The effect of nuclear factor of activated T-cells (NFAT) in kidney I/R mediated by C5a/C5aR.
Wuhan, China. In Int J Clin Exp Med, 2014
To investigate the relationship between NFAT and C5a/C5aR in C5a/C5aR-mediated kidney Ischemia/reperfusion (I/R) injury, the rats' NRK-52E cell line was used in this study and was distributed into 4 groups, I: the normal control (NC), II: the ischemia/reperfusion (I/R) injury cell model (MG), III: the ischemia/reperfusion (I/R) injury cell model treated with C5a (50 nmol/l) (MG + C5a), IV: the ischemia/reperfusion (I/R) injury cell model treated with C5aR antagonist (2.5 μmol/l) (MG + anti-C5aR).
Mining for novel candidate clock genes in the circadian regulatory network.
Berlin, Germany. In Bmc Syst Biol, 2014
Using the criteria of circadian proteomic expression, circadian expression in multiple tissues and independent gene knockdown data, we propose six genes (Por, Mtss1, Dgat2, Pim3, Ppp1r3b, Upp2) involved in metabolism and cancer for further experimental investigation.
Small molecule inhibitors of PIM1 kinase: July 2009 to February 2013 patent update.
Bengaluru, India. In Expert Opin Ther Pat, 2014
INTRODUCTION: The proviral insertion in murine (PIM) lymphoma proteins for which three isoforms, PIM1, PIM2 and PIM3 have been identified, belonging to the family of serine/threonine kinases has emerged recently as an important therapeutic target for the development of selective inhibitors as the new drugs for treating hematological malignancies and solid tumors.
The PIM family of serine/threonine kinases in cancer.
Madrid, Spain. In Med Res Rev, 2014
The proviral insertion site in Moloney murine leukemia virus, or PIM proteins, are a family of serine/threonine kinases composed of three different isoforms (PIM1, PIM2, and PIM3) that are highly evolutionarily conserved.
Pim3 negatively regulates glucose-stimulated insulin secretion.
Chicago, United States. In Islets, 2010
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