ABSTRACT: Expression data fom human capillary network-derived cells before and after adipogenic differentation, and after chronic adenylate cyclase activation of differentiated cells
Project description:Progenitors in human vasculature expanded in-vitro were differentiated with adipogenic cocktail for 12 days, following which they were stimulated with forskolin for 7 days Microarrays were used to detail the program of differentiation of thermogenic human adipose cells Adipose tissue from three individuals was cultured in hydrogel under pro-angiogenic conditions. Capillary networks emerging from the explants were subcultured on plastic, grown to confluence, subjected to adipogenic differentiation and after 12 days treated with vehicle or forskolin for 7 days
Project description:The whooping cough agent, Bordetella pertussis, subverts dendritic cell (DCs) functions through powerful immunomodulatory activities of its toxins. Here we focused on the signaling action of the adenylate cyclase toxin (CyaA) that targets myeloid cells expressing the αMβ2 integrin CD11b/CD18 (known as complement receptor 3 (CR3) or Mac-1). CyaA delivers an extremely catalytically potent adenylyl cyclase enzyme domain into the cytosol of phagocytes and disrupts their innate and adaptive immune functions through unregulated production of the key signaling molecule cAMP. Here we describe the global phosphoproteomic analysis of cAMP signaling in murine bone marrow-derived DCs exposed to CyaA. Gathered data reveal toxin-triggered alternations of phosphorylation status of proteins regulating actin cytoskeleton, chromatin remodeling, mTOR activity and IL-10 gene expression. The reported findings highlight the complexity of subversive physiological manipulation that is exerted on myeloid phagocytes by the cAMP-generating adenylate cyclase toxin of Bordetellae.
Project description:Investigation of transcriptional changes induced in adult primary neural stem cells when stimulated with the proliferative agent PACAP (pituitary adenylate cyclase-activating polypeptide). In addition the data was compared to results obtained from a proliferation control (stimulation with a transmembrane receptor agonist) and a differentiation control (primary neural stem cells induced to differentiate by withdrawing growth factors, adding serum and plating onto solid support).
Project description:The acidic tumor microenvironment in melanoma drives immune evasion by up-regulating cyclic adenosine monophosphate (cAMP) in tumor-infiltrating monocytes..Melanoma growth can be suppressed by releasing non-toxic concentrations of an adenylate cyclase (AC) inhibitor from polypept(o)id micelles at the tumor site in an immune cell-dependent manner.
Project description:Adenylate cyclase signaling pathway is suggested to be a key regulator of immune system functions. However, specific effects of cyclic adenosine monophosphate on T helper cell differentiation and functions are unclear. Involvement of cAMP in Th cell differentiation program, in particular development of Th1, Th2, and Th17 subsets, was evaluated employing forskolin (FSK), a labdane diterpene well known as AC activator.
Project description:The aim of this study was to evaluate changes in the transcriptome due to the lack of adenylate cyclase in light or darkness. As the cAMP pathway represents an output pathway of heterotrimeric G-protein signaling ACY1 is likely to be important for regulation of enzymes in response to different nutrient conditions. Also, a light dependent effect was found earlier.
Project description:hMSCs (Lonza) were differentiated towards adipocytes with three cycles of adipocyte differentiation induction and maintenance. hMSCs were differentiated towards osteocytes with osteogenic differentiation medium for 3 days and for 7 days. ArrayCGH experiments were performed before differentiation induction, after 2 and 3 cycles of adipogenic differentiation induction and after 3 days and 7 days of osteogenic differentiation induction.
