抗Human EGFR 抗体:
抗Rat (Rattus) EGFR 抗体:
抗Mouse (Murine) EGFR 抗体:
Human Polyclonal EGFR Primary Antibody for IHC, WB - ABIN6713327
Li, Sun, Fang, Han, Luo, Wang, Pan, Hu, Zhang, Pao, Shen, Ji, Chen: Lung adenocarcinomas with HER2-activating mutations are associated with distinct clinical features and HER2/EGFR copy number gains. in Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer 2012
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Human Polyclonal EGFR Primary Antibody for CyTOF, ELISA (Capture) - ABIN4899925
Sarup, Jin, Turin, Bai, Beryt, Brdlik, Higaki, Jorgensen, Lau, Lindley, Liu, Ni, Rozzelle, Kumari, Watson, Zhang, Shepard: Human epidermal growth factor receptor (HER-1:HER-3) Fc-mediated heterodimer has broad antiproliferative activity in vitro and in human tumor xenografts. in Molecular cancer therapeutics 2008
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Human Polyclonal EGFR Primary Antibody for WB - ABIN3042517
Ge, Yu, Petitte, Zhang: Epidermal growth factor-induced proliferation of chicken primordial germ cells: involvement of calcium/protein kinase C and NFKB1. in Biology of reproduction 2009
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Human Polyclonal EGFR Primary Antibody for IHC - ABIN966041
Buerger, Nagel-Wolfrum, Kunz, Wittig, Butz, Hoppe-Seyler, Groner: Sequence-specific peptide aptamers, interacting with the intracellular domain of the epidermal growth factor receptor, interfere with Stat3 activation and inhibit the growth of tumor cells. in The Journal of biological chemistry 2003
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Human Polyclonal EGFR Primary Antibody for ELISA (Detection), FACS - ABIN4899924
Gonzalez, Seurynck-Servoss, Crowley, Brown, Omenn, Hayes, Zangar: Development and validation of sandwich ELISA microarrays with minimal assay interference. in Journal of proteome research 2008
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Human Polyclonal EGFR Primary Antibody for CyTOF, FACS - ABIN4900628
Weissenbacher, Vrekoussis, Roeder, Makrigiannakis, Mayr, Ditsch, Friese, Jeschke, Dian: Analysis of Epithelial Growth Factor-Receptor (EGFR) Phosphorylation in Uterine Smooth Muscle Tumors: Correlation to Mucin-1 and Galectin-3 Expression. in International journal of molecular sciences 2013
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Human EGFR Primary Antibody for IHC - ABIN966039
Yamamasu, Sato, Ogita, Inoue: Role of glutathione metabolism and apoptosis in the regression of liver hemopoiesis. in Free radical biology & medicine 1997
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Human Polyclonal EGFR Primary Antibody for IHC - ABIN966047
Burnett, Barrow, Cohen, Snyder, Sabatini: RAFT1 phosphorylation of the translational regulators p70 S6 kinase and 4E-BP1. in Proceedings of the National Academy of Sciences of the United States of America 1998
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Human Monoclonal EGFR Primary Antibody for IHC (f), ICC - ABIN1027691
Fortunel, Hatzfeld, Rosemary, Ferraris, Monier, Haydont, Longuet, Brethon, Lim, Castiel, Schmidt, Hatzfeld: Long-term expansion of human functional epidermal precursor cells: promotion of extensive amplification by low TGF-beta1 concentrations. in Journal of cell science 2003
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Human Polyclonal EGFR Primary Antibody for WB - ABIN5518909
Salenius, Haapanen, Harju, Jokela, Riekkinen: Late carotid restenosis: aetiologic factors for recurrent carotid artery stenosis during long-term follow-up. in European journal of vascular surgery 1989
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Results indicated that most periocular squamous cell carcinomas of horses expressed epidermal growth factor receptor (EGFR) and human epidermal growth factor receptor 2 (HER2).
