemic lupus erythematosus and controls. In addition, there was significant association between the two groups in allelic frequency of the T allele. Gastrin-releasing peptide receptor mediates activation of the epidermal growth factor receptor in lung cancer cells. Gene 33 is a physiological feedback inhibitor of the EGFR, functioning to inhibit EGFR phosphorylation and all events induced by EGFR activation. GqPCR-induced FAK activation is mediated by via a pathway involving transactivation of the EGFr and alterations in the actin cytoskeleton. Grb2-mediated recruitment of the functional RING domain of Cbl to the EGFR is essential and sufficient to support receptor endocytosis. HB-EGF/HER-1 signaling is relevant to mesenchymal stem cell biology, by regulating both proliferation and differentiation. HDL blocks neuroblastoma differentiation by inhibition of EGFR. HEGFR was expressed in the subventricular zone embryologically. HER2-mediated effects on EGFR dimerization and trafficking were sufficient to explain the observed HER2-mediated amplification of epidermal growth factor-induced ERK signaling. Helicobacter pylori-stimulated EGF receptor transactivation requires metalloprotease cleavage of HB-EGF. High EGFR gene copy number identified by FISH may be an effective molecular predictor for gefitinib efficacy in advanced NSCLC. High frequency of epidermal growth factor receptor mutations with complex patterns in non-small cell lung cancers related to gefitinib responsiveness. Human colon carcinoma cells that overexpress cyclooxygenase exhibit growth stimulation and induction of this protein. Human cytomegalovirus infection inhibits epidermal growth factor (EGF) signalling by targeting EGF receptors. Human leukocyte elastase induces keratinocyte proliferation by proteolytic activation of an EGFR signaling cascade involving TGF-alpha. IL-1beta-dependent prolonged EGFR transactivation involves multiple pathways, including an IL-8-dependent pathway. Identification of epidermal growth factor receptor as a target of Cdc25A protein phosphatase. In addition to EGFR mutations, other factors in non-small cell lung carcinoma cells, such as high expression of ErbB family members, may constitutively activate AKT and sensitize cells to EGFR inhibitors. In each of these gliomas, the founding molecule was generated by a simple event that circularizes a chromosome fragment overlapping the epidermal growth factor receptor gene. In patients with breast cancer, most CNS metastatic tumor deposits showed expression for either EGFR or HER-2/neu, and less often for both. Increased levels of EGFR were significantly associated with adult soft tissue sarcomas. Infection of primary cells with adenoviruses carrying the relevant point mutations confirmed the crucial role of putative YXX Phi and dileucine (LL) transport motifs within Ad2 10.4-14.5 for down-regulation of Fas, TRAIL-R1, TRAIL-R2, and EGFR. Inhibition of erbB receptor family members protects HaCaT keratinocytes from ultraviolet-B-induced apoptosis. This inhibition was specific for the erbB receptor family and specific for ultraviolet-B-induced apoptosis. Intensive staining of EGF-R is associated with invasive tumours of bladder. Interaction of the extracellular domain of the epidermal growth factor receptor with gangliosides. Levels of this receptor are lowered in cryptorchism. Ligand-induced EGFR degradation is preceded by proteasome-dependent EGFR de-ubiquitination. Loss of PTEN/MMAC1/TEP in tumor cells expression this protein counteracts the antitumor action of EGFR tyrosine kinase inhibitors. Mitogenic effects of gastrin-releasing peptide in head and neck squamous cells are mediated by activation of EGFR. Mutations in either the EGFR TK domain or the KRAS gene can lead to lung cancer pathogenesis. EGFR TK domain mutations are the first molecular change known to occur specifically in never smokers. Mutations in the tyrosine kinase domain of the epidermal growth factor receptor is associated with non-small cell lung cancer. Mutual interaction of EGFR with c-Src is required for many EGFR-mediated cellular functions including proliferation, migration, survival and EGFR endocytosis, as discussed in this review. NHERF stabilizes EGFR at the cell surface and slows the rate of endocytosis without affecting recycling. Nitric oxide and nitric oxide donors induce EGF receptor phosphorylations, in A431 tumor cells. Our findings suggest that extracellular H(2)O(2) generated by EGFR-ligand interaction permeates the plasma membrane and inhibits EGFR-associated tyrosine phosphatase activity. Our results suggest a novel