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Mouse (Murine) ERBB3 Protein expressed in Human Cells - ABIN2008508
Alimandi, Romano, Curia, Muraro, Fedi, Aaronson, Di Fiore, Kraus: Cooperative signaling of ErbB3 and ErbB2 in neoplastic transformation and human mammary carcinomas. in Oncogene 1995
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Human ERBB3 Protein expressed in Human Cells - ABIN3216381
Wallasch, Weiss, Niederfellner, Jallal, Issing, Ullrich: Heregulin-dependent regulation of HER2/neu oncogenic signaling by heterodimerization with HER3. in The EMBO journal 1995
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Our results indicate that administration of U3-1402 alone or in combination with an EGFR-TKI may have potential as a novel therapy for EGFR-TKI-resistant EGFR-mutant non-small cell lung cancer (NSCLC)
High HER3 expression is associated with progression of breast cancer.
Low HER3 expression is suggested to be a valuable prognostic biomarker to predict recurrence in HER2-amplified breast cancer.
Results show that MEK inhibition promoted an ERK rebound during early phase treatment in head and neck squamous cell carcinoma (HNSCC) cells, which was due to feedback-induced, ligand-dependent activation of FGFR3 up-regulation.
Results show that silencing HER3 increased the radiosensitivity of luminal A breast cancer cells in vitro and in vivo providing evidence for its role in breast cancer radiotherapy resistance.
Study supports the involvement of EGFR, HER2 and HER3 in BCC aggressiveness of and in tumor differentiating towards different histological subtypes.
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.
ERBB3 mutations can be found in a wide variety of tumour types, and can be used to select treatment with HER family inhibitors.
identified P2RX2, KCNQ5, ERBB3 and SOCS3 to be associated with the progression of age-related hearing impairment
In this study, authors analyzed the immunoexpression of EGFR, HER2 (EGFR2) and HER3 (EGFR3) in 41 cases of serous borderline ovarian tumors and carcinomas, in relation to the degree of differentiation and tumor stage.
Results demonstrate that 4-PBA promotes gastric cancer cells migration through upregulation of HER3/HER4 subsequent to increased levels of acetyl-histone and activation of ERK signaling.
miR152 was found to be involved in the proliferation and metastasis of ovarian cancer cells through repression of ERBB3 expression.
NRG1-dependent activation of HER3 induces primary resistance to trastuzumab in HER2-overexpressing breast cancer cells. HER3 monoclonal antibody combined with trastuzumab may serve as a treatment choice for patients with primary resistance to trastuzumab.
This phase Ib study was designed to determine the MTD, safety, preliminary efficacy, and pharmacokinetics of the HER3 (ErbB3) mAb SAR256212 in combination with the oral PI3K inhibitor SAR245408 for patients with metastatic or locally advanced solid tumors.
the present study suggests that HER2 has an important role in the regulation of the cancer stem-like cells phenotype in ALK translocated lung cancers that is mainly orchestrated by HER2/HER3 heterodimers.
HER3 phosphorylation by EGFR depends on the ability of EGFR to homo-oligomerize.
To determine additional resistance mechanisms to cetuximab treatment besides HER3 signaling.
Study shows ErbB3 expression was markedly decreased in suicide completers compared to controls.
EGFR expression is increased in oesophageal and gastric adenocarcinomas after neoadjuvant therapy and was significantly associated with a prolonged overall survival in univariable analysis.
Using time-resolved-fluorescence energy transfer (TR-FRET), we demonstrated that in the presence of recombinant NRG1, binding of 9F7-F11 to HER3 is increased, whereas that of ligand-competing anti-HER3 antibodies (H4B-121, U3-1287, Ab#6, Mab205.10.2, and MOR09825) is decreased.
Widespread expression of ErbB3 receptor mRNAs was found throughout the telencephalon of juvenile and adult monkeys with in situ hybridization.
data confirmed that an ErbB3-driven pathway mediates a net positive influence in an in vivo model closely resembling human repair
Result suggest the potential for a paracrine signalling network whereby basal cells secrete neuregulin 1 (Nrg1), which acts on luminal cells via Erbb3 and Erbb4 receptors.
The authors demonstrate that ErbB3 signaling is required for the embryonic development of the enteric nervous system.
