Browse our anti-EGFR (EGFR) Antibodies

Horse (Equine) Epidermal Growth Factor Receptor (EGFR) interaction partners

1. Results indicated that most periocular squamous cell carcinomas of horses expressed epidermal growth factor receptor (EGFR) and human epidermal growth factor receptor 2 (HER2).

Fruit Fly (Drosophila melanogaster) Epidermal Growth Factor Receptor (EGFR) interaction partners

1. Regulation of cell growth by ROS is independent of the highly conserved TSC-TOR pathway.

2. 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.

3. 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.

4. Wnt signaling functions genetically upstream of EGFR signaling by activating the expression of the EGFR ligand, Spitz.

5. The somatic EGFR-ERK activity appeared to regulate the termination of Bam expression in the germline and promote subsequent differentiation to the spermatocyte stage.

6. stress-dependent EGFR/MAPK promotes gut regeneration via a novel mechanism that operates independently of Insulin/Pi3K/TOR signaling.

7. EGFR/ARF6 regulation of Hh signaling stimulates oncogenic Ras tumor overgrowth in Drosophila.

8. Graf functions to downregulate EGFR signaling.

9. 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.

10. The activity of Gro is antagonized by EGFR signaling, which inhibits Gro-dependent repression via p-ERK mediated phosphorylation.

11. 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.

12. 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

13. 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

14. 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.

15. These data demonstrate a strong genetic link between dG9a and the EGFR signaling pathway.

16. Avermectin directly interacts with EGFR and leads to the activation of the EGFR/AKT/ERK pathway.

17. The dorsoventral patterning and EGFR signaling genes play essential roles in correct identity determination and differentiation of lateral glia in the Drosophila nervous system.

18. 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.

19. 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.

20. 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.

Zebrafish Epidermal Growth Factor Receptor (EGFR) interaction partners

1. 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.

2. Study demonstrated that IGF-I can stimulate egfr expression in both follicles cell culture and intact follicles promoting oocyte maturation.

3. 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.

4. EGFR signaling in vertebrate oocytes can prevent meiotic progression.

5. the expression of EGFR was mainly restricted to the follicle cells with little expression in the oocytes

Human Epidermal Growth Factor Receptor (EGFR) interaction partners

1. It was confirmed that Osimertinib could inhibit the proliferation of tumor cells with EGFR mutation and T790M resistance mutation in zebrafish, which was consistent with the clinical research conclusion.

2. A predictive computational model reveals that GIV/girdin serves as a tunable valve for EGFR-stimulated cyclic AMP signals.

3. Our results suggest that SPP1 enhanced the second-generation EGFR TKI resistance in lung cancer, and inhibiting SPP1 might be a therapeutic target to overcome afatinib resistance.

4. EGFR T790M mutation is a major mechanism of acquired resistance to afatinib

5. The emergence of EGFR mutations determines the outcome of anti-EGFR treatment in colorectal cancer patients.

6. EGFR mutation testing should be performed in Asian patients with squamous cell carcinoma diagnosed from small lung biopsies

7. Study shows that skin and keratinocytes from Kindler syndrome patients have significantly reduced expression levels of the EGFR, resulting in defective EGF-dependent signaling and cell migration. Kindlin-1 can associate directly with EGFR in vitro and in keratinocytes in an EGF-dependent manner and formation of this complex protect EGFR from lysosomal-mediated degradation and required for EGF-dependent migration.

8. Loss of T790 M mutation at resistance was correlated with early progression and overall survival in response to osimertinib treatment in Chinese patients with NSCLC harboring acquired T790 M mutation.

9. We have developed a clinically translatable bispecific antibody that redirects human T cells to safely and effectively treat malignant glioma. On the basis of these results, we have developed a clinical study of hEGFRvIII-CD3 bi-scFv for patients with EGFRvIII-positive malignant glioma.

10. We identified EE02 as an EGFR/Eps8 complex inhibitor that demonstrated promising antitumor effects in breast cancer and non-small cell lung cancer (NSCLC). Our data suggest that the EGFR/Eps8 complex offers a no

11. EGFR-mutant non-small cell lung carcinomas can undergo small cell lung carcinoma transformation. This occurs at an average of 17.8 months after diagnosis and cases are often characterized by Rb1, TP53, and PIK3CA mutations.

12. FOXO3a activation is a crucial event in the response of glioblastoma cells to EGFR inhibition.

13. For those cases who developed resistance with circulating DNA showing an EGFR mutation, 50% were positive for T790M that is also comparable to the international literature.

14. Mechanistically, GPAA1 enhanced the levels of metastasis-associated GPI-anchored proteins to increase tumour metastasis and intensified lipid raft formation, which consequently promoted the interaction between EGFR and ERBB2 as well as downstream pro-proliferative signalling.

15. prosurvival response was partially mediated through enhanced DNA repair, as EGFR or MEK/ERK inhibitors delayed DNA damage resolution

16. extracellular domain of epithelial cell adhesion molecule -induced LIN28 expression reduces the expression of the microRNA LET7 and up-regulates that of the transcription factor high-mobility group AT-hook 2 (HMGA2), which activates the transcription of pluripotency factors.

