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Human HER2 Protein expressed in Human Cells - ABIN2001860
Yamamoto, Ikawa, Akiyama, Semba, Nomura, Miyajima, Saito, Toyoshima: Similarity of protein encoded by the human c-erb-B-2 gene to epidermal growth factor receptor. in Nature 1986
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Human HER2 Protein expressed in Wheat germ - ABIN1353011
He, Qu, Shen, Tan, Zeng, Liu, Jiang, Li: Highly specific recognition of breast tumors by an RNA-cleaving fluorogenic DNAzyme probe. in Analytical chemistry 2015
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Human HER2 Protein expressed in Human Cells - ABIN2001858
Lai, Lemke: An extended family of protein-tyrosine kinase genes differentially expressed in the vertebrate nervous system. in Neuron 1991
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Human HER2 Protein expressed in HEK-293 Cells - ABIN2181216
Piechocki, Wu, Jones, Jacob, Gibson, Ethier, Abrams, Yagita, Venuprasad, Wei: Induction of proapoptotic antibodies to triple-negative breast cancer by vaccination with TRAIL death receptor DR5 DNA. in International journal of cancer. Journal international du cancer 2012
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Human HER2 Protein expressed in HEK-293 Cells - ABIN2181214
NDong, Tate, Kett, Batra, Demidenko, Lewis, Hoopes, Gerngross, Griswold: Tumor Cell Targeting by Iron Oxide Nanoparticles Is Dominated by Different Factors In Vitro versus In Vivo. in PLoS ONE 2015
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auranofin could regulate the Her2/Akt (show AKT1 Proteins)/FOXO3 (show FOXO3 Proteins) signaling pathway in SKOV3 cells and be used as a potential antitumor agent considering the expression of MUC4 (show MUC4 Proteins) in ovarian cancer patients.
The results show that Somatic ERBB2 mutations were detected in 3.15% patients. The ERBB2 mutation rate differed amongst different histological types. Patients carrying ERBB2 mutations were found to have worse prognosis than those with wild-type or PIK3CA-mutated ICCs but a better prognosis than those with KRAS-mutated ICCs.
KRT19 (show KRT19 Proteins) intracellularly binds to HER2, playing a critical role in HER2 activation
The dipole potential exerts significant effects on the ligand binding, clustering and signaling of ErbB2 protein.
HER2 reactivation through acquisition of the HER2L755S mutation was identified as a mechanism of acquired resistance to lapatinib-containing HER2-targeted therapy in preclinical HER2-amplified breast cancer models, which can be overcome by irreversible HER1 (show EGFR Proteins)/2 inhibitors
FGFR1 (show FGFR1 Proteins) and/or FGF3 (show FGF3 Proteins) gene amplification correlated with a lower pathologic complete response in patients with HER2(+) early breast cancer treated with neoadjuvant anti-HER2 therapy.
Asbestos-exposed patients displayed a significantly lower rate of EGFR (show EGFR Proteins) mutations and a higher rate of HER2 mutations. Chrome-exposed patients exhibited enhanced HER2 and PIK3 (show PIK3CG Proteins) mutation frequency. In particular, asbestos-exposed patients have a lower chance of EGFR (show EGFR Proteins) mutations.
Electrochemical signals are significantly enhanced through the layer-by-layer assembly of pSC4-AuNPs due to its high conductivity and high effective area. With this innovative method, by taking the assay of a tumor marker as an example, human epidermal growth factor receptor (show EGFR Proteins) 2 (ErbB2) was successfully measured with a detection limit of 0.5ng/mL
Data have found that the prevalence of HER2 mutations is about 3%. These genetic alterations are independently associated with HER2 amplification status, occurring in both ER-positive/HER2-negative diseases or HER2-enriched cancers. [review]
Our study provides novel evidence of Endo II function in HER2+ cancer cell motility and trafficking of HER2 that relates to effective treatments with trastuzumab or T-DM1 (show DMPK Proteins). Thus, differential expression of Endo II may relate to sensitivity or resistance to trastuzumab-based therapies for HER2+ cancers
Over-expression of HER2 remarkably enhanced the proliferation, invasion and migration of B16 cells.
YAP (show YAP1 Proteins) accumulated in nuclei of mammary glands in ErbB2/EGFR (show EGFR Proteins)-transgenic mice, suggesting that EGFR (show EGFR Proteins) signaling affects YAP (show YAP1 Proteins) in vivo similar to cell culture. ErbB2/EGFR (show EGFR Proteins)-transgenic mice develop mammary tumors in 7-8 months, but surprisingly, MaSCs from these mice did not form tumors when transplanted into host mice.
Results indicate the importance of the LDL receptor (LDLR (show LDLR Proteins)) in the growth of triple-negative and HER2-overexpressing breast cancers in the setting of elevated circulating LDL cholesterol (LDL-C).
immunocompetent mouse models of HER2/ErbB2-driven breast cancer, CD73 expression by tumor cells and host cells significantly suppressed immune-mediated responses mediated by anti-ErbB2 mAb.
