Inhibition of tumor cell proliferation and motility by fibroblasts is both contact and soluble factor dependent.
Stockholm, Sweden. In Proc Natl Acad Sci U S A, 17 Dec 2014
Moreover, comparison of CCM and NCM with an antibody array for 507 different soluble human proteins revealed differential expression of growth differentiation factor 15, dickkopf-related protein 1, endothelial-monocyte-activating polypeptide II, ectodysplasin A2, Galectin-3, chemokine (C-X-C motif) ligand 2, Nidogen1, urokinase, and matrix metalloproteinase 3.
Proteases and small intestinal barrier function in health and disease.
London, United Kingdom. In Curr Opin Gastroenterol, Mar 2014
RECENT FINDINGS: It is now well established that intestinal proteases, such as matrix metalloproteinase (MMP)-1, MMP-3, MMP-10 and MMP-12, are key players in the development of ulcers in inflammatory bowel disease, have direct effects on epithelial barrier function and are involved in epithelial restitution.
Immune-metabolic interaction in Drosophila.
London, United Kingdom. In Fly (austin), Mar 2014
We have recently identified the transcription factor MEF2 as a critical switch between anabolic and immune function in the adult Drosophila fat body.
Hemorrhagic transformation after ischemic stroke in animals and humans.
Sacramento, United States. In J Cereb Blood Flow Metab, Feb 2014
This contrasts to delayed HT (>18 to 24 hours after stroke) that relates to ischemia activation of brain proteases (MMP-2, MMP-3, MMP-9, and endogenous tissue plasminogen activator), neuroinflammation, and factors that promote vascular remodeling (vascular endothelial growth factor and high-moblity-group-box-1). Processes that mediate BBB repair and reduce HT risk are discussed, including transforming growth factor beta signaling in monocytes, Src kinase signaling, MMP inhibitors, and inhibitors of reactive oxygen species.
Exercise, GLUT4, and skeletal muscle glucose uptake.
Copenhagen, Denmark. In Physiol Rev, Jul 2013
AMPK and CaMKII are key signaling kinases that appear to regulate GLUT4 expression via the HDAC4/5-MEF2 axis and MEF2-GEF interactions resulting in nuclear export of HDAC4/5 in turn leading to histone hyperacetylation on the GLUT4 promoter and increased GLUT4 transcription.