role for the juxtamembrane domain (JM) of EGFR in mediating intracellular dimerization and thus receptor kinase activation and function. Overall, these data suggest that GRK2 has a regulatory role in EGF-induced ERK/MAPK activation. Overexpression of EGFR is associated with recurrent non-small cell lung cancer. Overexpression of EGFR was observed in only a small fraction of colorectal carcinomas, but were frequently accompanied by gene amplification. Overexpression of an introduced EGFR, under an E1A-insensitive heterologous promoter, blocked E1A induction of apoptosis in SCC cells. E1A-mediated EGFR downregulation appears to be the cause not consequence of E1A-induced apoptosis in these cells. P. 445:""The EGF receptor (EGFR), a glycoprotein of 170 kDA, has also been intensily studied and finally located on chromosome 17, region p13l13-q22. PGE2 regulates cell migration via the EGFR, and affects cell division and neoplasm invasiveneess. PGF(2 alpha)-FP receptor may promote endometrial tumorigenesis via phospholipase C-mediated phosphorylation of EGF receptor and MAPK signaling pathways. PLSCR1, through its interaction with Shc, promotes Src kinase activation through the EGF receptor. PMA transactivates the EGFR and increases cell proliferation by activating the PKCdelta/c-Src pathway in glioblastoma cells. PPARgamma and EGFR signalling have roles in urothelial terminal differentiation. PTEN protein could inhibit cell invasion even in the presence of the constitutively active epidermal growth factor receptor(EGFR). Rac activation upon cell-cell contact formation is dependent on signaling from here. Results demonstrate that mice humanised for epidermal growth factor receptor (EGFR) display tissue-specific hypomorphic phenotypes and describe a novel function for EGFR in bone development. Results describe the role of epidermal growth factor receptor regulation in antiapoptosis, cell migration, and cell proliferation. Results provide an explanation for cell surface receptor cross-talk involving the Met receptor and link G protein-coupled receptors and the epidermal growth factor receptor to the oncogenic potential of Met signaling in human carcinoma cells. Results show that the juxtamembrane region of the epidermal growth factor receptor is necessary for accurate polarized expression of the native molecule. Results suggest that epidermal growth factor receptor and protein kinase C activation are involved in 12- O-tetradecanoylphorbol-13-acetate-induced cell signaling for modulation of cadherin-dependent cell-cell adhesion and cell shape in Caco-2 cells. Review. Mucin transcription in response to both gram-positive bacteria and tobacco smoke is mediated through activation of the epidermal growth factor receptor (EGFR). S1P transactivates c-Met and EGFR in gastric cancer cells. SHP-2/Gab1 association is critical for linking EGFR to NF-kappaB transcriptional activity via the PI3-kinase/Akt signaling axis in glioblastoma cells. SKMG-3 cells produced high levels of EGFR protein. Signals from overexpressed EGFRs contribute to the constitutive phosphorylation of Erk, but these signals may not be required for the constitutive activation of PI3K or AKT1. Seasonal allergic rhinitis subject showed significant elevation in EGFR expression, consistent with the observation of mucus hypersecretion in allergic rhinitis. Src-dependent phosphorylation of the EGFR at Tyr-845 is required for EGFR transactivation and zinc-induced Ras activation. Statistically significant relation existed between the ovarian cancer metastatic potential and EGFR expression level. Stimulation of cells with EGF rapidly leads to phosphorylation of Hrs, raising the question whether the EGF receptor tyrosine kinase phosphorylates Hrs directly. Several downstream kinases, rather than the active receptor kinase are responsible. Sustained hyaluronan depolymerization is expected to cause tissue kallikrein activation, EGF release, and EGFR signaling. Syk acts a negative control element of EGFR signalling. TPA-induced AP-1 activation requires EGFR protein, but not EGFR tyrosine kinase and EGFR autophosphorylation at tyrosine(1173), whereas both EGFR tyrosine kinase and EGFR autophosphorylation at Y(1173) play a critical role in EGF-induced AP-1 activation. The EGFR pathway may be a specific, signal transduction pathway that regulates reactive astrocytes to form cavernous spaces in the glial scars following CNS injury and in the compressed optic nerve in glaucomatous optic nerve neuropathy. The Id-1-induced androgen-independent prostate cancer cell growth was correlated with up-regulation