We further demonstrate that loss of one allele of PTEN is sufficient to shift isoform dependency from p110alpha (show PIK3CA Proteins) to p110beta in vivo. These results provide insight into the molecular mechanism by which ErbB2-positive breast cancer escapes p110alpha (show PIK3CA Proteins) inhibition.
sought to further echocardiographically characterize the ErbB2(tg) mouse line as a model of hypertrophic obstructive cardiomyopathy
investigations revealed that NUMB (show NUMB Proteins) and NUMBL (show NUMBL Proteins) interacted with small GTPase (show RACGAP1 Proteins) Rab7 (show RAB7A Proteins) to transition ERBB2 from early to late endosome for degradation.
Combined targeting of TGF-beta (show TGFB1 Proteins), EGFR (show EGFR Proteins) and HER2 signaling suppresses lymphangiogenesis and metastasis in a pancreatic ductal adenocarcinoma model.
The conjugation of benzylguanine-modified auristatin F to EGFR (show EGFR Proteins)-specific 425(scFv)-SNAP and HER2-specific alphaHER2(scFv)-SNAP resulted in two potent recombinant antibody-drug conjugates that specifically killed breast cancer cell lines by inducing apoptosis when applied at nanomolar concentrations.
ErbB2 is required for neonatal cardiomyocyte proliferation. ErbB2 conditional knockout heart exhibited an upregulation of negative cell cycle regulators.
Newly synthesized N-cadherin (show CDH2 Proteins) molecules move from the lateral to the basal surface of cardiomyocytes during trabeculation. This localization requires Erbb2 signaling.
these results suggest that Nrg1 (show NRG1 Proteins) is not the primary effector of trabeculation and/or that other EGF (show EGF Proteins)-like ligand(s) activates the ErbB2/ErbB4 (show ERBB4 Proteins) pathway, either through functioning as the primary ligand or acting in a redundant manner. Overall, our work provides an example of cross-species differences in EGF (show EGF Proteins) family member requirements for an evolutionary conserved process.
Embryos homozygous for a GBT insertion within neuregulin 2a (nrg2a) revealed a novel requirement for a Neuregulin 2a (Nrg2a)-ErbB2/3-AKT (show AKT1 Proteins) signaling pathway governing the organization of a subset of epidermal cells during median fin fold morphogenesis.
A direct link was found between Erbb2 activity and remodeling of myofibrils.
Study shows that, in addition to its role in cardiomyocyte proliferation, ErbB2 is also required for regulating cardiomyocyte migration (delamination) to initiate cardiac trabeculation.
erbb3 (show ERBB3 Proteins) and erbb2 are essential for schwann cell migration and myelination in zebrafish.
NRG1 (show NRG1 Proteins) and PI3K functionally interact with ErbB2 and ErbB3 (show ERBB3 Proteins) during regeneration
Results indicated that most periocular squamous cell carcinomas of horses expressed epidermal growth factor receptor (EGFR (show EGFR Proteins)) and human epidermal growth factor receptor (show EGFR Proteins) 2 (HER2).[HER2]
Widespread expression of ErbB2 receptor mRNAs was found throughout the telencephalon of juvenile and adult monkeys with in situ hybridization, with higher levels in grey matter compared to white matter.
We have isolated the cDNA encoding the rhesus monkey homolog of human Her2/neu (RhErbB2) to construct DNA plasmids and adenoviral vectors for the development of a cancer vaccine against this protein.
This gene encodes a member of the epidermal growth factor (EGF) receptor family of receptor tyrosine kinases. This protein has no ligand binding domain of its own and therefore cannot bind growth factors. However, it does bind tightly to other ligand-bound EGF receptor family members to form a heterodimer, stabilizing ligand binding and enhancing kinase-mediated activation of downstream signalling pathways, such as those involving mitogen-activated protein kinase and phosphatidylinositol-3 kinase. Allelic variations at amino acid positions 654 and 655 of isoform a (positions 624 and 625 of isoform b) have been reported, with the most common allele, Ile654/Ile655, shown here. Amplification and/or overexpression of this gene has been reported in numerous cancers, including breast and ovarian tumors. Alternative splicing results in several additional transcript variants, some encoding different isoforms and others that have not been fully characterized.
c-erb B2/neu protein
, metastatic lymph node gene 19 protein
, neuro/glioblastoma derived oncogene homolog
, neuroblastoma/glioblastoma derived oncogene homolog
, proto-oncogene Neu
, proto-oncogene c-ErbB-2
, receptor tyrosine-protein kinase erbB-2
, tyrosine kinase-type cell surface receptor HER2
, v-erb-b2 erythroblastic leukemia viral oncogene homolog 2, neuro/glioblastoma derived oncogene homolog
, Neu oncogene
, avian erythroblastosis oncogene B 2
, proto-oncogene NEU
, Avian erythroblastosis viral (v-erb-B2) oncogene homologue 2 (neuro/glioblastoma derived oncogene homolog)
, NEU proto-oncogene
, epidermal growth factor receptor-related protein
, v-erb-b2 avian erythroblastic leukemia viral oncogene homolog 2
, epidermal growth factor receptor type 2