In segmentation mutants, where specific peaks of EGFR ligands fail to form, gaps in signaling activity appear, leading to coincident hid up-regulation and subsequent cell death. In wild-type embryos, the segmentation cascade elicits the segmental production of several epidermal growth factor receptor (EGFR) ligands, including the transforming growth factor Spitz (TGFalpha), and the neuregulin, Vein.
In this study, whole genome expression analysis was performed to identify genes activated by JAK/STAT and/or EGFR..AdamTS-A mRNA becomes enriched at the anterior and posterior poles of the egg chamber at stages 6 to 7 and is regulated by JAK/STAT.
Wnt signaling functions genetically upstream of EGFR signaling by activating the expression of the EGFR ligand, Spitz.
The somatic EGFR-ERK activity appeared to regulate the termination of Bam expression in the germline and promote subsequent differentiation to the spermatocyte stage.
stress-dependent EGFR/MAPK promotes gut regeneration via a novel mechanism that operates independently of Insulin/Pi3K/TOR signaling.
EGFR/ARF6 regulation of Hh signaling stimulates oncogenic Ras tumor overgrowth in Drosophila.
Graf functions to downregulate EGFR signaling.
Data show that EGFR controls the proper formation of brain neuroblasts by regulating the number, survival and proneural gene expression of neuroectodermal progenitor cells which suggest that EGFR signalling is crucially important for patterning and early neurogenesis of the brain.
The activity of Gro is antagonized by EGFR signaling, which inhibits Gro-dependent repression via p-ERK mediated phosphorylation.
These results reveal that ESCRT-0 (ESCRT-0 components stam and hrs)mutants inhibit EGFR signaling by disrupting Rhomboid endosomal trafficking in the ligand-producing cells.
we find that EGFR regulates the apical determinant Crb and the extracellular matrix regulator Serp, two factors previously known to control tube length. EGFR regulates the organisation of endosomes in which Crb and Serp proteins are loaded
Here we uncover a cell non-autonomous requirement for the Epidermal growth factor receptor (Egfr) pathway in the lateral epidermis for sustained dpp expression in the LE. Specifically, we demonstrate that Egfr pathway activity in the lateral epidermis prevents expression of the gene scarface (scaf), encoding a secreted antagonist of JNK signaling
Loss of Usp5 results in upregulation of Notch signaling and downregulation of RTK signaling by EGF receptor (EGFR) and Sevenless (Sev), leading to impaired photoreceptor development.
These data demonstrate a strong genetic link between dG9a and the EGFR signaling pathway.
Avermectin directly interacts with EGFR and leads to the activation of the EGFR/AKT/ERK pathway.
The dorsoventral patterning and EGFR signaling genes play essential roles in correct identity determination and differentiation of lateral glia in the Drosophila nervous system.
Data suggest that OSCP1 (organic solute carrier partner 1) plays multiple roles during eye development in D. melanogaster; OSCP1 regulates developmental gene expression and epidermal growth factor receptor signaling pathway in imaginal discs of eye.
The vector of cell movement is regulated by localised epidermal growth factor (EGF) signalling from the distally placed tip cell lineage and the acquisition of planar polarity leads to asymmetric pulsatile Myosin II accumulation.
Our findings provide in vivo evidence for the role of adult neurons in the maintenance of glia and a novel role for EGFR signaling in the autophagic flux.
Gro inhibits rho expression in undifferentiated cells and represses the expression of both ato and rho in non-R8 precursors during initiation of photoreceptor differentiation in an E(spl)-dependent manner.
Combination of an EGFR tyrosine kinase inhibitor and a NF-kappaB inhibitor effectively suppressed cetuximab-resistant HNSCC and interfering with the EGFR-LTbeta interaction reverses resistance.
Study demonstrated that IGF-I can stimulate egfr expression in both follicles cell culture and intact follicles promoting oocyte maturation.