of EGF-R. The cytoplasmic overexpression of EGFr plays a significant role in the progression of pancreatic ductal adenocarcinoma, especially in the invasion and acquisition of aggressive clinical behavior. The data presented here demonstrate that, in contrast to activation by the cytokine, growth hormone (GH), the activation of STAT5b by the growth factor, epidermal growth factor (EGF), requires overexpression of the EGF receptor (EGFR). The effects of high glucose on proximal tubular cells proliferation, reduced apoptosis and increased NHE3 mRNA levels are mediated by EGFR-dependent up-regulation of SGK-1. The epidermal growth factor receptor (EGFR) is one of signalling pathways activated during premalignant proliferative changes in the airway epithelium. The expression of this protein was not different in the clone cell variants or the A431 parental line. The frequency of CA allele combinations was assessed in healthy women from Poland; results provide new data on EGFR microsatellite instability and may contribute to the understanding of EGFR gene expression regulation. The mechanism of deoxycholic acid-induced EGFR activation is ligand-dependent and is controlled, at least in part, at the level of amphiregulin release from the basolateral cell membrane. The membrane-anchoring domain of EGFR ligands dictates their ability to operate in juxtacrine mode. The optimization and specification of therapeutic approaches based on erbB-receptor targeting requires to account for EGFR coexpression as well as the potential presence of erbB-receptor relevant growth factors. The overall time-dependent activation of EGFR autophosphorylation was identical in cells treated with 1 nm BTC or 1.5 nm EGF. The reduction in EGFR levels and EGF-induced signaling in SOCS5-expressing cells requires both the Src homology-2 and SOCS box domains of SOCS5. The results of this study indicate that dual inhibition of focal adhesion kinase (FAK) and epidermal growth factor receptor (EGFR) signaling pathways can cooperatively enhance apoptosis in breast cancers. The results suggest that activation and nuclear localization of EGFR may be needed for induction of NOS-2 in response to elevated intraocular pressure in glaucomatous optic neuropathy. The study found that over-expression of EGFR occurred more often in cases of cervical cancer (50%) compared to breast cancer cases (36%), while in breast cancer EGFR expression correlated significantly with metastasis of the lymph nodes. The timing of lethality caused by homozygosity for a null allele of the epidermal growth factor receptor in mice is strongly dependent on genetic background. The tumor-specific mutation of epidermal growth factor receptor promotes cells survival and dimerization with the wild-type EGFR. These data demonstrate a distinct radiation response profile at the transcriptional level that is dependent on enhanced EGFR/Ras/MAPK signaling. These results demonstrate that 1,25(OH)(2)D(3) alters EGFR membrane trafficking and down-regulates EGFR growth signaling. These results identify CKLFSF8 as a novel regulator of EGF-induced signaling and indicate that the association of EGFR with four transmembrane proteins is critical for EGFR desensitization. These results indicate that epidermal growth factor (EGF) receptors can form a ligand-independent inactive dimer and that receptor dimerization and activation are mechanistically distinct and separable events. These results indicate that the EGFR signaling pathway is involved in urothelial regeneration. These results suggest a possible important ""cross-talk"" between SDF-1/CXCR4 and EGFR intracellular pathways that may link signals of cell proliferation in ovarian cancer. These results suggest that EGFR amplification is a relatively rare event in larynx carcinogenesis that obviously does not predispose to tumor progression. This study suggests that coexpression of LN-5 gamma2 and EGFR is closely related to the progression and poor prognosis of esophageal SCC. Trypsin exerts robust trophic action on colon cancer cells and underline the critical role of EGF-R transactivation. Two tyrosine residues in the C terminus of human TRPC4 phosphorylated following epidermal growth factor (EGF) receptor stimulation of COS-7 cells. Tyr-992 and Tyr-1173 are required for phosphorylation of the epidermal growth factor receptor by ionizing radiation and modulation by SHP2. Up-regulation of EGFR is associated with renal cell carcinoma. Upregulation of leucine-rich repeats and immunoglobulin-like domains 1 is followed by enhanced ubiquitylation and degradation of EGFR. Using the