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results demonstrate that PIM3 is induced upon mTORC1 inhibition, with potential implications for the effects of mTORC1 inhibitors in TSC, cancers, and the many other disease settings influenced by aberrant mTORC1 signaling.
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Study identified that PIM1 and PIM3 phosphorylate HIV-2 Vpx at Ser13 and stabilize the interaction of Vpx with SAMHD1 thereby promoting ubiquitin-mediated proteolysis of SAMHD1 and revealed a regulatory mechanism of virus-host interaction that governs viral escape from an intrinsic cellular immune defense via the post-translational modification of viral protein.
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show that PIM1 contributes to melanoma cell proliferation and tumor growth in vivo; however, the presence of PIM2 and PIM3 could also influence the outcome.
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These results demonstrate the involvement of PIM kinases in LIF-induced regulation in different trophoblastic cell lines which may indicate similar functions in primary cells.
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PIM kinases in classical Hodgkin lymphoma exhibit pleiotropic effects, orchestrating tumor immune escape and supporting Reed-Sternberg cell survival.
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Our study suggests that up-regulation of Pim-3 successfully accelerated Chronic Obstructive Pulmonary Disease development, and aggravated lung damage
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High PIM3 expression is associated with osteosarcoma.
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The expression status of Pim-3 mRNA was significantly associated with pathological parameters such as pre-surgery prostate specific antigen, Gleason score, pathological stage, and lymphoid metastasis.
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Pim-3 expression was inversely correlated with that of miR-377.
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SSRP1/Ets-1/Pim-3 signalling is tightly associated with the proliferation, apoptosis, autophagy, invasion and clonogenicity of nasopharyngeal carcinoma cells, and blockage of this signalling facilitates chemosensitivity of the cells to docetaxel.
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Pim-3 expression showed a positive correlation with tumor cell differentiation.
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Pim-3 has a role in human pancreatic cancer cell survival against radiation
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A high percentage of urothelial carcinomas express Pim kinases. Pim expression differs in NILG, NIHG, and IHG lesions.
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MicroRNA506 participates in pancreatic cancer pathogenesis by targeting PIM3
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Pim-3 kinase enhances growth and metastatic properties of prostate cancer xenografts. PC-3 prostate cancer cells overexpressing either Pim-1 or Pim-3 kinases form larger xenograft tumors than the parental PC-3 cells.
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Knockdown of Pim-3 by specific shRNA slowed decreased proliferation, induced cell cycle arrest in the G0/G1 phase, and increased apoptosis in glioblastoma cells.
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PIM3 expression is higher in ovarian cancer than in normal ovarian tissue. Upregulation of PIM3 promotes proliferation and migration of ovarian cancer cells.
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Data demonstrate the role of PIM kinases in driving myeloid leukemia, and as candidate molecules for therapy against human malignancies.
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we constructed a dual-function small hairpin RNA (shRNA) vector containing an shRNA targeting Pim-3 and a TLR7-stimulating ssRNA.
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Blocking the activities of PIM kinases(PIM1, PIM2 and PIM3) could prevent pancreatic cancer development. PIM kinases(PIM1, PIM2 and PIM3) may be a novel target for cancer therapy