Constraints on split-UED from Electroweak Precision Tests

We present strongly improved electroweak precision constraints on the split-UED model. We find that the dominating effect arises from contributions to the muon decay rate by the exchange of even-numbered W-boson Kaluza-Klein modes at tree-level, which so far have not been discussed in the context of UED models. The constraints on the split-UED parameter space are translated into bounds on the mass difference of the first Kaluza-Klein mode of fermions and the lightest Kaluza-Klein mode, which will be tested is the LHC.Comment: 4 pages, 2 figure

Constraints on UED from W' searches

We obtain contraints on three Universal Extra Dimensional models utilizing limits from the CMS Collaboration on W' production and decay into a single-top-quark final state. We find a weak constraint on the Minimal Universal Extra Dimensions model due to small Kaluza-Klein number violating terms. In contrast, the W' search puts a strong limit on the size of the Dirac mass term of the quarks in Split Universal Extra Dimension models. In Non-minimal Universal Extra Dimension models the W' search constrains the splitting between the boundary localized kinetic terms of the gauge bosons and the quarks. Each of these bounds can be translated into constraints on the mass splitting between the Kaluza-Klein excitations of the SU(2) charged quarks and the Klauza-Klein excitations of the W boson.Comment: 7 pages, 5 figures; Updated Draft and Figure

The activity of cAMP-Phosphodiesterase 4D7 (PDE4D7) is regulated by protein kinase A-dependent phosphorylation within its unique N-terminus

The cyclic AMP phosphodiesterases type 4 (PDE4s) are expressed in a cell specific manner, with intracellular targeting directed by unique N-terminal anchor domains. All long form PDE4s are phosphorylated and activated by PKA phosphorylation within their upstream conserved region 1 (UCR1). Here, we identify and characterise a novel PKA site (serine 42) within the N-terminal region of PDE4D7, an isoform whose activity is known to be important in prostate cancer progression and ischemic stroke. In contrast to the UCR1 site, PKA phosphorylation of the PDE4D7 N-terminus appears to occur constitutively and inhibits PDE4 activity to allow cAMP signalling under basal conditions