LightCycler PCR assay, the EGFR L858R mutation status might correlate with gender, pathologic subtypes, and gefitinib sensitivity of lung cancers. YB-1 overexpression can induce EGF independence in human mammary epithelial cells via activation of the EGFR pathway. ZO-1 bound to EGFR irrespective of the phosphorylation status of EGFR. EGFR associated ZO-1 was highly tyrosine-phosphorylated only in primary colorectal cancers but was dephosphorylated in the liver-metastasized cancers. A novel and important role for metalloprotease activation and EGFR transmodulation in mediating the cellular response to TNF. A novel regulatory role for Galphas in EGF receptor degradation and provide mechanistic insights into the function of Galphas in endocytic sorting. Activation regulates mutation and epidermal growth factor receptor activation regulates vascular endothelial growth factor mRNA expression in human glioblastoma cells by transactivating the proximal VEGF promoter. Amphiregulin- and ErbB1-dependent mechanism by which autocrine ERK activation is maintained in normal keratinocytes. An interrelationship is now known to exist between the IGF and EGF receptors [review]. Analysis of activating mutations in catalytic domain of EGFR in 3.5% (2 of 57) of ovarian cancers. Analysis of conformations of the epidermal growth factor receptor and antibody binding [review]. Analysis of ligand-induced dimer-tetramer transition during the epidermal growth factor receptor activation of the cell surface. Androgens promote an increase in the activity of the epidermal growth factor (EGF)-network by increasing ErbB1 levels, and this activity of is essential for androgen-induced proliferation and survival of the prostate cancer LNCaP cell line. Autocrine and/or paracrine NRG-1/erbB signaling promotes neoplastic Schwann cell proliferation. Betacellulin may play a role as a local growth factor in promoting the differentiated villous trophoblastic function via ErbB-1 in early placentas and in contributing to placental growth through EVT cell function via ErbB-4 in term placentas. Blocking of ubiquitination by inhibiting Src family kinases. C-erbB-2 and EGF-R are overexpressed in breast neoplasms and have an inverse association with Estrogen Receptor expression. Carboxyl-terminal mutation of the epidermal growth factor receptor alters tyrosine kinase activity and substrate specificity. Caveolin-1/EGFR association and is critical for the EGF-induced tyrosine phosphorylation of caveolin-1 that is associated with its inhibition of EGFR activation. Cholangiocarcinoma cells exhibit sustained EGFR activation due to defective receptor internalization. Cholesterol depletion with cyclodextrin induced an increase in both basal and EGF-stimulated EGF receptor phosphorylation, at specific tyrosine sites, that was associated with an increase in the intrinsic kinase activity of the EGF receptor kinase. Contig map for the EGFR region and markers positioned on its associated physical map to the analysis of 7p11.2 amplifications in a series of glioblastomas. Data demonstrate that prostaglandin E2 transactivates EGFR and triggers mitogenic signaling in gastric epithelial and colon cancer cells as well as in rat gastric mucosa in vivo. Data explain how thrombin exerts robust trophic action on colon cancer cells and underline the critical role of EGFR transactivation. Data indicate that altered expression of beta-catenin may play an important role in oral cancer progression through increased proliferation and invasiveness under epidermal growth factor receptor (EGFR) activation but not mutation or cyclin D1 expression. Data indicate that growth hormone, by activating extracellular signal related kinases, can modulate epidermal growth factor-induced epidermal growth factor receptor trafficking and signaling. Data suggest that agonist-induced binding of Src kinase to the Src homology 3 binding sites in the P2Y(2) purinergic receptor facilitates Src activation and allows Src to efficiently phosphorylate the epidermal growth factor receptor. Data suggest that mutations of epidermal growth factor receptor (EGFR) and K-RAS genes might separately, but not cooperatively, contribute to lung adenocarcinoma pathogenesis. Decreased EGF receptor tyrosine phosphorylation and aberrant recruitment of the adaptor proteins ShcA and Grb2 to the EGF receptor in cells harbouring the hepatitis C virus subgenomic replicon. DeltaEGFR may contribute to glioblastoma development. Demonstration that metalloproteinase-mediated transactivation of the EGFR is a key mechanism of the cellular signalling network that promotes