Person:
Varela Peña, Pilar

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First Name
Pilar
Last Name
Varela Peña
Affiliation
Universidad Complutense de Madrid
Faculty / Institute
Medicina
Department
Area
Inmunología
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UCM identifierScopus Author IDDialnet ID

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Now showing 1 - 2 of 2
  • Item
    Phylogeography of crossbills, bullfinches, grosbeaks, and rosefinches
    (Cellular and Molecular Life Sciences CMLS, 2001) Arnaiz Villena, Antonio; Guillén, J.; Ruiz del Valle, V.; Lowy, E.; Zamora, J.; Varela Peña, Pilar; Stefani, D.; Allende Martínez, Luis Miguel
    Mitochondrial cytochrome b (cyt b) from 24 Carduelini species including crossbills, bullfinches, grosbeaks, rosefinches, and other related, but not conclusively classified species, was sequenced. These sequences were also compared with all the available sequences from the genera Carduelis, Serinus, and Passer. Phylogenetic analyses consistently gave the same groups of finches and the calculated divergence times suggest that speciation of the studied species occurred between 14 and 3 million years ago (Miocene-Pliocene), appearing before the Passer, Carduelis, and Serinus genera. Pleistocene glaciations may have been important in subspeciation. Crossbills are integrated within the genus Carduelis, and within redpolls; the common crossbill shows subspeciation with Loxia japonica in the Pleistocene epoch. Pinicola enucleator groups together with bullfinches and is probably the ancestor of the group. Hawfinch is only distantly related to the studied groups, and might either represent an isolated genus or be related to the New World genus Hesperiphona. The grosbeak genera Eophona and Mycerobas are clearly sister groups, and species belonging to the former might have given rise to Mycerobas species. The isolated (in classification) Uragus sibiricus and Haematospiza sipahi are included within the genus Carpodacus (rosefinches); Carpodacus nipalensis is outside the genus Carpodacus in the molecular analyses and might be an isolated species or related to the genus Montifringilla.
  • Item
    A Point Mutation in a Domain of Gamma Interferon Receptor 1 Provokes Severe Immunodeficiency
    (Clinical and Diagnostic Laboratory Immunology, 2001) Allende Martínez, Luis Miguel; López Goyanes, Alberto; Paz Artal, Estela Natividad; Corell, Alfredo; García Pérez, Miguel Ángel; Varela Peña, Pilar; Scarpellini, Atilio; Negreira, Sagrario; Palenque Mataix, Elia; Arnaiz Villena, Antonio
    Gamma interferon (IFN-γ) and the cellular responses induced by it are essential for controlling mycobacterial infections. Most patients bearing an IFN-γ receptor ligand-binding chain (IFN-γR1) deficiency present gross mutations that truncate the protein and prevent its expression, giving rise to severe mycobacterial infections and, frequently, a fatal outcome. In this report a new mutation that affects the IFN-γR1 ligand-binding domain in a Spanish patient with mycobacterial disseminated infection and multifocal osteomyelitis is characterized. The mutation generates an amino acid change that does not abrogate protein expression on the cellular surface but that severely impairs responses after the binding of IFN-γ (CD64 and HLA class II induction and tumor necrosis factor alpha and interleukin-12 production). A patient's younger brother, who was also probably homozygous for the mutation, died from meningitis due to Mycobacterium bovis. These findings suggest that a point mutation may be fatal when it affects functionally important domains of the receptor and that the severity is not directly related to a lack of IFN-γ receptor expression. Future research on these nontruncating mutations will make it possible to develop new therapeutical alternatives in this group of patients.