Aranaz-Oroz, P. (Paula)

Filtering

Settings

Author search.filters.isAuthorOfPublication.8f6060d1-d2d4-425b-ac46-ffe00907395a

Search Results

Now showing 1 - 10 of 28
  • Thumbnail Image
    Estudio mediante dHPLC del perfil mutacional de los genes SYK y ZAP70 en pacientes con Síndromes Mieloproliferativos Crónicos BCR-ABL negativos
    (Editorial Doyma, 2007-10-25) Ormazábal, C. (Cristina); Hurtado, C. (Cristina); Novo-Villaverde, F. J. (Francisco Javier); Vizmanos-Pérez, J.L. (José Luis); García-Delgado, M. (Marina); Aranaz-Oroz, P. (Paula); Calasanz-Abinzano, M.J. (Maria Jose)
  • Thumbnail Image
    FISH and mutational screening of the ABL, SYK and JAK tirosine kinase family genes in BCR-ABL1 negative and V617FJAK2 negative chronic myeloproliferative neoplasms (CMPNs)
    (Ferrata-Storti Foundation, 2009-06-04) Ormazábal, C. (Cristina); Hurtado, C. (Cristina); Novo-Villaverde, F. J. (Francisco Javier); Vizmanos-Pérez, J.L. (José Luis); Erquiaga, I. (Ignacio); Aranaz-Oroz, P. (Paula); Calasanz-Abinzano, M.J. (Maria Jose)
  • Thumbnail Image
    ¿Existen más mutaciones en JAK2 en pacientes con Síndromes Mieloproliferativos Crónicos BCR-ABL negativos?
    (Editorial Doyma, 2007-10-25) Ormazábal, C. (Cristina); Hurtado, C. (Cristina); Novo-Villaverde, F. J. (Francisco Javier); Vizmanos-Pérez, J.L. (José Luis); García-Delgado, M. (Marina); Aranaz-Oroz, P. (Paula); Calasanz-Abinzano, M.J. (Maria Jose)
  • Thumbnail Image
    Análisis de la expresión diferencial de distintos transcritos de PDGFRA en neoplasias hematológicas con eosinofilia
    (Editorial Doyma, 2009-11-12) Ormazábal, C. (Cristina); Hurtado, C. (Cristina); Novo-Villaverde, F. J. (Francisco Javier); Vizmanos-Pérez, J.L. (José Luis); García-Delgado, M. (Marina); Erquiaga, I. (Ignacio); Aranaz-Oroz, P. (Paula); Calasanz-Abinzano, M.J. (Maria Jose)
  • Thumbnail Image
    Phenolic compounds inhibit 3T3-L1 adipogenesis depending on the stage of differentiation and their binding affinity to PPAR gamma
    (2019) Martinez, J.A. (José Alfredo); Miguéliz-Basterra, I. (Itziar); Milagro-Yoldi, F.I. (Fermín Ignacio); Gonzalez-Navarro, C.J. (Carlos Javier); Vizmanos-Pérez, J.L. (José Luis); Aranaz-Oroz, P. (Paula); Romo‐Hualde, A. (Ana); Zabala-Navó, M. (María); López-Yoldi, M. (Miguel); Navarro-Herrera, D. (David)
    Phenolic compounds might modulate adiposity. Here, we report our observation that polyphenols and phenolic acids inhibit adipogenesis in 3T3-L1 with different intensity depending on the family and the stage of differentiation. While quercetin and resveratrol inhibited lipid accumulation along the whole process of differentiation, apigenin and myricetin were active during the early and latest stages, but not intermediate, contrary to hesperidin. The activity of phenolic acids was limited to the early stages of the differentiation process, except p-coumaric and ellagic acids. This anti-adipogenic effect was accompanied by down-regulation of Scd1 and Lpl. Molecular docking analysis revealed that the inhibitory activity of these phenolic compounds over the early stages of adipogenesis exhibits a significant correlation (r = 0.7034; p = 0.005) with their binding affinity to the ligand-binding domain of PPAR¿. Results show that polyphenols and phenolic acids would interact with specific residues of the receptor, which could determine their potential anti-adipogenic activity during the early stages of the differentiation. Residues Phe264, His266, Ile281, Cys285 and Met348 are the most frequently involved in these interactions, which might suggest a crucial role for these amino acids modulating the activity of the receptor. These data contribute to elucidate the possible mechanisms of phenolic compounds in the control of adipogenesis.
  • Thumbnail Image
    Phenolic compounds reduce the fat content in caenorhabditis elegans by affecting lipogenesis, lipolysis, and different stress responses
    (MDPI AG, 2020) Milagro-Yoldi, F.I. (Fermín Ignacio); Gonzalez-Navarro, C.J. (Carlos Javier); Vizmanos-Pérez, J.L. (José Luis); Aranaz-Oroz, P. (Paula); Romo‐Hualde, A. (Ana); Zabala-Navó, M. (María); López-Yoldi, M. (Miguel); Navarro-Herrera, D. (David)