These studies demonstrate that ErbB3, like ErbB4, enhances lactogenic expansion and differentiation of the mammary gland during pregnancy, through activation of Akt and STAT5A, two targets crucial for lactation.
The data suggest that ErbB3 restricts Paneth cells numbers through PI3K-mediated suppression of Atoh1 levels leading to inhibition of Paneth cells differentiation, with important implications for regulation of the intestinal stem cells niche.
Our results support a role for the hepatocellular ERBB tyrosine kinases in fibrogenesis. Maximal impact to fibrogenesis occurred in the ERBB3 and EGFR-ERBB3 DKO models, suggesting that EGFR-ERBB3 heterodimeric signaling in damaged hepatocytes may play a more important role in liver fibrosis than EGFR-EGFR homodimeric signaling.
nuc-ErbB3 directly regulates levels of H3K27me3 in Schwann cells
Data indicate that Sonic hedgehog (Shh) stimulate branching morphogenesis (BrM) and induced synthesis of mRNAs for Ptch1 protein, epidermal growth factor (EGF) and receptors of the ErbB receptors ErbB1, ErbB2 and ErbB3.
ERBB3 is required for wound healing and for the progression of skin tumors in mice.
The expression of ERBB3 in combination with ERBB4 significantly amplifies proliferation of lymphocytes upon ligand stimulation.
Data indicate that increased expression of erbB3 plays a pivotal role in activating downstream PI-3K/Akt pathway and promoting erbB2-driven mammary/breast tumorigenesis.
Suggest that ERBB3 may promote hepatocellular carcinoma through STAT3 activation.
ERBB3 is crucial for the proliferation of Bergmann glia in the developing cerebellum.
ErbB3 plays a key role in migration, as well as in myelination, in mouse Schwann lineage cells.
Knock-down of Erbb3 with siRNA during early differentiation inhibits cardiomyogenesis in embryonic stem cells.
Myocilin binds to ErbB2/ErbB3, activates these receptors, and affects the downstream PI3K-AKT signaling pathway
PIK3CA(H1047R)-driven tumor growth and PI3K signaling can occur independently of ErbB3 receptor tyrosine kinases.
downregulation of ErbB3 induced by Wnt3a contributes to Wnt3a-induced early osteoblast differentiation of Mesenchymal stem cells through increased canonical Wnt/beta-catenin signaling and decreased Src signaling.
findings indicate that although ErbB3-associated PI3K activity is critical for mammary development, it is dispensable for ErbB2-induced mammary tumor progression
our findings suggest that ErbB3 promotes HER2-induced changes in the breast epithelium before, during, and after tumor formation.
Bone marrow-derived mesenchymal stem cells up-regulate skeletal muscle acetylcholine receptor delta subunit through NRG/ErbB3-mediated mitogen-activated protein kinase pathway.
This gene encodes a member of the epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases. This membrane-bound protein has a neuregulin binding domain but not an active kinase domain. It therefore can bind this ligand but not convey the signal into the cell through protein phosphorylation. However, it does form heterodimers with other EGF receptor family members which do have kinase activity. Heterodimerization leads to the activation of pathways which lead to cell proliferation or differentiation. Amplification of this gene and/or overexpression of its protein have been reported in numerous cancers, including prostate, bladder, and breast tumors. Alternate transcriptional splice variants encoding different isoforms have been characterized. One isoform lacks the intermembrane region and is secreted outside the cell. This form acts to modulate the activity of the membrane-bound form. Additional splice variants have also been reported, but they have not been thoroughly characterized.
proto-oncogene-like protein c-ErbB-3
, receptor tyrosine-protein kinase erbB-3
, tyrosine kinase-type cell surface receptor HER3
, v-erb-b2 erythroblastic leukemia viral oncogene homolog 3 (avian)
, receptor tyrosine kinase ErbB3
, receptor tyrosine-protein kinase erbB-3-like
, avian erythroblastosis oncogene B 3 receptor
, glial growth factor receptor
, receptor tyrosine kinase
, avian erythroblastosis oncogene B 3
, v-erb-b2 erythroblastic leukemia viral oncogene homolog 3
, v-erb-b2 avian erythroblastic leukemia viral oncogene homolog 3