ArticlePloS one2012
Activation of cell cycle arrest and apoptosis by the proto-oncogene Pim-2.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 22 citations in OpenAlex.
- A zebrafish-based in vivo model of Zika virus infection unveils alterations of the glutamatergic neuronal development and NS4A as a key viral determinant of neuropathogenesis.PLoS pathogens · 2024Article
- The Role of PIM Kinases in Pediatric Solid Tumors.Cancers · 2022Review
- Pathogenesis and treatment of multiple myeloma bone disease.The Japanese dental science review · 2021Review
- Protein kinase PIM2: A simple PIM family kinase with complex functions in cancer metabolism and therapeutics.Journal of Cancer · 2021Review
- Inhibition of PIM2 in liver cancer decreases tumor cell proliferation in vitro and in vivo primarily through the modulation of cell cycle progression.International journal of oncology · 2020Article
- PIM-2 protein kinase negatively regulates T cell responses in transplantation and tumor immunity.The Journal of clinical investigation · 2018Article
- Critical reanalysis of the methods that discriminate the activity of CDK2 from CDK1.Cell cycle (Georgetown, Tex.) · 2016Review
- Control of Pim2 kinase stability and expression in transformed human haematopoietic cells.Bioscience reports · 2015Article
- Article
- The PIM-2 kinase is an essential component of the ultraviolet damage response that acts upstream to E2F-1 and ATM.The Journal of biological chemistry · 2013Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Potent survival effects have been ascribed to the serine/threonine kinase proto-oncogene PIM-2. Elevated levels of PIM-2 are associated with various malignancies. In human cells, a single Pim-2 transcript gives rise mainly to two protein isoforms (34, 41 kDa) that share an identical catalytic site but differ at their N-terminus, due to in-frame alternative translation initiation sites. In this study we observed that the 34 kDa PIM-2 isoform has differential nuclear and cytoplasmic forms in all tested cell lines, suggesting a possible role for the balance between these forms for PIM-2's function. To further study the cellular role of the 34 kDa isoform of PIM-2, an N-terminally HA-tagged form of this isoform was transiently expressed in HeLa cells. Surprisingly, this resulted in increased level of G1 arrested cells, as well as of apoptotic cells. These effects could not be obtained by a Flag-tagged form of the 41 kDa isoform. The G1 arrest and apoptotic effects were associated with an increase in T14/Y15 phosphorylation of CDK2 and proteasom-dependent down-regulation of CDC25A, as well as with up-regulation of p57, E2F-1, and p73. No such effects were obtained upon over-expression of a kinase-dead form of the HA-tagged 34 kDa PIM-2. By either using a dominant negative form of p73, or by over-expressing the 34 kDa PIM-2 in p73-silenced cells, we demonstrated that these effects were p73-dependent. These results demonstrate that while PIM-2 can function as a potent survival factor, it can, under certain circumstances, exhibit pro-apoptotic effects as well.
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Registered trials
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