    Supplementation with bioactive compounds capable of regulating energy homeostasis is a promising strategy to manage obesity. Here, we have screened the ability of different phenolic compounds (myricetin, kaempferol, naringin, hesperidin, apigenin, luteolin, resveratrol, curcumin, and epicatechin) and phenolic acids (p-coumaric, ellagic, ferulic, gallic, and vanillic acids) regulating C. elegans fat accumulation. Resveratrol exhibited the strongest lipid-reducing activity, which was accompanied by the improvement of lifespan, oxidative stress, and aging, without affecting worm development. Whole-genome expression microarrays demonstrated that resveratrol affected fat mobilization, fatty acid metabolism, and unfolded protein response of the endoplasmic reticulum (UPRER), mimicking the response to calorie restriction. Apigenin induced the oxidative stress response and lipid mobilization, while vanillic acid affected the unfolded-protein response in ER. In summary, our data demonstrates that phenolic compounds exert a lipid-reducing activity in C. elegans through different biological processes and signaling pathways, including those related with lipid mobilization and fatty acid metabolism, oxidative stress, aging, and UPR-ER response. These findings open the door to the possibility of combining them in order to achieve complementary activity against obesity-related disorders.
  • Thumbnail Image
    Absence of rearrangements or activating mutations in the RTK III and IV family genes in BCR-ABL1 negative and V617FJAK2 negative chronic myeloproliferative neoplasms (CMPNs)
    (Ferrata-Storti Foundation, 2009-06-04) Ormazábal, C. (Cristina); Hurtado, C. (Cristina); Novo-Villaverde, F. J. (Francisco Javier); Vizmanos-Pérez, J.L. (José Luis); García-Delgado, M. (Marina); Erquiaga, I. (Ignacio); Aranaz-Oroz, P. (Paula); Calasanz-Abinzano, M.J. (Maria Jose)
  • Thumbnail Image
    FISH screening of Receptor- and Cytoplasmatic Tyrosine Kinase genes in BCR-ABL1 negative and JAK2V617F negative chronic myeloproliferative neoplasms (CMPNs)
    (Springer, 2009-07-04) Ormazábal, C. (Cristina); Hurtado, C. (Cristina); Novo-Villaverde, F. J. (Francisco Javier); Vizmanos-Pérez, J.L. (José Luis); García-Delgado, M. (Marina); Erquiaga, I. (Ignacio); Aranaz-Oroz, P. (Paula); Calasanz-Abinzano, M.J. (Maria Jose)
  • Thumbnail Image
    A new potential oncogenic mutation in the FERM domain of JAK2 in BCR-ABL1 negative and V617F negative chronic myeloproliferative neoplasms (CMPNs) revealed by a comprehensive screening of 17 tyrosine kinase coding genes
    (Elsevier Inc., 2010-05-01) Ormazábal, C. (Cristina); Hurtado, C. (Cristina); Novo-Villaverde, F. J. (Francisco Javier); Vizmanos-Pérez, J.L. (José Luis); García-Delgado, M. (Marina); Erquiaga, I. (Ignacio); Aranaz-Oroz, P. (Paula); Calasanz-Abinzano, M.J. (Maria Jose)
    BCR/ABL1-negative chronic myeloproliferative neoplasms (CMPNs) are a heterogeneous group of clonal hematological malignancies. Over recent years, some genetic events in tyrosine kinase (TK) genes have been described as causal events of these diseases. To identify new genetic aberrations underlying these diseases, we used denaturing high performance liquid chromatography and fluorescence in situ hybridization (FISH) to analyze 17 genes from two receptor-TK families (III and IV) and from three cytoplasmic-TK families (Syk, Abl, and Jak) on samples from 44 BCR/ABL1-negative and JAK2(V617F)-negative CMPN patients with different clinical phenotypes. Although screening by FISH did not reveal novel chromosomal aberrations, several sequence changes were detected. None of them were frequent events, but we identified a new potential activating mutation in the FERM domain of JAK2(R340Q). None of the germline JAK2(V617F) single-nucleotide polymorphisms detected differed in distribution between patients and control subjects. In summary, data presented here show that these genes are not frequently mutated or rearranged in CMPNs, suggesting that molecular events causing these disorders must be located in other genes.
  • Thumbnail Image
    Mutational analysis of the EGF Receptor gene in BCR-ABL1 negative and JAK2V617F negative chronic myeloproliferative neoplasms
    (Ferrata-Storti Foundation, 2010-06-10) Ormazábal, C. (Cristina); Hurtado, C. (Cristina); Novo-Villaverde, F. J. (Francisco Javier); Vizmanos-Pérez, J.L. (José Luis); García-Delgado, M. (Marina); Erquiaga, I. (Ignacio); Aranaz-Oroz, P. (Paula); Calasanz-Abinzano, M.J. (Maria Jose)