MAPK activation as well as tumour cell migration and invasion. Depending on their localization, oxytocin receptors transactivate EGFR and activate ERK1/2 using different signalling intermediates. The final outcome is a different temporal pattern of EGFR and ERK1/2 phosphorylation. Determination of decorin binding site. Determination of whether G protein-coupled receptor kinase-2 can phosphorylate and desensitize epidermal growth factor receptor. Effects of receptor-selective retinoid ligands on EGFR-associated signal transduction. Endosomal epidermal growth factor receptor stimulates cell growth. Epidermal growth factor receptor (avian erythroblastic leukemia viral (v-erb-b) oncogene homolog). Epidermal growth factor receptor activity on fertilization capacity of testicular harvested spermatozoa. Epidermal growth factor receptor and CD95 activation are triggered by Src family kinase Yes. Epidermal growth factor receptor interacts with gastrointestinal peptide hormone receptors to regulate mitogenic signaling and cell migration [review]. Epidermal growth factor receptor is activated by imatinib mesylate, resulting in cyclooxygenase-2 induction and prostaglandin E2 accumulation. Epidermal growth factor receptor is dephosphorylated at endomembranes after ligand-mediated endocytosis. Epidermal growth factor receptor may have a role in disease relapse and progression to androgen-independence in human prostate cancer. Estrogen transactivates the epidermal growth factor receptor (EGFR) to MAP K signaling axis via GPR30;implications for breast cancer biology. Fibrin can support the wound healing process of the epidermis via the TGF-alpha/EGF-R pathway. Findings establish Cbl protein as the major endogenous ubiquitin ligase responsible for epidermal growth factor receptor degradation. Findings suggest an increase in functional TGF-alpha and activation of the EGFr in response to IFN-gamma. Findings suggest that the coexpression of c-erbB-2 oncogene protein, epidermal growth factor receptor, and TGF-beta1 in pancreatic ductal adenocarcinoma is related to the histopathological grades and clinical stages of tumors. Ganglioside GM3 inhibits integrin-induced, ligand-independent epidermal growth factor receptor phosphorylation (cross-talk) through suppression of Src family kinase and phosphatidylinositol 3-kinase signaling. Heregulin/EGFR system as a possible important physiologic growth regulatory system in melanocytes in which multiple deregulations may occur during progression toward melanoma, all resulting in, or indicating, growth factor independence. Heterogeneity in the density of EGFR due to localization in certain regions of the plasma membrane, which has been experimentally reported, can also lead to concave up shape of the Scatchard plot of the EGF binding on EGFR. Hydrogen peroxide increases cPLA(2) activity through its phosphorylation utilizing an epithelial growth factor/Ras/extracellular signal-regulated kinase and p38 pathway. Identification of ligand-induced site-specific phosphorylation of epidermal growth factor receptor. In glioblastoma multiforme patients a complex relationship exists between epidermal growth factor receptor expression and age. Involvement urokinase plasminogen activator secretion and cell motility in breast cancer cells. Ligand-independent activation of the epidermal growth factor receptor is triggered by cholesterol depletion from the plasma membrane. Lysosomal degradation by adenovirus E3 RIDalpha protein dependent on specific domains. Mediates increased cell proliferation, migration, and aggregation in esophageal keratinocytes in vitro and in vivo. Mediation of synergism with c-src by STAT5b. Misfolding of the LDLR epidermal growth factor-AB pair results from low density lipoprotein receptor familial hypercholesterolemia mutations. Mutant EGFRs selectively transduce survival signals on which nonsmall cell lung cancers become dependent. Novel mechanism by which IGF-I induces ERK activation in a manner that is dependent on the basal level of EGFR-TK activity, but is independent of receptor transactivation. Novel mechanism of EGFR internalization that does not require ligand binding, receptor kinase activity, or ubiquitylation and does not direct the receptor into a degradative pathway. Overexpression of the active form of the small GTPase RhoA induces the activation of Epidermal Growth Factor Receptor and promotes cell motility. P38 mediates EGF receptor activation after oxidant injury; Src activates MMK3, which, in turn, activates p38; and the EGF receptor signaling pathway plays a critical role in renal