During FY13, we accomplished the following: 1) Initiated studies of NF-kappaB function in senescent cells. IMR90 diploid human fibroblasts were induced to senesce after exposure to etoposide. We standardized the dose-response and time-course for etoposile treatment, and assayed the development of senescence by beta-galactosidase expression and pl6 induction. We are currently evaluating NF-kappaB-dependent gene expression in these cells. 2) Initiated studies to determine whether Rel suppression by celecoxib is mediated by the induction of ER stress by this drug. 3) Collaborated with Dr. Mollie Meffert (Johns Hopkins School of Medicine) to carry out RelA ChiP studies in primary neuronal cultures. 4) Studied the interaction between glucocorticoid receptor (GR) and NFB in a human B cell line. BJAB cells were activated with PMA and ionomycin (to mimic BCR signaling) in the presence or absence of dexamethasone. Microarray analyses were carried out using RNA samples obtained at various time of activation. Anti-RelA ChIP was carried out from the same samples to measure the effects of dexamethasone on RelA recruitment genome-wide.
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|Sen, Ranjan (2011) The origins of NF-ÎºB. Nat Immunol 12:686-8|
|Olkhanud, Purevdorj B; Damdinsuren, Bazarragchaa; Bodogai, Monica et al. (2011) Tumor-evoked regulatory B cells promote breast cancer metastasis by converting resting CD4âº T cells to T-regulatory cells. Cancer Res 71:3505-15|