0000000001217074
AUTHOR
J. Friedman
De novo CCND2 mutations leading to stabilization of cyclin D2 cause megalencephaly-polymicrogyria-polydactyly-hydrocephalus syndrome
Activating mutations in genes encoding phosphatidylinositol 3-kinase (PI3K)-AKT pathway components cause megalencephaly-polymicrogyria-polydactyly-hydrocephalus syndrome (MPPH, OMIM 603387)(1-3). Here we report that individuals with MPPH lacking upstream PI3K-AKT pathway mutations carry de novo mutations in CCND2 (encoding cyclin D2) that are clustered around a residue that can be phosphorylated by glycogen synthase kinase 313 (GSK-3 beta)(4). Mutant CCND2 was resistant to proteasomal degradation in vitro compared to wild-type CCND2. The PI3K-AKT pathway modulates GSK-3 beta activity(4), and cells from individuals with PIK3CA, PIK3R2 or AKT3 mutations showed similar CCND2 accumulation. CCND…
Direct measurement of the W boson width
We present a direct measurement of the width of the W boson using the shape of the transverse mass distribution of W->enu candidates selected in 1 fb-1 of data collected with the D0 detector at the Fermilab Tevatron collider in ppbar collisions at sqrt{s}=1.96 TeV. We use the same methods and data sample that were used for our recently published W boson mass measurement, except for the modeling of the recoil, which is done with a new method based on a recoil library. Our result, 2.028 +- 0.072 GeV, is in agreement with the predictions of the standard model.