epithelial cell dedifferentiation. Propose a role of Ent-1 in the trafficking of EGFR to down-regulate intestinal mitogenic signals, highlighting the mechanisms of cell growth arrest associated with enterocytic differentiation. Protein kinase B/Akt phosphorylation is stimulated by mechanical stretch in epidermal cells via angiotensin II type 1 receptor and epidermal growth factor receptor. Regulation of LMP1 on the nuclear translocation of EGFR is critical for the process of nasopharyngeal carcinoma. Regulation of phosphorylation of ER-alpha and EGFR may play critical roles in EGF-induced transcriptional activation of WISP-2 gene in breast tumor cells. Results demonstrate that tamoxifen resistant MCF-7 cell growth is mediated by the autocrine release and action of an epidermal growth factor receptor-specific ligand inducing preferential epidermal growth factor receptor/c-erbB2 dimerization. Results show that EGFR are present on normal human melanocytes. Results suggest a potential mechanism by which maintenance of low levels of EGFR expression and subsequent EGFR upregulation may be attributed to the loss of transcriptional repression of EGFR gene expression in hormone-dependent breast cancer cells. Results support a structural model for oligomerization of EGF receptors in which dimers are positioned head-to-head with respect to the ligand-binding site. Role for EGFR activity in the lifespan and inflammatory potential of RSV-infected epithelial cells. Role in mediating thromboxane A2-dependent -signal-regulated kinase activation. Second cysteine-rich region contains targeting information for caveolae/rafts. Sequestration in non-caveolar lipid rafts inhibits lipid binding. Serum epidermal growth factor receptor and HER2 have roles in response of advanced non-small cell lung cancer to chemotherapy. Signaling intensity determines intracellular protein interactions, ubiquitination, and internalization. Simulation results show the formation of a channel under Thr766 following the movement of the side chain of Gln767 away from the hinge in EGFR. Somatic mutations of EGFR were found in 15 of 58 non-small cell lung cancer tumors from Japan and 1 of 61 from the United States; EGFR mutations may predict sensitivity to gefitinib. Sorting of endocytosed epidermal growth factor receptor into the degradation pathway requires both its kinase activity and actin-binding domain. Study reveals a novel cross-talk between the EP1 receptor and EGFR signaling that synergistically promotes cancer cell growth and invasion. Targeting in cancer, involved in apoptosis (REVIEW). The EGF receptor is abundantly expressed in epithelioid vascular smooth muscle cells and the activation of this receptor results in cell cycle arrest through activation of the mitogen-activated protein kinase pathway. The EGF receptor plays a central role in the signaling pathway that links albumin to the activation of ERK1/ERK2 and increased expression of IL-8. The acceleration of EBV LMP1 on the G1/S transition via the nuclear accumulation of EGFR was critical in the process of nasopharyngeal carcinoma. The adhesion-dependent activation of EGF receptor signaling is promoted by L1-type CAMs in vitro and in vivo. The effect of interleukin-8 (IL-8) induced by H. pylori infection on EGFR transactivation and epithelial cell growth. The epidermal growth factor receptor has a role in activating ERK with extracellular oxidation by taurine chloramine. The mechanism of attenuated ERK signaling in EGFR-overexpressing cells is a sequestration of ERKs at the cell membrane in EGFR-containing complexes. The relationship between the egfr polymorphism and breast cancer risk. Therapeutic potential of siRNA to impact DeltaEGFR as a glioma-specific target. This study, 11 analogs of a fragment of the B-loop of EGF-related peptides from several species were synthesized to study binding to A431 human epidermoid carcinoma using both 125I-EGF and [3'4'-3H-Tyr(22,29), Abu(20,31)]EGF(20-31)-NH(2). Thrombomodulin induces Ca2+ signals and nitric oxide synthesis through EGFR and calmodulin kinase II. Trans-activation by calcium-sensing receptor. Transactivation of the EGFr is required for the full expression of cAMP-dependent Cl- secretory responses. Transactivation through CCR3 is a critical pathway that elicits mitogen-activated protein kinase activation and cytokine production in bronchial epithelial cells. Whole gene amplifications of egfr are rare in invasive breast cancer and explain protein overexpression in only about 12.5% of invasive breast cancer cases.
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