{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wright KD"],"funding":["Wisconsin Breast Cancer Showhouse Inc and Medical College of Wisconsin Cancer Center","Advancing a Healthier Wisconsin Endowment","American Cancer Society and the MCW Cancer Center","National Institute of Diabetes and Digestive and Kidney Diseases","NIDDK NIH HHS","Medical College of Wisconsin","The Mary Kay Foundation","METAvivor Foundation","National Cancer Institute","NCI NIH HHS"],"pagination":["74"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6570928"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["21(1)"],"pubmed_abstract":["<h4>Background</h4>SHC1 proteins (also called SHCA) exist in three functionally distinct isoforms (p46SHC, p52SHC, and p66SHC) that serve as intracellular adaptors for several key signaling pathways in breast cancer. Despite the broad evidence implicating SHC1 gene products as a central mediator of breast cancer, testing the isoform-specific roles of SHC1 proteins have been inaccessible due to the lack of isoform-specific inhibitors or gene knockout models.<h4>Methods</h4>Here, we addressed this issue by generating the first isoform-specific gene knockout models for p52SHC and p66SHC, using germline gene editing in the salt-sensitive rat strain. Compared with the wild-type (WT) rats, we found that genetic ablation of the p52SHC isoform significantly attenuated mammary tumor formation, wher"],"journal":["Breast cancer research : BCR"],"pubmed_title":["The p52 isoform of SHC1 is a key driver of breast cancer initiation."],"pmcid":["PMC6570928"],"funding_grant_id":["R01 CA193343","R01 DK098159","#14-247-29","R01CA193343","R01 CA188575","Grant No. 024.16","R01DK098159","Cancer Center Pilot Grant"],"pubmed_authors":["Wright KD","Rui H","Miller BS","Geurts AM","Sheinin Y","El-Meanawy S","Sun Y","Kalyanaraman B","Flister MJ","Banerjee A","Tsaih SW","Sorokin A"],"additional_accession":[]},"is_claimable":false,"name":"The p52 isoform of SHC1 is a key driver of breast cancer initiation.","description":"<h4>Background</h4>SHC1 proteins (also called SHCA) exist in three functionally distinct isoforms (p46SHC, p52SHC, and p66SHC) that serve as intracellular adaptors for several key signaling pathways in breast cancer. Despite the broad evidence implicating SHC1 gene products as a central mediator of breast cancer, testing the isoform-specific roles of SHC1 proteins have been inaccessible due to the lack of isoform-specific inhibitors or gene knockout models.<h4>Methods</h4>Here, we addressed this issue by generating the first isoform-specific gene knockout models for p52SHC and p66SHC, using germline gene editing in the salt-sensitive rat strain. Compared with the wild-type (WT) rats, we found that genetic ablation of the p52SHC isoform significantly attenuated mammary tumor formation, wher","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Jun","modification":"2025-04-04T22:09:04.155Z","creation":"2019-07-24T07:18:57Z"},"accession":"S-EPMC6570928","cross_references":{"pubmed":["31202267"],"doi":["10.1186/s13058-019-1155-7"]}}