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Zinc finger protein 354A

kidney 1, Pim-3, Kid-1, kidney I
C2H2 class zinc finger-containing DNA-binding protein; may act as a transcription factor [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: pim-1, HAD, PIM2, CAN, AGE
Papers on kidney 1
Design and synthesis of an in vivo-efficacious PIM3 kinase inhibitor as a candidate anti-pancreatic cancer agent.
Nagano et al., Tokyo, Japan. In Bioorg Med Chem Lett, Jan 2016
Serine/threonine kinase PIM3 is a potential therapeutic target for pancreatic cancer.
Binding site identification and role of permanent water molecule of PIM-3 kinase: A molecular dynamics study.
Khan et al., Karāchi, Pakistan. In J Mol Graph Model, Nov 2015
PIM-3, sub-member of PIM kinases is a proto-oncogene, its overexpression inhibits apoptosis, and results in progression of hepatocellular carcinoma.
[Protective effect of phloroglucinol on renal ischemia and reperfusion injury].
Ma et al., Beijing, China. In Beijing Da Xue Xue Bao, Nov 2015
CONCLUSION: PG protects murine kidney I/R injury by suppressing oxidative stress, inflammation, and cell apoptosis.
MicroRNA‑506 participates in pancreatic cancer pathogenesis by targeting PIM3.
Jiao et al., Beijing, China. In Mol Med Report, Oct 2015
PIM-3 is a member of the proto-oncogene PIM family, the aberrant expression of which exists in human pancreatic cancer tissues.
The Effect of Autophagy on Inflammation Cytokines in Renal Ischemia/Reperfusion Injury.
Xie et al., Zhangjiakou, China. In Inflammation, Oct 2015
In this study, we discuss how autophagy regulated inflammation response in the kidney I/R.
Overexpression of pim-3 and protective role in lipopolysaccharide-stimulated hepatic stellate cells.
Cheng et al., Nanchang, China. In World J Gastroenterol, Sep 2015
To study the effect of pim-3 kinase on HSC-T6 cells, si-pim3 (siRNA against pim-3) was transfected into HSC-T6 cells.
The protective effect of apelin on ischemia/reperfusion injury.
Chen et al., Kaifeng, China. In Peptides, 2015
Apelin could activate multiple protective mechanisms to prevent heart, brain, liver and kidney I/R injury.
The effect of nuclear factor of activated T-cells (NFAT) in kidney I/R mediated by C5a/C5aR.
Liu et al., 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.
Ananthasubramaniam et al., 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.
PIM kinases: an overview in tumors and recent advances in pancreatic cancer.
Zhao et al., Beijing, China. In Future Oncol, 2014
The PIM kinases represent a family of serine/threonine kinases, which is composed of three different members (PIM1, PIM2 and PIM3).
Small molecule inhibitors of PIM1 kinase: July 2009 to February 2013 patent update.
Viswanadhan et al., 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.
Carnero et al., 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.
Genetic Modeling of PIM Proteins in Cancer: Proviral Tagging and Cooperation with Oncogenes, Tumor Suppressor Genes, and Carcinogens.
Blanco-Aparicio et al., Madrid, Spain. In Front Oncol, 2013
Mouse models have also been used to study whether the inhibition of specific PIM isoforms is required to prevent carcinogen-induced sarcomas, indicating that the absence of Pim2 and Pim3 greatly reduces sarcoma growth and bone invasion; the extent of this effect is similar to that observed in the absence of all three isoforms.
Pim protein kinase-3 is regulated by TNF-α and promotes endothelial cell sprouting.
Huang et al., Wuhan, China. In Mol Cells, 2011
Pim protein kinase-3 is regulated by TNF-alpha and promotes endothelial cell sprouting.
The direct Myc target Pim3 cooperates with other Pim kinases in supporting viability of Myc-induced B-cell lymphomas.
Nilsson et al., Umeå, Sweden. In Oncotarget, 2011
Pim3 cooperates with other Pim kinases in supporting viability of Myc-induced B-cell lymphomas.
Mutations in lectin complement pathway genes COLEC11 and MASP1 cause 3MC syndrome.
Beales et al., London, United Kingdom. In Nat Genet, 2011
Here we studied 11 families with 3MC syndrome and identified two mutated genes, COLEC11 and MASP1, both of which encode proteins in the lectin complement pathway (collectin kidney 1 (CL-K1) and MASP-1 and MASP-3, respectively).
The Pim protein kinases regulate energy metabolism and cell growth.
Kraft et al., Charleston, United States. In Proc Natl Acad Sci U S A, 2011
Pim-3 has an important role in modulating c-Myc and PGC-1alpha protein levels and cell growth
Pim3 negatively regulates glucose-stimulated insulin secretion.
Steiner et al., 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
Fighting tumor cell survival: advances in the design and evaluation of Pim inhibitors.
Moreau et al., Clermont-Ferrand, France. In Curr Med Chem, 2009
A cell-based test system useful for rapid and inexpensive pre-screening of compounds capable of preventing Pim-mediated phosphorylation is discussed.
High-throughput retroviral tagging to identify components of specific signaling pathways in cancer.
Romeyn et al., Amsterdam, Netherlands. In Nat Genet, 2002
In addition, we found that Pim3 is selectively activated in Pim-null tumor cells, which supports the validity of our approach.
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