404 research outputs found
Mutation of the phospholipase C-γ1–binding site of LAT affects both positive and negative thymocyte selection
Linker for activation of T cells (LAT) is a scaffolding adaptor protein that is critical for T cell development and function. A mutation of LAT (Y136F) that disrupts phospholipase C-γ1 activation and subsequent calcium influx causes a partial block in T cell development and leads to a severe lymphoproliferative disease in homozygous knock-in mice. One possible contribution to the fatal disease of LAT Y136F knock-in mice could be from autoreactive T cells generated in these mice because of altered thymocyte selection. To examine the impact of the LAT Y136F mutation on thymocyte positive and negative selection, we bred this mutation onto the HY T cell receptor (TCR) transgenic, recombination activating gene-2 knockout background. Female mice with this genotype showed a severe defect in positive selection, whereas male mice exhibited a phenotype resembling positive selection (i.e., development and survival of CD8(hi) HY TCR-specific T cells) instead of negative selection. These results support the hypothesis that in non-TCR transgenic, LAT Y136F knock-in mice, altered thymocyte selection leads to the survival and proliferation of autoreactive T cells that would otherwise be negatively selected in the thymus
The structure of quantum Lie algebras for the classical series B_l, C_l and D_l
The structure constants of quantum Lie algebras depend on a quantum
deformation parameter q and they reduce to the classical structure constants of
a Lie algebra at . We explain the relationship between the structure
constants of quantum Lie algebras and quantum Clebsch-Gordan coefficients for
adjoint x adjoint ---> adjoint. We present a practical method for the
determination of these quantum Clebsch-Gordan coefficients and are thus able to
give explicit expressions for the structure constants of the quantum Lie
algebras associated to the classical Lie algebras B_l, C_l and D_l.
In the quantum case also the structure constants of the Cartan subalgebra are
non-zero and we observe that they are determined in terms of the simple quantum
roots. We introduce an invariant Killing form on the quantum Lie algebras and
find that it takes values which are simple q-deformations of the classical
ones.Comment: 25 pages, amslatex, eepic. Final version for publication in J. Phys.
A. Minor misprints in eqs. 5.11 and 5.12 correcte
The Four Distal Tyrosines Are Required for LAT-dependent Signaling in FcɛRI-mediated Mast Cell Activation
The linker for activation of T cells (LAT) is an adaptor protein critical for FcɛRI-mediated mast cell activation. LAT is a substrate of the tyrosine kinases activated after TCR and FcɛRI engagement. After phosphorylation of the cytosolic domain of LAT, multiple signaling molecules such as phospholipase C–γ1, Grb2, and Gads associate with phosphorylated LAT via their SH2 domains. The essential role of the four distal tyrosines in TCR-mediated signaling and T cell development has been demonstrated by experiments using LAT-deficient cell lines and genetically modified mice. To investigate the role of these four tyrosines of LAT in FcɛRI-mediated mast cell activation, bone marrow–derived mast cells from LAT-deficient mice were infected with retroviral vectors designed to express wild-type or mutant LAT. Examination of bone marrow–derived mast cells expressing various tyrosine to phenylalanine mutants in LAT demonstrates a differential requirement for these different binding sites. In these studies, assays of biochemical pathways, degranulation, and cytokine and chemokine release were performed. Finally, the role of these tyrosines was also evaluated in vivo using genetically modified animals. Deletion of all four distal tyrosines, and in particular, loss of the primary phospholipase C–γ-binding tyrosine had a significant effect on antigen-induced histamine release
Inactivation of c-Cbl Reverses Neonatal Lethality and T Cell Developmental Arrest of SLP-76–deficient Mice
c-Cbl is an adaptor protein that negatively regulates signal transduction events involved in thymic-positive selection. To further characterize the function of c-Cbl in T cell development, we analyzed the effect of c-Cbl inactivation in mice deficient in the scaffolding molecule SLP-76. SLP-76–deficient mice show a high frequency of neonatal lethality; and in surviving mice, T cell development is blocked at the DN3 stage. Inactivation of c-cbl completely reversed the neonatal lethality seen in SLP-76–deficient mice and partially reversed the T cell development arrest in these mice. SLP-76−/− Cbl−/− mice exhibited marked expansion of polarized T helper type (Th)1 and Th2 cell peripheral CD4+ T cells, lymphoid infiltrates of parenchymal organs, and premature death. This rescue of T cell development is T cell receptor dependent because it does not occur in recombination activating gene 2−/− SLP-76−/− Cbl−/− triple knockout mice. Analysis of the signal transduction properties of SLP-76−/− Cbl−/− T cells reveals a novel SLP-76– and linker for activation of T cells–independent pathway of extracellular signal–regulated kinase activation, which is normally down-regulated by c-Cbl
On Quantum Lie Algebras and Quantum Root Systems
As a natural generalization of ordinary Lie algebras we introduce the concept
of quantum Lie algebras . We define these in terms of certain
adjoint submodules of quantized enveloping algebras endowed with a
quantum Lie bracket given by the quantum adjoint action. The structure
constants of these algebras depend on the quantum deformation parameter and
they go over into the usual Lie algebras when .
The notions of q-conjugation and q-linearity are introduced. q-linear
analogues of the classical antipode and Cartan involution are defined and a
generalised Killing form, q-linear in the first entry and linear in the second,
is obtained. These structures allow the derivation of symmetries between the
structure constants of quantum Lie algebras.
The explicitly worked out examples of and illustrate the
results.Comment: 22 pages, latex, version to appear in J. Phys. A. see
http://www.mth.kcl.ac.uk/~delius/q-lie.html for calculations and further
informatio
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On the Coupling of Wind Stress and Sea Surface Temperature
A simple quasi-equilibrium analytical model is used to explore hypotheses related to observed spatial correlations between sea surface temperatures and wind stress on horizontal scales of 50–500 km. It is argued that a plausible contributor to the observed correlations is the approximate linear relationship between the surface wind stress and stress boundary layer depth under conditions in which the stress boundary layer has come into approximate equilibrium with steady free-atmospheric forcing. Warmer sea surface temperature is associated with deeper boundary layers and stronger wind stress, while colder temperature is associated with shallower boundary layers and weaker wind stress. Two interpretations of a previous hypothesis involving the downward mixing of horizontal momentum are discussed, and it is argued that neither is appropriate for the warm-to-cold transition or quasi-equilibrium conditions, while one may be appropriate for the cold-to-warm transition. Solutions of a turbulent large-eddy simulation numerical model illustrate some of the processes represented in the analytical model. A dimensionless ratio γτA is introduced to measure the relative influence of lateral momentum advection and local surface stress on the boundary layer wind profile. It is argued that when γ[subscript]τA < 1, and under conditions in which the thermodynamically induced lateral pressure gradients are small, the boundary layer depth effect will dominate lateral advection and control the surface stress
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