Dysfunctions in ribosome biogenesis cause developmental defects and increased cancer susceptibility; however, the connection between ribosome assembly and tumorigenesis remains unestablished. Here we show that hCINAP (also named AK6) is required for human 18S rRNA processing and 40S subunit assembly. Homozygous CINAP−/− mice show embryonic lethality. The heterozygotes are viable and show defects in 18S rRNA processing, whereas no delayed cell growth is observed. However, during rapid growth, CINAP haploinsufficiency impairs protein synthesis. Consistently, hCINAP depletion in fast-growing cancer cells inhibits ribosome assembly and abolishes tumorigenesis. These data demonstrate that hCINAP reduction is a specific rate-limiting controller during rapid growth. Notably, hCINAP is highly expressed in cancers and correlated with a worse prognosis. Genome-wide polysome profiling shows that hCINAP selectively modulates cancer-associated translatome to promote malignancy. Our results connect the role of hCINAP in ribosome assembly with tumorigenesis. Modulation of hCINAP expression may be a promising target for cancer therapy.

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In this paper, we show that the stationary solution u(t, ω) of the differentiable random dynamical system U: ℝ+ × L2[0, 1] × Ω → L2[0, 1] generated by the stochastic Burgers' equation with large viscosity, denoted by ν, driven by a Brownian motion in L2[0, 1], is given by: u(t, ω) = U(t, Y(ω), ω) = Y(θ(t, ω)), where Y(ω) can be represented by the following integral equation: [Formula: see text] Here θ is the group of P-preserving ergodic transformations on the canonical probability space [Formula: see text] such that θ(t, ω)(s) = W(t + s) - W(t), where W is the L2[0, 1]-valued Brownian motion on the probability space [Formula: see text], Tν is the linear operator semigroup on L2[0, 1] generated by νΔ.

Background: PB2 cap is critical for the initiation of influenza virus transcription. Results: FluB PB2 cap binds to GDP and m 7 GDP utilizing unique structural features, which is corroborated by data from ITC. Conclusion: FluB PB2 cap has a unique cap recognition mechanism compared with FluA PB2 cap . Significance: We characterize the cap recognition mechanism of FluB PB2 cap , consequently providing insight into inhibitor design targeting FluB PB2 cap .

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For a sequence of complex Wiener-Itô multiple integrals, the equivalence between the convergence of the symmetrized contraction norms and that of the non-symmetrized contraction norms is shown directly by means of a new version of complex Mallivian calculus using the Wirtinger derivatives of complex-valued functions.

Linear Algebra and Its Applications 416 (2006) 815-834. doi:10.1016/j.laa.2005.12.024Received by publisher: 2005-04-26Harvest Date: 2016-01-04 12:20:29DOI: 10.1016/j.laa.2005.12.024Page Range: 815-83