17. APE1 stimulates EGFR-tyrosine kinase inhibitors resistance by activating Akt signaling through a redox-dependent mechanism in lung adenocarcinoma.

18. The T790M mutation rate was 8.4% in overall patients. The T790M mutation was more frequent in patients with brain metastasis 30.0% . We found that post-TKI (tyrosine kinase inhibitors) samples 42.8% were associated with a higher T790M mutation rate. Subgroup analysis showed that the duration of TKI therapy for 6 to 10 months 66.6% and >10 months 75.0% were also associated with higher T790M mutation rate.

19. The expression of lncRNA EGFR-AS1 is decreased in preeclampsia patients, promoting disease progression by inhibiting EGFR-JAK/STAT signaling pathway.

20. The esophageal squamous cell carcinoma patients with the CC genotype of PLCE1 rs17109671 and EGFR rs2072454 have poor overall survival.

Mouse (Murine) Epidermal Growth Factor Receptor (EGFR) interaction partners

1. ErbB receptor controls the transformation of oligodendrocyte progenitor cells into functional remyelinating Schwann cells after spinal cord injury.

2. The RAS-PI3K interaction is an important signaling node and potential therapeutic target in EGFR-mutant lung cancer.

3. Inhibiting miR-129-5p function and restoring EGFR protein levels in vivo is sufficient to reverse LC-induced defects in cortical NPC self-renewal.

4. This study demonstrates that IL-17A activates the IL-17R-EGFR axis in Lrig1(+) stem cells linking wound healing to tumorigenesis.

5. data point to ZBTB20 as a critical regulator of EGFR expression and hepatocyte proliferation in mouse liver regeneration, and may serve as a potential therapeutic target in clinical settings of liver regeneration.

6. a novel role for SMAD7 as a tumor promoter in skin carcinogenesis where SMAD7 stimulates the DNA repair pathway and EGFR signaling activation.

7. these results indicate that EGFR plays an important role in NAFLD and is a potential therapeutic target.

8. Mig6 regulates the production of inflammatory mediators (TNF-alpha, il-1beta) through inhibiting the over activation of EGFR.

9. results demonstrate that suppression of the IGF-1R/mTOR-pathway by EGFR/ERK/IGFBP-3 signaling is necessary for balanced osteoblast maturation providing a mechanism for the skeletal phenotype observed in EGFR-deficient mice.

10. Increased blood pressure in mice with selective smooth muscle cell ablation of EMILIN-1 depends on transactivation of EGFR and enhanced myogenic tone.

11. 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.

12. 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

13. EGFR regulates CCN2 fibrotic signalling in the kidney

14. 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.

15. only tumors expressing both EGFR and c-Fos responded to anti-EGFR therapy

16. ADAM17 is needed for EGF-R-mediated induction of IL-6 synthesis, which via IL-6 trans-signaling induces beta-catenin-dependent tumorigenesis.

17. Low EGFR expression is associated with impaired neural stem cell expansion and hypersensitivity leading to epileptic seizures.

18. 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.

19. 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.

20. The results identify a novel mechanism of TRAF4-mediated EGFR activation and signaling.

Pig (Porcine) Epidermal Growth Factor Receptor (EGFR) interaction partners

1. 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.

2. this study shows that anemonin may ameliorate LPS-induced intestinal injury and improve restoration by regulating the TGF-b1 and EGFR signaling pathways

3. Syndecan-4 mediates porcine respiratory and reproductive syndrome virus entry by interacting with EGFR.

4. 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.

5. 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

6. Report EGFR expression in the normal pancreas.

7. Injury and activation of purinergic receptors and direct activation of EGFR via EGF induce distinct downstream pathways.

8. Data suggest that the mechanism of hypoxia-induced increased activation of EGFR kinase is mediated by nNOS-derived nitric oxide.

9. An expressed transition SNP was identified in Meishan and white composite swine breeds.

10. EGFR, VEGFR and FGFR are expressed in porcine oviduct and endometrium during the time of implantation [review]

11. 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

12. 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.

13. This result suggests that ubiquitination of the kinase-impaired receptor can mediate its internalization by the clathrin pathway.

14. 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.

15. mRNA expression of EGF receptor

16. EGFR activation, by PKC signal pathway, participates in FSH-induced porcine oocyte meiotic resumption.

17. 20-HETE activates the Raf/MEK/ERK pathway in renal epithelial cells through an EGFR- and c-Src-dependent mechanism.

Cow (Bovine) Epidermal Growth Factor Receptor (EGFR) interaction partners

1. 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.

2. 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.

3. Regulation of the sperm EGFR by ouabain leads to initiation of the acrosome reaction.

4. 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.

5. 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

6. Data suggest that epidermal growth factor (EGF) and EGF receptors are important paracrine and/or autocrine regulators of spermatogenesis in bovine.

7. MT1-MMP has a role in signaling events mediating EGFR transactivation

8. 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

9. 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.

Rabbit Epidermal Growth Factor Receptor (EGFR) interaction partners

1. These results show that MMP-2 activates the EGFR and triggers downstream signaling pathways increasing Reactive Oxygen Species formation and promoting vasoconstriction.