Disease relevance of PIM2

• This was further confirmed using purified PIM2 and PIM6 from M. bovis BCG that decreased by half the internalization of M. smegmatis [1].
• Disease progression may be related to proangiogenic processes and strong Pim2 expression [2].

High impact information on PIM2

• Targeted down-regulation of PIM-2 by RNA interference (RNAi) selectively abrogated survival of Ba/F3 cells transformed by various Fms-like tyrosine kinase 3 (FLT3)-activating mutants [internal tandem duplication (ITD) and kinase domain] and attenuated growth of human cell lines containing FLT3 mutations [3].
• Our observations indicate that combined inactivation of PIM-1 and PIM-2 interferes with oncogenic PTKs and suggest that PIMs are alternative therapeutic targets in PTK-mediated leukemia [3].
• Cells expressing activated forms of KIT or platelet-derived growth factor receptor (PDGFR), two additional targets of imatinib, were unaffected by SKI-606, whereas activity was found against PIM2 [4].
• Three of 15 genes up-regulated in the cDNA microarray were involved in the apoptosis signaling pathway (NFkappaB), and its downstream targets defender against cell death 1 and PIM-2 [5].
• The additional two mannoses in PIM4, relative to PIM2, are located at the distal 6' carbon of the alpha1-alpha6-linked mannose and would project away from the CD1d binding groove for interaction with the TCR [6].

Biological context of PIM2

• The PIM-2 kinase phosphorylates BAD on serine 112 and reverses BAD-induced cell death [7].

Associations of PIM2 with chemical compounds

• Quercetagetin was a highly selective inhibitor of PIM1 compared with PIM2 and seven other serine-threonine kinases [8].
• When coated on latex beads, PIM2 and polar GPL (GPL III) favored the particle entry through complement receptor 3 [1].
• Inhibition was essentially attributable to phosphatidylinositol mannosides (PIMs), namely PIM2 and PIM6, because the purified phosphatidylethanolamine, phosphatidylglycerol, and phosphatidylinositol were inactive [1].
• Addition of genistein and BAY 11-7085 resulted in a decrease in NFkappaB, PIM-2 and defender against cell death 1 as well as a reversal of the inhibition of apoptosis [5].

Other interactions of PIM2

• RT-PCR was performed, and we found that MDM2, BCL2, PKCZ and PIM2 expression levels were increased in A549 cells and decreased in NCI-H446 cells after irradiation [9].

Analytical, diagnostic and therapeutic context of PIM2

• CONCLUSIONS: PIM2 has been re-calibrated to reflect the improvement that has occurred in intensive care outcome [10].
• Age, PIM 2, mortality and length of stay were compared between treated and non treated patients [11].

References