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1.
Fig 1

Fig 1. From: Signal transducer and activator of transcription 1 (STAT1) gain-of-function mutations and disseminated coccidioidomycosis and histoplasmosis.

Patient 1. A, Extensive right upper lung, mediastinal, and pleural involvement with C immitis. B, MRI showing an intramedullary spinal cord lesion (arrow) with edema and cord compression.

Elizabeth P. Sampaio, et al. J Allergy Clin Immunol. ;131(6):1624-1634.
2.
Fig 2

Fig 2. From: Signal transducer and activator of transcription 1 (STAT1) gain-of-function mutations and disseminated coccidioidomycosis and histoplasmosis.

STAT1 mutants. A, STAT1 coding region. TAD, Transactivation domain. Mutations were associated with (blue arrows) disseminated coccidioidomycosis and (green arrows) disseminated histoplasmosis. L706S was the dominant negative mutation. B, U3A cells transfected with STAT1 mutants, WT or empty vector, and WB with anti-STAT1 and anti-tubulin antibodies.

Elizabeth P. Sampaio, et al. J Allergy Clin Immunol. ;131(6):1624-1634.
3.

Fig 5. From: Signal transducer and activator of transcription 1 (STAT1) gain-of-function mutations and disseminated coccidioidomycosis and histoplasmosis.

Gene expression: restimulation experiments in transfected U3A cells. Cells were stimulated or not (NS) with IFN-γ, washed, and restimulated (IFN-γ/IFN-γ) or not (IFN-γ rest). Expression of IFN-γ (CXCL9 [A] and CXCL10 [B]) target genes was evaluated. Results are means ± SDs of 3 independent experiments. *P < .05 compared with IFN-γ rest.

Elizabeth P. Sampaio, et al. J Allergy Clin Immunol. ;131(6):1624-1634.
4.
Fig 4

Fig 4. From: Signal transducer and activator of transcription 1 (STAT1) gain-of-function mutations and disseminated coccidioidomycosis and histoplasmosis.

Increased STAT1/PIAS1 association. A, After interferon stimulation, cell lysates from EBV-B cells of patients and control subjects (Nm) were IP:WB anti-STAT1: anti-PIAS1 antibody. B, EBV-B cells treated with SAMe were evaluated as above. Blots are representative of 3 independent experiments for each condition. Numbers are band densities normalized to the nonstimulated samples (NS).

Elizabeth P. Sampaio, et al. J Allergy Clin Immunol. ;131(6):1624-1634.
5.

Fig 6. From: Signal transducer and activator of transcription 1 (STAT1) gain-of-function mutations and disseminated coccidioidomycosis and histoplasmosis.

Reduction of PIAS1 modulates the IFN-γ–induced gene response. Evaluation of gene expression in U3A cells cotransfected with WT or mutant STAT1 and with siRNA directed against PIAS1. Cells were treated as described in Fig5. Restimulated cells =IFN-γ/IFN-γ or PIAS siRNA IFN-γ/IFN-γ. Results are means ± SDs of 3 independent experiments. NS, Nonstimulated. *P < .05 when compared with IFN-γ rest. A, WT and E353K with and without PIAS siRNA. B, WT, A267V, and R274G with and without PIAS siRNA.

Elizabeth P. Sampaio, et al. J Allergy Clin Immunol. ;131(6):1624-1634.
6.

Fig 3. From: Signal transducer and activator of transcription 1 (STAT1) gain-of-function mutations and disseminated coccidioidomycosis and histoplasmosis.

STAT1 mutants lead to delayed dephosphorylation and enhanced luciferase GAS-induced activity. A, Dephosphorylation in EBV-B cells from patients and control subjects (Nm) stimulated with IFN-γ for the indicated periods. B, Dephosphorylation assayed by means of flow cytometry in U3A cells. Results are representative of at least 3 independent experiments. MFI, Mean fluorescence intensity; NS, nonstimulated. C, Transcriptional responses to IFN-γ and IFN-α in U3A cells transfected with STAT1 mutant constructs and when cotransfected with WT STAT1. D, U3A cells transfected with L706S showed no negative effect on the mutants A267V and E353K. Data show the mean fold increase relative to the WT nonstimulated specimens from a total of 5 experiments. *P < .05 when compared with stimulated WT, respectively. **P < .01 compared with L706S.

Elizabeth P. Sampaio, et al. J Allergy Clin Immunol. ;131(6):1624-1634.

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