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1. The People's Progress . Frank Ireson 1911

   https://ncsu.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV3dS8MwED90PuiLzCn4bR5EH6Rb6UeawBjIUPStyN5L1g-Gggyr_7-XXNNmikzxJTShCc39ksv1ch8Al3MeVlxWBe60oPCipBCeCKLYCyupuIq5Un61qsyh7J71T1bso39Di20IrnaV_QO87aDYgM8IMpYIM5a_Bjo1duBG955qgyvNvoZGKH25ecRaQ_vnrocjiC7JBA4rZd65OBTkGqdVm4nVBDiW-cInflZahpZ4cUhWkC3Hkw6yicO-OGWgbU7CpvaNyfrmzke7vPpBd4zYq_Mvp0tr82duuwXPqN8mbAWJlDrnxNM0dQJ--WEb3x1n4mSDon6O-ODIAbM-7DZ0Y7cExB5slK8D2Lb-3fUA-qmlJ2sY5z5owxZGIF3XzELEhmy8mBiUGKE0Hi0mB3B1fzebPnj2C7IlRQTJVucWHgKLhcRlHomqmKtI87kojysldeikHH9ByyO4WDPK8do3TmCnWwan0Ht_-yjPoKd3zbkh6ycmChJ-

   The Journal Of Political Economy, Vol. 19, Issue 7, p. 607.

   Journal Article  |  Full Text Online

2. Silencing of protein kinase D2 induces glioma cell senescence via p53-dependent and -independent... 2014

   https://ncsu.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1NT9wwEB0BB8QFtYDo0nZlJNRbyCZ2nORYURCXFUhQiVvk-KO1YJ0Vybbqv-84TqBLJQ4ckzhKMjPOzLNn3gCc1JwaXhqFMy1VEctVERUpyyJqSsFFxoWYmfXFHMjGWpg-aV_W9tQ9LE6d_dnnVi4XMh7zxOLr-ZkPMhBbxZuwmVM2QvQBZSEgCSSpiLJ84_mBWBORe-z0qnEydk2HP25PA4xYiFJf5fevT_ov0HyZLxkyJXsHdPEOdofIkXwNb_geNrTbg-35sDe-D_bG-gIidEWkMaTnX7CO3FuHfop8SwmCb1RjS3482GYhiF-xJ63_00k_uckvK8gyo9HYFbcjwikSWfd8wncv_i3-tAfw_eL89uwyGhopRJKlsy7iOtGK1aI0gmeC01T6Y5krxCqqNLo2tJA8EbQomM4TJWuDCuSMK13Xs8zQD0CyokS9scKoWjA_cZnMjCg9F5BETKUn8GWUYbUMRBlV2OCmVZB7FeQ-geNRwhWasv9a4XSzaqt-084zhiWvjikxYuM8ncBh0MrT40Z1TiBf09fTAE-lvX4FLayn1B4s6ujNd36EHQylWEjk_QRb3eNKf4YtX4cxRfu8upv2VvoXKa_whA

   Bernhart, Eva; Damm, Sabine; Heffeter, Petra; Wintersperger, Andrea...

   Neuro Oncology (Charlottesville, Va.), Vol. 16, Issue 7, pp. 933 - 945.

   Glioblastoma multiforme (GBM) is a highly aggressive tumor of the central nervous system with a dismal prognosis for affected patients. Aberrant protein kinase C (PKC) signaling has been implicated... Read more

   Glioblastoma multiforme (GBM) is a highly aggressive tumor of the central nervous system with a dismal prognosis for affected patients. Aberrant protein kinase C (PKC) signaling has been implicated in gliomagenesis, and a member of the PKC-activated protein kinase D (PRKD) family, PRKD2, was identified as mediator of GBM growth in vitro and in vivo. The outcome of PRKD2 silencing and pharmacological inhibition on glioma cell proliferation was established with different glioma cell lines. Western blotting, senescence assays, co-immunoprecipitation, fluorescence activated cell sorting, quantitative PCR, and immunofluorescence microscopy were utilized to analyze downstream signaling. RNA-interference (21-mer siRNA) and pharmacological inhibition (CRT0066101) of PRKD2 profoundly inhibited proliferation of p53(wt) (U87MG, A172, and primary GBM2), and p53(mut) (GM133, T98G, U251, and primary Gli25) glioma cells. In a xenograft experiment, PRKD2 silencing significantly delayed tumor growth of U87MG cells. PRKD2 silencing in p53(wt) and p53(mut) cells was associated with typical hallmarks of senescence and cell cycle arrest in G1. Attenuated AKT/PKB phosphorylation in response to PRKD2 silencing was a common observation made in p53(wt) and p53(mut) GBM cells. PRKD2 knockdown in p53(wt) cells induced upregulation of p53, p21, and p27 expression, decreased phosphorylation of CDK2 and/or CDK4, hypophosphorylation of retinoblastoma protein (pRb), and reduced transcription of E2F1. In p53(mut) GM133 and primary Gli25 cells, PRKD2 silencing increased p27 and p15 and reduced E2F1 transcription but did not affect pRb phosphorylation. PRKD2 silencing induces glioma cell senescence via p53-dependent and -independent pathways. Read less

   Journal Article  |  Full Text Online

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