These results indicate that maintenance of Pgrmc1 signaling is required for Egfr expression on zebrafish oocyte cell membranes and for conserving the functions of Egfr in maintaining meiotic arrest through estrogen activation of Gper.
EGFR signaling in vertebrate oocytes can prevent meiotic progression.
the expression of EGFR was mainly restricted to the follicle cells with little expression in the oocytes
microRNA-21 and microRNA-206 closely correlate with ER, PR, and HER2 expression, which can be considered as clinical biomarkers
Patients with EGFR exon20ins have similar clinical characteristics.
The de novo T790M EGFR mutation is a relatively unfavorable prognosis factor for lung adenocarcinoma patients receiving first-line tyrosine kinase-inhibitor treatment.
MAT2B was markedly increased in osteosarcoma (OS) specimens compared with the normal bone tissues, and it was additionally abundantly expressed in OS cell lines. Inhibition of MAT2B expression caused a marked decrease in proliferation and significant increase in apoptosis. Results demonstrated that MAT2B functions as a tumor oncogene in OS in vivo and in vitro via regulation of EGFR and PCNA.
In the case of CNS failure of first-line EGFR inhibition.
G719S and T790M mutations are not associated with cervical cancer
EGFR was significantly upregulated in the hepatocellular carcinoma tissues.MCM3AP-AS1 regulates EGFR expression.
Results show that after treatment with tyrosine kinase inhibitors of EGFR, lung adenocarcinoma with EGFR mutation develops resistance through a mechanism involving USP22 which prevents ubiquitination-mediated EGFR degradation.
In the largest consecutive routine Asian non-small cell lung cancer (NSCLC) cohort analyzed to date, we found that high PD-L1 expression frequently overlapped with ROS1 rearrangement, while it negatively correlated with EGFR mutations.
Treated in neoadjuvant setting with EGFR tyrosine kinase inhibitor.
EGFR mutations are associated with recurrence in pN0M0 lung adenocarcinoma. EGFR mutation status and histological subtype should be considered when evaluating the risk of recurrence in resected lung adenocarcinoma patients.
the glioblastoma cell line 170-MG-BA exhibits a high level of EGFR amplification
Adenocarcinomas with EGFR mutations had a higher GGO proportion than those with wild-type EGFR after matching of clinical variables. Lesions with an exon 21 mutation had a higher GGO proportion than lesions with other mutations.
Positive EGFR mutation status is a favorable prognostic factor in patients with surgically resected Lung Adenocarcinomas; however, EGFR mutation subtype (exon 21 L858R mutation or exon 19 deletion) exhibits no prognostic impact.
In modulating drug resistance to EGFR-TKI treatment.
EGFR-TKIs plus local therapy showed prolonged survival benefit.
Report reduced EMILIN-1 and enhanced myogenic tone, dependent on increased TGF-beta-EGFR signaling, in resistance arteries from hypertensive patients.
Study identify MED12 as an important molecular regulator of epithelial ovarian cancer (EOC) tumor dormancy. MED12 knockout (KO) induced dormancy of EOC cells in vitro and in vivo, and microarray analysis showed that MED12 KO decreased expression of EGFR. MED12 bound to the promoter of EGFR, and MED12 expression positively correlated with EGFR expression in EOC patient samples.
Patients younger than 64 years and carriers of EGFR gene -191CC genotype have significantly higher risk for adenocarcinoma than carriers of -191CA or -191AA genotype. Further studies on larger cohorts are necessary to evaluate -191C/A SNP as a potential biomarker.
The mRNA and protein expression levels of LRIG1 in U251 cells were up-regulated after resveratrol treatment, accompanied with decreased Epidermal Growth Factor Receptor (EGFR)
Increased blood pressure in mice with selective smooth muscle cell ablation of EMILIN-1 depends on transactivation of EGFR and enhanced myogenic tone.
Osteoglycin negatively regulates cardiac fibrotic remodelling by attenuating myofibroblast proliferation and migration through LPA3-mediated and Rho/ROCK-dependent inhibition of MT1-MMP translocation, MMP2 activation and EGFR transactivation.
