To address these questions, we generated mice lacking mCAP1/ Prss8 in the alveolar epithelium using tissue-specific Cre-loxP-mediated recombination, and studied the consequences of CAP1/ Prss8 deficiency in distal lung Na+ and fluid transport.
To specifically address this point, we injected IL-1β and other cytokines/chemokines with known pro-inflammatory functions like TNF-α [ 14], IFN-γ [ 15], IL-6 [ 7, 16], and CXCL2 into the striatum, and studied the consequences of this treatment for the recruitment of AQP4-specific antibodies, complement and neutrophils to the CNS.
In this study, we have manipulated the copy number of native motor complexes on a physiological type of cargo, by incubating cellular extracts with RNA variants, and studied the consequences on motility in a defined in vitro setting using high spatiotemporal resolution imaging.
To investigate the possibility of function blocking antibodies to NRP1 as potential therapeutics, and study the consequence of targeting NRP1 in murine tumor models, panels of antibodies that cross-react with human and murine NRP1 were generated from a designed antibody phage library.
We model in-register intermolecular β-sheet β-sheet associations and study the consequences of Alzheimer's mutations (E22G, E22Q, E22K, and M35A) on the organization.
In particular, we consider how fiscal stringency requirements like the Stability and Growth Pact affect fiscal policy design under EMU and study the consequences of the introduction of a fiscal transfer mechanism between countries.
By directing expression of an engineered protein to the heart, one is now able to effectively remodel the cardiac protein profile and study the consequences of a single genetic manipulation at the molecular, biochemical, cytological and physiologic levels, both under normal and stress stimuli.
Thus we can now ablate or augment expression of a engineered protein in the heart and are able to effectively remodel the cardiac protein profile and study the consequences of a single genetic manipulation at the molecular, biochemical, cytological and physiologic levels.
In order to further test the concept of balance between initiation and development, we decided to artificially perturb the primordium initiation process and study the consequences on the development process.
Here, we present a model that includes explicitly the downstream signaling pathways from p53 and AKT to apoptosis, and study the consequences of p53 oscillations on the regulation of caspase-dependent apoptosis.
