<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Pradip D</submitter><funding>NCI NIH HHS</funding><pagination>173-95</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3623837</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>3(2)</volume><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</pubmed_abstract><journal>American journal of cancer research</journal><pubmed_title>Dissecting GRB7-mediated signals for proliferation and migration in HER2 overexpressing breast tumor cells: GTP-ase rules.</pubmed_title><pmcid>PMC3623837</pmcid><funding_grant_id>R21 CA139428</funding_grant_id><pubmed_authors>Leyland-Jones B</pubmed_authors><pubmed_authors>Bouzyk M</pubmed_authors><pubmed_authors>Dey N</pubmed_authors><pubmed_authors>Pradip D</pubmed_authors></additional><is_claimable>false</is_claimable><name>Dissecting GRB7-mediated signals for proliferation and migration in HER2 overexpressing breast tumor cells: GTP-ase rules.</name><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</description><dates><release>2013-01-01T00:00:00Z</release><publication>2013</publication><modification>2025-04-26T21:06:49.723Z</modification><creation>2019-03-27T01:07:21Z</creation></dates><accession>S-EPMC3623837</accession><cross_references><pubmed>23593540</pubmed></cross_references></HashMap>