ISMB 2008 Toronto

The International Society for Computational Biology (ISCB) presents the Sixteenth International Conference on Intelligent Systems for Molecular Biology (ISMB 2008), to be held in Toronto, Canada, July 19–23, 2008. Now in the final phases of scheduling selected presentations, demonstrations, and posters, the organizers are preparing what will likely be recognized as the premier conference on computational biology in 2008. ISMB 2008 (http://www.iscb.org/ismb2008/) will follow the road paved by the ISMB/ ECCB 2007 (http://www.iscb.org/ ismbeccb2007/) in Vienna in the attempt to specifically encourage increased participation from previously under-represented disciplines of computational biology. This conference will feature the best of the computer and life sciences through a variety of core sessions running in multiple parallel tracks, along with single-tracked Keynote Presentations, posters on display throughout the duration of the conference, and an extensive commercial exposition. The first day (July 18) of the meeting is reserved for two-day Special Interest Group (SIG) and Satellite meetings, the second day (July 19) runs SIGs for the first time in parallel with Tutorials and the Student Council Symposium, and for the first time two SIGs are running in parallel with the main ISMB meeting (July 20–23)Other Research Uni

Counting BPS Operators in Gauge Theories: Quivers, Syzygies and Plethystics

We develop a systematic and efficient method of counting single-trace and multi-trace BPS operators with two supercharges, for world-volume gauge theories of $N$ D-brane probes for both $N \to \infty$ and finite $N$. The techniques are applicable to generic singularities, orbifold, toric, non-toric, complete intersections, et cetera, even to geometries whose precise field theory duals are not yet known. The so-called ``Plethystic Exponential'' provides a simple bridge between (1) the defining equation of the Calabi-Yau, (2) the generating function of single-trace BPS operators and (3) the generating function of multi-trace operators. Mathematically, fascinating and intricate inter-relations between gauge theory, algebraic geometry, combinatorics and number theory exhibit themselves in the form of plethystics and syzygies.Comment: 59+1 pages, 7 Figure

The scaffold protein KSR1, a novel therapeutic target for the treatment of Merlin-deficient tumors

Merlin has broad tumor-suppressor functions as its mutations have been identified in multiple benign tumors and malignant cancers. In all schwannomas, the majority of meningiomas and 1/3 of ependymomas Merlin loss is causative. In neurofibromatosis type 2, a dominantly inherited tumor disease because of the loss of Merlin, patients suffer from multiple nervous system tumors and die on average around age 40. Chemotherapy is not effective and tumor localization and multiplicity make surgery and radiosurgery challenging and morbidity is often considerable. Thus, a new therapeutic approach is needed for these tumors. Using a primary human in vitro model for Merlin-deficient tumors, we report that the Ras/Raf/mitogen-activated protein, extracellular signal-regulated kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) scaffold, kinase suppressor of Ras 1 (KSR1), has a vital role in promoting schwannomas development. We show that KSR1 overexpression is involved in many pathological phenotypes caused by Merlin loss, namely multipolar morphology, enhanced cell-matrix adhesion, focal adhesion and, most importantly, increased proliferation and survival. Our data demonstrate that KSR1 has a wider role than MEK1/2 in the development of schwannomas because adhesion is more dependent on KSR1 than MEK1/2. Immunoprecipitation analysis reveals that KSR1 is a novel binding partner of Merlin, which suppresses KSR1's function by inhibiting the binding between KSR1 and c-Raf. Our proteomic analysis also demonstrates that KSR1 interacts with several Merlin downstream effectors, including E3 ubiquitin ligase CRL4DCAF1. Further functional studies suggests that KSR1 and DCAF1 may co-operate to regulate schwannomas formation. Taken together, these findings suggest that KSR1 serves as a potential therapeutic target for Merlin-deficient tumors