Richard, C. (Carlos)
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- Nuclear factor κ B is activated in myelodysplastic bone marrow cells(Ferrata Storti Foundation, 2002) Fernandez-Luna, J.L. (J.L.); Richard, C. (Carlos); Sanz, C. (C.); Prosper-Cardoso, F. (Felipe)
- Identification of c-Kit gene mutations in patients with polycythemia vera(Elsevier, 2006) Fernandez-Luna, J.L. (J.L.); Real, P.J. (Pedro J.); Richard, C. (Carlos); Prosper-Cardoso, F. (Felipe); Aguirre-Ena, X. (Xabier); Fontalba, A. (A.)Imatinib mesylate has recently been reported to have clinical activity in the treatment of polycythemia vera (PV), suggesting the involvement of one of the kinases targeted by this inhibitor, including c-Kit and PDGFR. Activating c-Kit mutations have been identified in patients with mastocytosis and other myeloid disorders such as acute myeloid leukemia. Thus, we wanted to analyze the presence of mutations of c-Kit in polycythemia vera patients. We found that 7 out of 20 patients carried missense mutations in the c-Kit gene whereas no sequence variation was detected in 15 healthy controls.
- NALP1 is a transcriptional target for cAMP-response-element-binding protein (CREB) in myeloid leukaemia cells(Biochemical Society, 2004) Andreu, E.J. (Enrique José); Fernandez-Luna, J.L. (J.L.); Richard, C. (Carlos); Sanz, C. (C.); Prosper-Cardoso, F. (Felipe); Calasanz-Abinzano, M.J. (Maria Jose)NALP1 (also called DEFCAP, NAC, CARD7) has been shown to play a central role in the activation of inflammatory caspases and processing of pro-IL1β (pro-interleukin-1β). Previous studies showed that NALP1 is highly expressed in peripheral blood mononuclear cells. In the present study, we report that expression of NALP1 is absent from CD34+ haematopoietic blast cells, and its levels are upregulated upon differentiation of CD34+ cells into granulocytes and to a lesser extent into monocytes. In peripheral blood cells, the highest levels of NALP1 were observed in CD3+ (T-lymphocytes), CD15+ (granulocytes) and CD14+ (monocytes) cell populations. Notably, the expression of NALP1 was significantly increased in the bone marrow blast cell population of some patients with acute leukaemia, but not among tissue samples from thyroid and renal cancer. A search for consensus sites within the NALP1 promoter revealed a sequence for CREB (cAMP-response-element-binding protein) that was required for transcriptional activity. Moreover, treatment of TF1 myeloid leukaemia cells with protein kinase C and protein kinase A activators induced CREB phosphorylation and upregulated the mRNA and protein levels of NALP1. Conversely, ectopic expression of a dominant negative form of CREB in TF1 cells blocked the transcriptional activity of the NALP1 promoter and significantly reduced the expression of NALP1. Thus NALP1 is transcriptionally regulated by CREB in myeloid cells, a mechanism that may contribute to modulate the response of these cells to pro-inflammatory stimuli.