{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Pradip D"],"funding":["NCI NIH HHS"],"pagination":["173-95"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3623837"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["3(2)"],"pubmed_abstract":["Amplification of human Her2 and its aberrant signaling in 20-30% of early breast cancer patients is responsible for highly aggressive tumors with poor outcome. Grb7 is reported to be co-amplified with Her2. We report a concurrent high expression of mRNA (from FFPE tumor samples; mRNA correlation, Pearson r(2)= 0.806), and high levels of GRB7 protein (immunoblot) in HER2+ breast cancer cell lines. We demonstrated the signaling mechanism of HER2 and downstream effectors that contributes to proliferation and migration. Using HER2+ and trastuzumab-resistant breast cancer cell lines, we identified the interaction between GRB7 and HER2 in the control of HER2+ cell proliferation. Our co-IP data show that GRB7 recruits SHC into the HER2-GRB7 signaling complex. This complex formation leads to activ"],"journal":["American journal of cancer research"],"pubmed_title":["Dissecting GRB7-mediated signals for proliferation and migration in HER2 overexpressing breast tumor cells: GTP-ase rules."],"pmcid":["PMC3623837"],"funding_grant_id":["R21 CA139428"],"pubmed_authors":["Leyland-Jones B","Bouzyk M","Dey N","Pradip D"],"additional_accession":[]},"is_claimable":false,"name":"Dissecting GRB7-mediated signals for proliferation and migration in HER2 overexpressing breast tumor cells: GTP-ase rules.","description":"Amplification of human Her2 and its aberrant signaling in 20-30% of early breast cancer patients is responsible for highly aggressive tumors with poor outcome. Grb7 is reported to be co-amplified with Her2. We report a concurrent high expression of mRNA (from FFPE tumor samples; mRNA correlation, Pearson r(2)= 0.806), and high levels of GRB7 protein (immunoblot) in HER2+ breast cancer cell lines. We demonstrated the signaling mechanism of HER2 and downstream effectors that contributes to proliferation and migration. Using HER2+ and trastuzumab-resistant breast cancer cell lines, we identified the interaction between GRB7 and HER2 in the control of HER2+ cell proliferation. Our co-IP data show that GRB7 recruits SHC into the HER2-GRB7 signaling complex. This complex formation leads to activ","dates":{"release":"2013-01-01T00:00:00Z","publication":"2013","modification":"2025-04-26T21:06:49.723Z","creation":"2019-03-27T01:07:21Z"},"accession":"S-EPMC3623837","cross_references":{"pubmed":["23593540"]}}