The Evidence for a Pentaquark Signal and Kinematic Reflections

Several recent experiments have reported evidence for a narrow baryon resonance with positive strangeness ($\Theta^+$) at a mass of 1.54 GeV/$c^2$. Baryons with $S=+1$ cannot be conventional $qqq$ states and the reports have thus generated much theoretical speculation about the nature of possible $S=+1$ baryons, including a 5-quark, or pentaquark, interpretation. We show that narrow enhancements in the $K^+n$ effective mass spectrum can be generated as kinematic reflections resulting from the decay of mesons, such as the $f_2(1275)$, the $a_2(1320)$ and the $\rho_3(1690)$.Comment: 4 pages, 4 figure

TNF-stimulated MAP kinase activation mediated by a Rho family GTPase signaling pathway

The biological response to tumor necrosis factor (TNF) involves activation of MAP kinases. Here we report a mechanism of MAP kinase activation by TNF that is mediated by the Rho GTPase family members Rac/Cdc42. This signaling pathway requires Src-dependent activation of the guanosine nucleotide exchange factor Vav, activation of Rac/Cdc42, and the engagement of the Rac/Cdc42 interaction site (CRIB motif) on mixed-lineage protein kinases (MLKs). We show that this pathway is essential for full MAP kinase activation during the response to TNF. Moreover, this MLK pathway contributes to inflammation in vivo

A search for J^{PC}=1^{-+} exotic mesons in the pi- pi- pi+ and pi- pi0 pi0 systems

A partial wave analysis (PWA) of the pi-pi-pi+ and pi-pi0pi0 systems produced in the reaction pi- p -> (3pi)-p at 18 GeV/c was carried out using an isobar model assumption. This analysis is based on 3.0M pi-pi0pi0 events and 2.6M pi-pi-pi+ events and shows production of the a2(1320), pi2(1670) and \pi(1800) mesons. An earlier analysis of 250K pi-pi-pi+ events from the same experiment showed possible evidence for a J^{PC}=1^{-+}$ exotic meson with a mass of 1.6 GeV/c^2 decaying into rho pi. In this analysis of a higher statistics sample of the (3pi)- system in two charged modes we find no evidence of an exotic meson.Comment: 4 pages, 5 figures, added comment about the negative reflectivity exotic wave

A Protein Scaffold Coordinates SRC-Mediated JNK Activation in Response to Metabolic Stress

Obesity is a major risk factor for the development of metabolic syndrome and type 2 diabetes. How obesity contributes to metabolic syndrome is unclear. Free fatty acid (FFA) activation of a non-receptor tyrosine kinase (SRC)-dependent cJun NH2-terminal kinase (JNK) signaling pathway is implicated in this process. However, the mechanism that mediates SRC-dependent JNK activation is unclear. Here, we identify a role for the scaffold protein JIP1 in SRC-dependent JNK activation. SRC phosphorylation of JIP1 creates phosphotyrosine interaction motifs that bind the SH2 domains of SRC and the guanine nucleotide exchange factor VAV. These interactions are required for SRC-induced activation of VAV and the subsequent engagement of a JIP1-tethered JNK signaling module. The JIP1 scaffold protein, therefore, plays a dual role in FFA signaling by coordinating upstream SRC functions together with downstream effector signaling by the JNK pathway

Systems Biology Markup Language (SBML) Level 3 Package: Distributions, Version 1, Release 1

Biological models often contain elements that have inexact numerical values, since they are based on values that are stochastic in nature or data that contains uncertainty. The Systems Biology Markup Language (SBML) Level 3 Core specification does not include an explicit mechanism to include inexact or stochastic values in a model, but it does provide a mechanism for SBML packages to extend the Core specification and add additional syntactic constructs. The SBML Distributions package for SBML Level 3 adds the necessary features to allow models to encode information about the distribution and uncertainty of values underlying a quantity

Adhesion between cells, diffusion of growth factors, and elasticity of the AER produce the paddle shape of the chick limb

This paper has been withdrawnComment: This paper has been withdraw

Discs large (Dlg1) complexes in lymphocyte activation

T cell antigen recognition involves the formation of a structured interface between antigen-presenting and T cells that facilitates the specific transmission of activating and desensitizing stimuli. The molecular machinery that organizes the signaling molecules and controls their disposition in response to activation remains poorly understood. We show here that in T cells Discs large (Dlg1), a PDZ domain-containing protein, is recruited upon activation to cortical actin and forms complexes with early participants in T cell activation. Transient overexpression of Dlg1 attenuates basal and Vav1-induced NFAT reporter activation. Reduction of Dlg1 expression by RNA interference enhances both CD3- and superantigen-mediated NFAT activation. Attenuation of antigen receptor signaling appears to be a complex, highly orchestrated event that involves the mutual segregation of important elements of the early signaling complex

Loss of DAP12 and FcRγ drives exaggerated IL-12 production and CD8(+) T cell response by CCR2(+) Mo-DCs

Dap12 and FcRγ, the two transmembrane ITAM-containing signaling adaptors expressed in dendritic cells (DC), are implicated in the regulation of DC function. Several activating and adhesion receptors including integrins require these chains for their function in triggering downstream signaling and effector pathways, however the exact role(s) for Dap12 and FcRγ remains elusive as their loss can lead to both attenuating and enhancing effects. Here, we report that mice congenitally lacking both Dap12 and FcRγ chains (DF) show a massively enhanced effector CD8(+) T cell response to protein antigen immunization or West Nile Virus (WNV) infection. Thus, immunization of DF mice with MHCI-restricted OVA peptide leads to accumulation of IL-12-producing monocyte-derived dendritic cells (Mo-DC) in draining lymph nodes, followed by vastly enhanced generation of antigen-specific IFNγ-producing CD8(+) T cells. Moreover, DF mice show increased viral clearance in the WNV infection model. Depletion of CCR2+ monocytes/macrophages in vivo by administration anti-CCR2 antibodies or clodronate liposomes completely prevents the exaggerated CD8+ T cell response in DF mice. Mechanistically, we show that the loss of Dap12 and FcRγ-mediated signals in Mo-DC leads to a disruption of GM-CSF receptor-induced STAT5 activation resulting in upregulation of expression of IRF8, a transcription factor. Consequently, Dap12- and FcRγ-deficiency exacerbates GM-CSF-driven monocyte differentiation and production of inflammatory Mo-DC. Our data suggest a novel cross-talk between DC-ITAM and GM-CSF signaling pathways, which controls Mo-DC differentiation, IL-12 production, and CD8(+) T cell responses