Publications by authors named "Noemi Cruz-Orcutt"

Phospholipase C-γ1 (PLC-γ1) is a key regulator of T cell receptor (TCR)-induced signaling. Activation of the TCR enhances PLC-γ1 enzymatic function, resulting in calcium influx and the activation of PKC family members and RasGRP. The current model is that phosphorylation of LAT tyrosine 132 facilitates the recruitment of PLC-γ1, leading to its activation and function at the LAT complex.

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Toll-like receptor 2 (TLR2) serves as a co-stimulatory receptor for human T cells by enhancing T cell receptor (TCR)-induced cytokine production and proliferation. However, it is unknown where signals from the TCR and TLR2 converge to enhance T cell activation. To address this gap, we examined changes in TCR-induced signaling following concurrent TLR2 activation in human T cells.

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Objective: To assess and compare examiner reliability of clinical and photographic fluorosis examinations using the Fluorosis Risk Index (FRI) among children in the Iowa Fluoride Study (IFS).

Methods: The IFS examined 538 children for fluorosis and dental caries at age 13 and obtained intraoral photographs from nearly all of them. To assess examiner reliability, duplicate clinical examinations were conducted for 40 of the subjects.

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The induction of the T cell receptor (TCR) is necessary for the activation and function of human T cells. TCR activation results in the tyrosine phosphorylation of LAT, leading to the direct interaction with several proteins, including PLC-gamma 1, Grb2 and Gads. These direct ligands then mediate the indirect interaction of LAT with proteins, such as SLP-76, Vav1 and Itk.

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Background: Human T cells play an important role in pathogen clearance, but their aberrant activation is also linked to numerous diseases. T cells are activated by the concurrent induction of the T cell receptor (TCR) and one or more costimulatory receptors. The characterization of signaling pathways induced by TCR and/or costimulatory receptor activation is critical, since these pathways are excellent targets for novel therapies for human disease.

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