Explorations of the Extended ncKP Hierarchy

A recently obtained extension (xncKP) of the Moyal-deformed KP hierarchy (ncKP hierarchy) by a set of evolution equations in the Moyal-deformation parameters is further explored. Formulae are derived to compute these equations efficiently. Reductions of the xncKP hierarchy are treated, in particular to the extended ncKdV and ncBoussinesq hierarchies. Furthermore, a good part of the Sato formalism for the KP hierarchy is carried over to the generalized framework. In particular, the well-known bilinear identity theorem for the KP hierarchy, expressed in terms of the (formal) Baker-Akhiezer function, extends to the xncKP hierarchy. Moreover, it is demonstrated that N-soliton solutions of the ncKP equation are also solutions of the first few deformation equations. This is shown to be related to the existence of certain families of algebraic identities.Comment: 34 pages, correction of typos in (7.2) and (7.5

Display of both N- and C-terminal target fusion proteins on the Aspergillus oryzae cell surface using a chitin-binding module

A novel cell surface display system in Aspergillus oryzae was established by using a chitin-binding module (CBM) from Saccharomyces cerevisiae as an anchor protein. CBM was fused to the N or C terminus of green fluorescent protein (GFP) and the fusion proteins (GFP-CBM and CBM-GFP) were expressed using A. oryzae as a host. Western blotting and fluorescence microscopy analysis showed that both GFP-CBM and CBM-GFP were successfully expressed on the cell surface. In addition, cell surface display of triacylglycerol lipase from A. oryzae (tglA), while retaining its activity, was also successfully demonstrated using CBM as an anchor protein. The activity of tglA was significantly higher when tglA was fused to the C terminus than N terminus of CBM. Together, these results show that CBM used as a first anchor protein enables the fusion of both the N and/or C terminus of a target protein

A new current algebra and the reflection equation

We establish an explicit algebra isomorphism between the quantum reflection algebra for the $U_q(\hat{sl_2})$ R-matrix and a new type of current algebra. These two algebras are shown to be two realizations of a special case of tridiagonal algebras (q-Onsager).Comment: 14 pages; v2: More details in Section 4; Typos corrected; References added; To appear in Lett. Math. Phy

Atr-atrip kinase complex triggers activation of the fanconi anemia dna repair pathway

Abstract ATR kinase activates the S-phase checkpoint when replication forks stall at sites of DNA damage. This event also causes phosphorylation of the Fanconi anemia (FA) protein FANCI, triggering its monoubiquitination of the key DNA repair factor FANCD2 by the FA core E3 ligase complex, thereby promoting this central pathway of DNA repair which permits replication to be restarted. However, the interplay between ATR and the FA pathway has been unclear. In this study, we present evidence that their action is directly linked, gaining insights into this relationship in a DT40 mutant cell line that is conditionally deficient in the critical ATR-binding partner protein ATRIP. Using this system, we showed that ATRIP was crucial for DNA damage–induced FANCD2 monoubiquitination and FANCI phosphorylation. ATR kinase phosphorylated recombinant FANCI protein in vitro, which was facilitated by the presence of FANCD2. Mechanistic investigations revealed that the RPA region but not the TopBP1 region of ATRIP was required for FANCD2 monoubiquitination, whereas Chk1 phosphorylation relied upon both domains. Together, our findings identify ATR as the kinase responsible for activating the FA pathway of DNA repair. Cancer Res; 72(5); 1149–56. ©2012 AACR.</jats:p