76 research outputs found
The Relation of Ear Rot Prevalence in Illinois Corn Fields to Ear Coverage by Husks
is peer reviewedOpe
Amazons letzte Meile: Ein OnlinehÀndler als Prekarisierungstreiber in der Paketlogistik - Eine Fallstudie zum Verteilzentrum Erfurt-Stotternheim
Protein Kinase CK2 Contributes to Glucose Homeostasis by Targeting Fructose-1,6-Bisphosphatase 1
Glucose homeostasis is of critical importance for the survival of organisms. It is under hormonal control and often coordinated by the action of kinases and phosphatases. We have previously
shown that CK2 regulates insulin production and secretion in pancreatic ÎČ-cells. In order to shed more
light on the CK2-regulated network of glucose homeostasis, in the present study, a qRT-PCR array was
carried out with 84 diabetes-associated genes. After inhibition of CK2, fructose-1,6-bisphosphatase 1
(FBP1) showed a significant lower gene expression. Moreover, FBP1 activity was down-regulated.
Being a central enzyme of gluconeogenesis, the secretion of glucose was decreased as well. Thus,
FBP1 is a new factor in the CK2-regulated network implicated in carbohydrate metabolism control
Protein Kinase CK2 Regulates Nerve/Glial Antigen (NG)2-Mediated Angiogenic Activity of Human Pericytes
Protein kinase CK2 is a crucial regulator of endothelial cell proliferation, migration and
sprouting during angiogenesis. However, it is still unknown whether this kinase additionally affects
the angiogenic activity of other vessel-associated cells. In this study, we investigated the effect of
CK2 inhibition on primary human pericytes. We found that CK2 inhibition reduces the expression of
nerve/glial antigen (NG)2, a crucial factor which is involved in angiogenic processes. Reporter gene
assays revealed a 114 bp transcriptional active region of the human NG2 promoter, whose activity
was decreased after CK2 inhibition. Functional analyses demonstrated that the pharmacological
inhibition of CK2 by CX-4945 suppresses pericyte proliferation, migration, spheroid sprouting and
the stabilization of endothelial tubes. Moreover, aortic rings of NG2â/â mice showed a significantly
reduced vascular sprouting when compared to rings of NG2+/+ mice, indicating that NG2 is an
important regulator of the angiogenic activity of pericytes. In vivo, implanted Matrigel plugs
containing CX-4945-treated pericytes exhibited a lower microvessel density when compared to
controls. These findings demonstrate that CK2 regulates the angiogenic activity of pericytes through
NG2 gene expression. Hence, the inhibition of CK2 represents a promising anti-angiogenic strategy,
because it does not only target endothelial cells, but also vessel-associated pericytes
Inhibition of CK2 Reduces NG2 Expression in Juvenile Angiofibroma
Juvenile angiofibroma (JA) is a rare fibrovascular neoplasm predominately found within the
posterior nasal cavity of adolescent males. JA expresses the proteoglycan nerveâglial antigen (NG)2,
which crucially determines the migratory capacity of distinct cancer cells. Moreover, it is known that
the protein kinase CK2 regulates NG2 gene expression. Therefore, in the present study, we analyzed
whether the inhibition of CK2 suppresses NG2-dependent JA cell proliferation and migration. For
this purpose, we assessed the expression of NG2 and CK2 in patient-derived JA tissue samples, as
well as in patient-derived JA cell cultures by Western blot, immunohistochemistry, flow cytometry
and quantitative real-time PCR. The mitochondrial activity, proliferation and migratory capacity
of the JA cells were determined by water-soluble tetrazolium (WST)-1, 5-bromo-20
-deoxyuridine
(BrdU) and collagen sprouting assays. We found that NG2 and CK2 were expressed in both the JA
tissue samples and cell cultures. The treatment of the JA cells with the two CK2 inhibitors, CX-4945
and SGC-CK2-1, significantly reduced NG2 gene and protein expression when compared to the
vehicle-treated cells. In addition, the loss of CK2 activity suppressed the JA cell proliferation and
migration. These findings indicate that the inhibition of CK2 may represent a promising therapeutic
approach for the treatment of NG2-expressing JA
CK2 Activity Mediates the Aggressive Molecular Signature of Glioblastoma Multiforme by Inducing Nerve/Glial Antigen (NG)2 Expression
Nerve/glial antigen (NG)2 expression crucially determines the aggressiveness of glioblastoma multiforme (GBM). Recent evidence suggests that protein kinase CK2 regulates NG2 expression.