Our data show in vivo and ex vivo the necessity of vascular smooth muscle cell -EGFR for angiotensin II-induced structural and functional vascular remodelling
EGFR regulates CCN2 fibrotic signalling in the kidney
NIH3T3 transfected with EGFR-PPARGC1A as well as A431 showed increased cell proliferation activity. With regard to underlying mechanism, EGFR-PPARGC1A protein causes constitutive tyrosine phosphorylation, and induces the phosphorylation of wild-type full-length epidermal growth factor receptor (EGFR) by dimerization.
only tumors expressing both EGFR and c-Fos responded to anti-EGFR therapy
ADAM17 is needed for EGF-R-mediated induction of IL-6 synthesis, which via IL-6 trans-signaling induces beta-catenin-dependent tumorigenesis.
Low EGFR expression is associated with impaired neural stem cell expansion and hypersensitivity leading to epileptic seizures.
G protein-coupled receptor family C group 5 member A (GPRC5A) deficiency contributes to dysregulated proto-oncogene protein c-mdm2 (MDM2) via activated epidermal growth factor receptor (EGFR) signaling, which promotes lung tumor development.
These findings define a novel mechanism that integrates EGFR and Wnt/beta-catenin pathways to coordinate the delicate balance between proliferation and differentiation during development.
The results identify a novel mechanism of TRAF4-mediated EGFR activation and signaling.
Rotational dynamics of the epidermal growth factor receptor.
Staphylococcus aureus protein A enhances osteoclastogenesis via TNFR1 and EGFR signaling
High EGFR expression is associated with angiogenesis in B16 melanoma.
Chi3l3 activates EGFR to promote oligodendrogenesis.
Gene deletion of Egfr in myeloid cells limits IL-6 and TNF-alpha production, lipid uptake, and consecutively reduces atherosclerosis development.
Our results identify a key role for NRG1/ErbB signalling in the regulation of hippocampal mGluRI-dependent synaptic and cognitive functions, whose alteration might contribute to the pathogenesis of different brain diseases.
Amphiregulin plays an important role in promoting cardiac fibrosis after myocardial infarction partly though activating the EGFR pathway.
We further show that EGFR is activated through toll-like receptor 4. Disruption of toll-like receptor 4 or the EGFR pathway led to reduced inflammatory activity and foam cell formation
HER2 and HER3 expression was detected in 22.2% and 86.1% of samples, respectively. The frequency of EGFR mutation was 45.7% and was not significantly different between stage 0 and IA1 (40.0% and 48.0%, respectively), suggesting that EGFR mutation does not correlate with cancer progression from stage 0 to IA1.
These results show that EGFR is a co-factor of Transmissible gastroenteritis virus (TGEV), and that it plays a synergistic role with Aminopeptidase N early in TGEV infection.
this study shows that anemonin may ameliorate LPS-induced intestinal injury and improve restoration by regulating the TGF-b1 and EGFR signaling pathways
Syndecan-4 mediates porcine respiratory and reproductive syndrome virus entry by interacting with EGFR.
These results indicate that cAMP and oocyte-secreted factors cooperate to promote EGF receptor functionality in developing cumulus oocyte complexes, representing a key component of the acquisition of oocyte developmental competence.
patients experiencing gefitinib dose reduction or short-term treatment interruption due to toxicities did not show inferior survival, compared to those receiving full dose of gefitinib in non-small cell lung cancer patients with EGFR mutation
Report EGFR expression in the normal pancreas.
Injury and activation of purinergic receptors and direct activation of EGFR via EGF induce distinct downstream pathways.
Data suggest that the mechanism of hypoxia-induced increased activation of EGFR kinase is mediated by nNOS-derived nitric oxide.
An expressed transition SNP was identified in Meishan and white composite swine breeds.
