Il n’y a pas de produits dans votre liste de comparaison.
Votre panier est vide.
Afficher toutes les espèces
Afficher tous les synonymes
Sélectionnez vos espèces et l'application
anti-Human ERBB3 Anticorps:
anti-Mouse (Murine) ERBB3 Anticorps:
anti-Rat (Rattus) ERBB3 Anticorps:
Vous arrivez à notre recherche pré-filtrée.
Human Polyclonal ERBB3 Primary Antibody pour CyTOF, FACS - ABIN4899525
Lin, Cheng, Lee, Ye, Tsai, Kim, Pasqualini, Arap, Navone, Tu, Hu, Yu-Lee, Logothetis: A 45-kDa ErbB3 secreted by prostate cancer cells promotes bone formation. dans Oncogene 2008
Show all 7 Pubmed References
Human Monoclonal ERBB3 Primary Antibody pour FACS - ABIN4896268
MacLeod, Elgadi, Bossi, Sankar, Pisio, Agopsowicz, Sharon, Graham, Hitt: HER3 targeting of adenovirus by fiber modification increases infection of breast cancer cells in vitro, but not following intratumoral injection in mice. dans Cancer gene therapy 2012
Show all 5 Pubmed References
Human Monoclonal ERBB3 Primary Antibody pour CyTOF, ELISA (Capture) - ABIN4899526
Liu, Leng, Gunasekaran, Pentony, Shen, Howard, Stoops, Manchulenko, Razinkov, Liu, Fanslow, Hu, Sun, Hasegawa, Clark, Foltz, Yan: A Novel Antibody Engineering Strategy for Making Monovalent Bispecific Heterodimeric IgG Antibodies by Electrostatic Steering Mechanism. dans The Journal of biological chemistry 2015
Show all 5 Pubmed References
Human Monoclonal ERBB3 Primary Antibody pour IHC (f), IHC (fro) - ABIN967437
Carraway, Cantley: A neu acquaintance for erbB3 and erbB4: a role for receptor heterodimerization in growth signaling. dans Cell 1994
Show all 4 Pubmed References
Polyclonal ERBB3 Primary Antibody pour IF, IHC (p) - ABIN4948293
Yarden, Sliwkowski: Untangling the ErbB signalling network. dans Nature reviews. Molecular cell biology 2001
Show all 3 Pubmed References
Polyclonal ERBB3 Primary Antibody pour IF, IHC (p) - ABIN4948299
Kobayashi, Iwamatsu, Shinohara-Kanda, Ihara, Fukui: Activation of ErbB3-PI3-kinase pathway is correlated with malignant phenotypes of adenocarcinomas. dans Oncogene 2003
Show all 3 Pubmed References
Human Monoclonal ERBB3 Primary Antibody pour ELISA, WB - ABIN969113
Sakai, Yokote, Murakami-Murofushi, Tamura, Saijo, Nishio: Pertuzumab, a novel HER dimerization inhibitor, inhibits the growth of human lung cancer cells mediated by the HER3 signaling pathway. dans Cancer science 2007
Show all 2 Pubmed References
Human Monoclonal ERBB3 Primary Antibody pour IHC, ELISA - ABIN969112
Sassen, Rochon, Wild, Hartmann, Hofstaedter, Schwarz, Brockhoff: Cytogenetic analysis of HER1/EGFR, HER2, HER3 and HER4 in 278 breast cancer patients. dans Breast cancer research : BCR 2008
Show all 2 Pubmed References
Human Polyclonal ERBB3 Primary Antibody pour IHC (p), ELISA - ABIN543997
Plowman, Whitney, Neubauer, Green, McDonald, Todaro, Shoyab: Molecular cloning and expression of an additional epidermal growth factor receptor-related gene. dans Proceedings of the National Academy of Sciences of the United States of America 1990
Show all 4 Pubmed References
Mutations in ERBB3 gene are associated with colorectal cancer.
we further dissected the diarrhea profile of the various patient dose cohorts and carried out in vitro investigations in human colon cell lines and explants to decipher the contribution and the mechanism of anti-HER2/3 therapeutic antibodies to intestinal epithelium malfunction
This study demonstrates that the Ig-like region of neuregulin exerts an important role in their capability to activate ErbB/HER receptors and mitogenic responses.
Observed that ERBB3/HER3 expression in gastric tumors correlates with female gender, high grade tumors, diffuse gastric carcinoma, diffuse to focal p53 positivity, and a high to moderate Ki-67 proliferation index in 75 in Saudi cohort study.
an involvement of CD151 in regulation of ErbB2/ErbB3 heterodimerization and its impact on cell response to Herceptin, is reported.
Our data support the combination of therapies targeting ERBB2/3 and mTORC1 signalling, together with fulvestrant, in patients who relapse on endocrine therapy and retain a functional ER.
Despite both ligands binding to the EGFR, BTC biases the EGFR to dimerize with ErbB3 to regulate the biologic response.
miR-125a-5p was downregulated in HBV-HCC tissues and cells. miR-125a-5p could inhibit the secretion of HBV proteins indirectly, but not inhibit HBV replication at the DNA level. Moreover, the upregulation of miR-125a-5p after HBV infection leads to an increased expression of one target, ErbB3, which might play important roles in chronic HBV infection and HCC development.
ERBB3 and NGFR mark a distinct skeletal muscle progenitor cell in human development and pluripotent stem cells.
High-throughput sequencing revealed a significant increase in HER3 mRNA and protein levels by the HER2 3'untranslated region (3'UTR). The HER2 3'UTR harboring a shared miR-125a/b response element induced miR-125a/b sequestration and thus resulted in HER3 mRNA derepression. Trastuzumab treatment upregulated HER3 via elevated HER2 mRNA expression, leading to trastuzumab resistance.
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.
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