Abstract:Introduction: Breast cancer onset and disease progression has been linked to members of the TGFb superfamily and their downstream signaling components, the Smads. Changes in Smad signaling have been associated with the dichotomous role of TGFβ in malignancy, mediating both tumor suppressant and tumor promoting behaviors in breast cancer. Our previous work showed that cyclin/CDK mediated phosphorylation of Smad3 resulted in the inhibition of canonical tumor suppressant Smad3 action. We thus hypothesized that ac… Show more
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