Proto-Oncogene Pim-2 (Serine Threonine Kinase) (PIM2) ELISA Kits

Zebrafish Proto-Oncogene Pim-2 (Serine Threonine Kinase) (PIM2) Interaktionspartner

1. Inhibition of the Pim1 oncogene results in diminished visual function.

Human Proto-Oncogene Pim-2 (Serine Threonine Kinase) (PIM2) Interaktionspartner

1. PIM2 is upregulated by strongly activated tumor suppressor protein p53.

2. PIM2 might function as an important oncogene in gastric cancer

3. These findings demonstrate an important role for the PIM2-TTP complex in breast cancer tumorigenesis.

4. High PIM2 expression is associated with Malignant Grade in Prostate Cancer.

5. our findings indicated that PIM2 was a novel regulator of HK2, and suggested a new strategy to treat breast cancer.

6. we showed that RPS6KA3 knockdown reduced the propagation of human AML cells in vivo in mice. Our results point to RSK2 as a novel Pim2 target with translational therapeutic potential in FLT3-ITD AML.

7. Inhibition of PIM2 attenuated asthma symptoms and increased expression levels of interleukin (IL)10 and forkhead box protein 3 (FOXP3) in bronchoalveolar lavage fluid.

8. data suggest that PIM1/2 kinase overexpression is a common feature of male reproductive organs tumors, which provoke tissue alterations and a large inflammatory response that may act synergistically during the process of tumorigenesis.

9. 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.

10. the elevated expression of PIM2 in blastic cells is associated with poor prognosis of AML patients and their resistance to induction therapy.

11. Our data provide evidence for a novel role for Pim2 in the regulation of the DNA damage response (DDR). Knockdown of Pim2 upregulates several downstream DDR markers, mimicking the effects of doxorubicin (Dox) treatment of MM cells, and suggesting a role for the kinase as a negative regulator of this pathway.

12. 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.

13. PIM kinases in classical Hodgkin lymphoma exhibit pleiotropic effects, orchestrating tumor immune escape and supporting Reed-Sternberg cell survival.

14. High PIM2 expression is associated with osteosarcoma.

15. We show that Pim2 inhibitors and proteasome inhibitors, such as bortezomib, have additive effects to inhibit the growth of myeloma cells, suggesting that Pim2 could be an interesting target for the treatment of multiple myeloma.

16. PIM2 gene knockdown enhances the anti-proliferative effect of AZD1208 in non-Hodgkin lymphoma cell line.

17. A high percentage of urothelial carcinomas express Pim kinases. Pim expression differs in NILG, NIHG, and IHG lesions.

18. Our findings suggest that Pim-2-mediated aerobic glycolysis is critical for monitoring Warburg effect in colorectal tumor cells, highlighting Pim-2 as a potential metabolic target for colorectal tumor therapy.

19. our findings will help to uncover novel signaling pathways between inflammations and oxidative stress in rheumatoid arthritis development and imply that Pim-2/mTORC1 pathway may be critical for the initiation of inflammatory reactions.

20. Persistent activation of STAT3 by PIM2-driven positive feedback loop for epithelial-mesenchymal transition in breast cancer.

Mouse (Murine) Proto-Oncogene Pim-2 (Serine Threonine Kinase) (PIM2) Interaktionspartner

1. PIM2 might function as an important oncogene in gastric cancer

2. studies define a pathway for limiting the regulation of Foxp3 function because the Pim-2 kinase represents a potential therapeutic target for modulating the Treg cell suppressive activities in controlling immune responses

3. Pim2 facilitated allograft rejection primarily by modulating the apoptosis of effector T cells and the function of regulatory T cells.

4. Loss of PIM2 is associated with abnormal hematopoietic phenotypes.

5. signals from IL-7 and RAG DSBs activate distinct Pim kinase family members that have context-dependent activities in regulating pre-B cell proliferation and survival.

6. Targeting cap-dependent translation blocks converging survival signals by AKT and PIM 1, 2 kinases in lymphoma

7. PIM2 controls the expression of the pro-inflammatory cytokine IL-6.

8. results support the hypothesis that Pim2, which is also a known target of Flt3-ITD (another gene that cooperates with PML-RARalpha), cooperates with PRalpha to induce acute promyelocytic leukemia-like disease

9. Pim-2 is a direct link between growth factor-induced transcription and a novel, kinase-dependent pathway that promotes cell-autonomous survival

10. pim-2 functions similarly to pim-1 as a pro-survival kinase; BAD is a legitimate PIM-2 substrate

11. Pim-2 and Akt-1 are critical components of overlapping but independent pathways, either of which is sufficient to promote the growth and survival of nontransformed hematopoietic cells

12. PIM-2 regulates a new intermediate stage in the differentiation pathway, the induction of autophagy.

13. BLyS stimulation activates 2 independent signaling pathways, Akt/mTOR and Pim 2, associated with cell growth and survival.

14. Overexpression of Pim2 together with Flt3-Wt or D835Y receptor is associated with neoplastic transformation

15. Pim kinases play a key role in the v-Abl transformation, possibly via participating in modulation of SOCS-1 and via regulating the apoptotic signaling

16. expression of the Myc and Pim proto-oncogenes by Jak2V617F was found to be FERM domain dependent.

17. through stabilizing c-Myc, Pim-1/Pim-2 kinases enhance the transcriptional activity of c-Myc. Also knocking down either Pim-1 or Pim-2 dramatically decreases the endogenous levels of c-Myc and thus, its transcriptional activity

18. PIM2 triggered significant p65 nuclear factor -kappaB (NF-kappaB) nuclear translocation that was dependent on activation of PI3K or Notch1 signaling

19. Invitro transcription/translation, site-directed mutagenesis, and immunoprecipitation studies described here, show that translation initiates at three different start sites, with the two major upstream sites initiating at non-AUG (CUG) codons.