Therefore, we investigated in the present study whether CK2 inhibition suppresses proliferation
and migration of NG2-positive GBM cells. For this purpose, CK2 activity was suppressed in the
NG2-positive cell lines A1207 and U87 by the pharmacological inhibitor CX-4945 and CRISPR/Cas9-
mediated knockout of CK2α. As shown by quantitative real-time PCR, luciferase-reporter assays,
flow cytometry and western blot, this significantly reduced NG2 gene and protein expression when
compared to vehicle-treated and wild type controls. In addition, CK2 inhibition markedly reduced
NG2-dependent A1207 and U87 cell proliferation and migration. The Cancer Genome Atlas (TCGA)-
based data further revealed not only a high expression of both NG2 and CK2 in GBM but also
a positive correlation between the mRNA expression of the two proteins. Finally, we verified a
decreased NG2 expression after CX-4945 treatment in patient-derived GBM cells. These findings
indicate that the inhibition of CK2 represents a promising approach to suppress the aggressive
molecular signature of NG2-positive GBM cells. Therefore, CX-4945 may be a suitable drug for the
future treatment of NG2-positive GBM
Hypoxia-induced downregulation of microRNA-186-5p in endothelial cells promotes non-small cell lung cancer angiogenesis by upregulating protein kinase C alpha
The tumor microenvironment stimulates the angiogenic activity of endothelial cells (ECs) to facilitate tumor vascularization,
growth, and metastasis. The involvement of microRNA-186-5p
(miR-186) in regulating the aberrant activity of tumor-associated ECs has so far not been clarified. In the present study,
we demonstrated that miR-186 is significantly downregulated
in ECs microdissected from human non-small cell lung cancer
(NSCLC) tissues compared with matched non-malignant lung
tissues. In vitro analyses of primary human dermal microvascular ECs (HDMECs) exposed to different stimuli indicated
that this miR-186 downregulation is triggered by hypoxia
via activation of hypoxia-inducible factor 1 alpha (HIF1a).
Transfection of HDMECs with miR-186 mimic (miR-186m)
significantly inhibited their proliferation, migration, tube
formation, and spheroid sprouting. In contrast, miR-186
inhibitor (miR-186i) exerted pro-angiogenic effects. In vivo,
endothelial miR-186 overexpression inhibited the vascularization of Matrigel plugs and the initial growth of tumors
composed of NSCLC cells (NCI-H460) and HDMECs. Mechanistic analyses revealed that the gene encoding for protein
kinase C alpha (PKCa) is a bona fide target of miR-186. Activation of this kinase significantly reversed the miR-186mrepressed angiogenic activity of HDMECs. These findings
indicate that downregulation of miR-186 in ECs mediates hypoxia-stimulated NSCLC angiogenesis by upregulating PKCa
Experimental evaluation of the energy efficiency of a CO2 refrigerating plant working in transcritical conditions
[EN] This work presents the experimental evaluation of the energy efficiency and optimal gas-cooler pressures of a single-stage refrigerating plant working with carbon dioxide as refrigerant in transcritical conditions. The performance of the plant was tested at three different evaporating temperatures (-0.9, -10.1 and -18.1 degrees C), for three gas-cooler refrigerant outlet temperatures (31.2, 33.6 and 40.0 degrees C) at each evaporating temperature and in a wide range of gas-cooler pressures (74.4-104.7 bar).
The experimental tests enabled us to calculate accurately the optimal gas-cooler pressures and compare them with the most commonly used relations to define this value in single-stage refrigerating cycles operating with carbon dioxide in transcritical conditions. Furthermore, an analysis of the reduction in energy efficiency produced in the plant if the optimum pressure is not well defined is also presented.The authors are indebted to Frost-Trol S.A. (www.frosttrol.com) and the Spanish Ministry of Education and Science (ENE2006-09972/CON) for the economical support given to the present work and for the Grant BES-2007-16820 linked to the Ministry projectCabello, R.; Sanchez, D.; Llopis, R.; Torrella Alcaraz, E. (2008). Experimental evaluation of the energy efficiency of a CO2 refrigerating plant working in transcritical conditions. Applied Thermal Engineering. 28(13):1596-1604. https://doi.org/10.1016/j.applthermaleng.2007.10.026S15961604281
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