EGFR, VEGFR and FGFR are expressed in porcine oviduct and endometrium during the time of implantation [review]
the restricted presence of the functional full-size receptor to the epithelial layer indicates a specific role during early embryonic development, whereas truncated EGF-R forms may potentially regulate contractions and blood flow in the oviduct
The phase-related expression of EGF and EGFR in the endothelium of the uterine artery and its branches suggest the modulatory effect of EGF and its receptor on the uterine artery and the region supplying these vessels.
This result suggests that ubiquitination of the kinase-impaired receptor can mediate its internalization by the clathrin pathway.
A linear relationship of EGF/EGFR, PI3-kinase, MAPK and geminal vesicle breakdown, presents a relatively definitive mechanism of EGF-induced meiotic resumption of porcine oocyte.
mRNA expression of EGF receptor
EGFR activation, by PKC signal pathway, participates in FSH-induced porcine oocyte meiotic resumption.
20-HETE activates the Raf/MEK/ERK pathway in renal epithelial cells through an EGFR- and c-Src-dependent mechanism.
Stimulation of bovine oviduct epithelial cell EGFR with EGF (human recombinant EGF) alone or with EGF in postovulatory/follicular phases (not luteal phase) up-regulates phosphorylation of MAPKs; heat blocks effects of EGF on phosphorylation of MAPKs.
Expression of the erbB/HER receptor family in the bovine uterus during the sexual cycle and the relation of this family to serum sex steroids.
Regulation of the sperm EGFR by ouabain leads to initiation of the acrosome reaction.
EGFR may simultaneously activate c-Src and PI3K to amplify the oxytocin signaling to increase the output of PGF(2 alpha) in endometrial epithelial cells.
results indicate that arginase induction depends in part on epidermal growth factor (EGF) receptor activity, and that EGFR inhibitors may attenuate vascular remodeling without affecting nitric oxide release
Data suggest that epidermal growth factor (EGF) and EGF receptors are important paracrine and/or autocrine regulators of spermatogenesis in bovine.
MT1-MMP has a role in signaling events mediating EGFR transactivation
possible cooperative role of the EGF and HGF pathways and indicate that cross-talk between their respective receptors may modulate mammary gland development in the cow
EGFR is stimulated during capacitation via PKA activation. More activation induces the acrosome reaction, which is induced by GPCR via EGFR transactivation by a signaling pathway involving PKA, SRC & metalloproteinase & effectors PI3K, PLC & PKC.
These results show that MMP-2 activates the EGFR and triggers downstream signaling pathways increasing Reactive Oxygen Species formation and promoting vasoconstriction.
The protein encoded by this gene is a transmembrane glycoprotein that is a member of the protein kinase superfamily. This protein is a receptor for members of the epidermal growth factor family. EGFR is a cell surface protein that binds to epidermal growth factor. Binding of the protein to a ligand induces receptor dimerization and tyrosine autophosphorylation and leads to cell proliferation. Mutations in this gene are associated with lung cancer. Multiple alternatively spliced transcript variants that encode different protein isoforms have been found for this gene.
, Egf receptor
, drosophila epidermal growth factor receptor homologue
, ellipse torpedo
, epidermal growth factor receptor
, faint little ball
, morphological defects 1
, avian erythroblastic leukemia viral (v-erb-b) oncogene homolog
, cell growth inhibiting protein 40
, cell proliferation-inducing protein 61
, proto-oncogene c-ErbB-1
, receptor tyrosine-protein kinase erbB-1
, EGFR-related peptide
, Epidermal growth factor receptor formerly avian erythroblastic leukemia viral (v-erbB) oncogene homolog (Erbb1)
, avian erythroblastic leukemia viral (v-erbB) oncogene homolog
, epidermal growth factor receptor, formerly avian erythroblastic leukemia viral (v-erbB) oncogene homolog (Erbb1)
, waved 2
, epidermal growth factor receptor (erythroblastic leukemia viral (v-erb-b) oncogene homolog, avian)
, egf receptor
, receptor tyrosine kinase ErbB1