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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.
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.
PIM kinases in classical Hodgkin lymphoma exhibit pleiotropic effects, orchestrating tumor immune escape and supporting Reed-Sternberg cell survival.
Our study suggests that up-regulation of Pim-3 successfully accelerated Chronic Obstructive Pulmonary Disease development, and aggravated lung damage
High PIM3 expression is associated with osteosarcoma.
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.
Pim-3 expression was inversely correlated with that of miR-377.
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.
Pim-3 expression showed a positive correlation with tumor cell differentiation.
Pim-3 has a role in human pancreatic cancer cell survival against radiation
A high percentage of urothelial carcinomas express Pim kinases. Pim expression differs in NILG, NIHG, and IHG lesions.
MicroRNA506 participates in pancreatic cancer pathogenesis by targeting PIM3
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.
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.
PIM3 expression is higher in ovarian cancer than in normal ovarian tissue. Upregulation of PIM3 promotes proliferation and migration of ovarian cancer cells.
Data demonstrate the role of PIM kinases in driving myeloid leukemia, and as candidate molecules for therapy against human malignancies.
we constructed a dual-function small hairpin RNA (shRNA) vector containing an shRNA targeting Pim-3 and a TLR7-stimulating ssRNA.
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
cancer development and in promoting tumor neovascularization and subsequent tumor growth. Targeting Pim-3 may play a dual role in halting tumor progression, by promoting tumor cell death and blocking angiogenesis
Our study indicates that the expression of Pim kinases is physiologically related to DNA-PKcs and ATM in ECs.
Study found that by promoting the phosphorylation of Stat3 Pim-3 induced the expression of Slug, Snail, and Zeb1, which enhanced epithelial-mesenchymal transition-related changes and induced melanoma migration and invasion. Exploration of the mechanism revealed that Pim-3 bound directly to Stat3 and promoted its phosphorylation.
Loss of PIM3 is associated with abnormal hematopoietic phenotypes.
investigation of physiological role of Pim3 in beta-cell function: regulates glucose-stimulated insulin secretion; limits ERK signaling; interacts with SOCS6; Pim3 localized to beta-cell; Pim3 knockout mice display increased glucose tolerance
Pim-3 has an important role in modulating c-Myc and PGC-1alpha protein levels and cell growth
All three Pim kinase family members predominantly phosphorylate Bad on Ser112 and in addition are capable of phosphorylating Bad on multiple sites associated with the inhibition of the pro-apoptotic function of Bad in HEK-293 cells
Pim-3 kinase has a novel role in the control of self-renewal of embryonic stem cells.
Pim-3 is expressed in endothelial cells and promotes vascular tube formation.
The protein encoded by this gene belongs to the Ser/Thr protein kinase family, and PIM subfamily. This gene is overexpressed in hematological and epithelial tumors and is associated with MYC coexpression. It plays a role in the regulation of signal transduction cascades, contributing to both cell proliferation and survival, and provides a selective advantage in tumorigenesis.
serine/threonine protein kinase pim-3
, non-specific serine/threonine protein kinase
, serine/threonine-protein kinase pim-3
, serine/threonine kinase Pim-3
, kinase induced by depolarization
, protein kinase Kid-1
, proviral integration site 3
, serine threonine kinase pim3
, KID-1/kinase induced by depolarization