about
The small GTPase Rab29 is a common regulator of immune synapse assembly and ciliogenesisSAP-mediated inhibition of diacylglycerol kinase α regulates TCR-induced diacylglycerol signaling.The CXCL12/CXCR4 axis as a therapeutic target in cancer and HIV-1 infection.Inhibition of diacylglycerol kinase α restores restimulation-induced cell death and reduces immunopathology in XLP-1.The small GTPase Rab8 interacts with VAMP-3 to regulate the delivery of recycling T-cell receptors to the immune synapse.Analysis of TCR/CD3 Recycling at the Immune Synapse.Expression of the p66Shc protein adaptor is regulated by the activator of transcription STAT4 in normal and chronic lymphocytic leukemia B cells.Specific recycling receptors are targeted to the immune synapse by the intraflagellar transport systemNegative regulation of chemokine receptor signaling and B-cell chemotaxis by p66Shc.The Rab GTPase Rab8 as a shared regulator of ciliogenesis and immune synapse assembly: From a conserved pathway to diverse cellular structures.p66SHC promotes apoptosis and antagonizes mitogenic signaling in T cells.The Helicobacter pylori vacuolating toxin inhibits T cell activation by two independent mechanisms.F-actin dynamics control segregation of the TCR signaling cascade to clustered lipid rafts.Nonsteroidal anti-inflammatory drugs inhibit a Fyn-dependent pathway coupled to Rac and stress kinase activation in TCR signaling.Simvastatin inhibits T-cell activation by selectively impairing the function of Ras superfamily GTPases.Defective Vav expression and impaired F-actin reorganization in a subset of patients with common variable immunodeficiency characterized by T-cell defects.p66Shc deficiency enhances CXCR4 and CCR7 recycling in CLL B cells by facilitating their dephosphorylation-dependent release from β-arrestin at early endosomes.Simvastatin inhibits the MHC class II pathway of antigen presentation by impairing Ras superfamily GTPases.Enhanced Chemokine Receptor Recycling and Impaired S1P1 Expression Promote Leukemic Cell Infiltration of Lymph Nodes in Chronic Lymphocytic Leukemia.Glycerophosphoinositol-4-phosphate enhances SDF-1α-stimulated T-cell chemotaxis through PTK-dependent activation of VavS1P1 expression is controlled by the pro-oxidant activity of p66Shc and is impaired in B-CLL patients with unfavorable prognosisAnthrax toxins inhibit immune cell chemotaxis by perturbing chemokine receptor signallingp52Shc is required for CXCR4-dependent signaling and chemotaxis in T cellsp66Shc-dependent apoptosis requires Lck and CamKII activityThemis releases the brakes on TCR signaling during thymocyte selection by disabling SHP-1p66Shc deficiency in the Eμ-TCL1 mouse model of chronic lymphocytic leukemia enhances leukemogenesis by altering the chemokine receptor landscapeAbnormalities in chemokine receptor recycling in chronic lymphocytic leukemiaP66Shc: A Pleiotropic Regulator of B Cell Trafficking and a Gatekeeper in Chronic Lymphocytic Leukemia
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description
forsker
@nb
onderzoeker
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researcher
@en
հետազոտող
@hy
name
L. Patrussi
@ast
L. Patrussi
@nl
Laura Patrussi
@en
Laura Patrussi
@es
Laura Patrussi
@nb
type
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L. Patrussi
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L. Patrussi
@nl
Laura Patrussi
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Laura Patrussi
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Laura Patrussi
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L. Patrussi
@en
prefLabel
L. Patrussi
@ast
L. Patrussi
@nl
Laura Patrussi
@en
Laura Patrussi
@es
Laura Patrussi
@nb
P106
P1153
6506110569
P31
P496
0000-0003-1542-6955