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Digital.CSIC (162.855 recursos)

Repositorio institucional del Consejo Superior de Investigaciones Científicas. Digital.CSIC es un depósito de documentos digitales, cuyo objetivo es organizar, archivar, preservar y difundir en modo de acceso abierto la producción intelectual resultante de la actividad investigadora del CSIC.

(IN) Artículos post-print

Mostrando recursos 1 - 20 de 38

  1. Identification of a 31-bp deletion in the RELN gene causing lissencephaly with cerebellar hypoplasia in sheep

    Suárez-Vega, Aroa; Gutiérrez Gil, Beatriz; Cuchillo-Ibáñez, Inmaculada; Sáez-Valero, Javier; Pérez Pérez, Valentín; Garciá-Gámez, E.; Benavides, Julio; Arranz, Juan José
    12 páginas, 5 figuras, 1 tabla.

  2. An interview with Angela Nieto. Interviewed by Eva Amsen.

    Nieto, M. Ángela
    Angela Nieto is Full Professor at the Instituto de Neurociencias (CSIC-UMH) in Alicante, Spain, and Head of the institute's Developmental Neurobiology Unit. She is also the current president of the Spanish Society for Developmental Biology (Sociedad Española de Biología del Desarollo, SEBD). We interviewed her to talk about the plans of the SEBD for the coming years.

  3. EPAC signalling pathways are involved in low PO2 chemoreception in carotid body chemoreceptor cells

    Rocher, Asunción; Cáceres, Ana Isabel; Almaraz, Laura; González, Constancio
    Chemoreceptor cells of the carotid bodies (CB) are activated by hypoxia and acidosis, responding with an increase in their rate of neurotransmitter release, which in turn increases the electrical activity in the carotid sinus nerve and evokes a homeostatic hyperventilation. Studies in isolated chemoreceptor cells have shown that moderate hypoxias (PO2 ≈ 46 mmHg) produces smaller depolarisations and comparable Ca2+ transients but a much higher catecholamine (CA) release response in intact CBs than intense acidic/hypercapnic stimuli (20% CO2, pH 6.6). Similarly, intense hypoxia (PO2 ≈ 20 mmHg) produces smaller depolarizations and Ca2+ transients in isolated chemoreceptor cells but a higher...

  4. The epithelial-mesenchymal transition under control: Global programs to regulate epithelial plasticity

    Nieto, M. Ángela; Nieto, M. Ángela; Cano, Amparo
    The epithelial to mesenchymal transition or EMT has become one of the most exciting fields in cancer research. Nevertheless, its relevance in tumor biology and the metastatic process still faces some controversy. Clarification may arise when considering the EMT as a reversible and often incomplete process, essentially a manifestation of strong epithelial plasticity. Transient cellular states are generated to fulfill specific requirements in each and all the steps of the metastatic process, from primary tumor cell detachment to dissemination and colonization. Opposing multiple cellular programs that promote or prevent EMT, thereby destabilizing or reinforcing epithelial integrity, play a central role...

  5. Mutual exclusion of transcription factors and cell behaviour in the definition of vertebrate embryonic territories

    Acloque, Hervé; Ocaña, Oscar H.; Nieto, M. Ángela
    Early embryonic territories are transient entities under permanent remodelling to form newly derived cell populations that will eventually give rise to the adult tissues and organs. A vast effort has been devoted to identifying the determinants and mechanisms that define embryonic territories. Indeed, studies in the vertebrate embryo from the morula stage to the segregation of the main embryonic layers - ectoderm, mesoderm and endoderm - have highlighted the importance of the mutual exclusion/repression between pairs of transcription factors, in coordination with the control exerted over cell division, adhesion and motility. © 2012 Elsevier Ltd.

  6. Metastatic colonization requires the repression of the epithelial-mesenchymal transition inducer Prrx1

    Ocaña, Oscar H.; Córcoles, Rebeca; Fabra, Àngels; Moreno-Bueno, Gema; Acloque, Hervé; Vega, Sonia; Barrallo-Gimeno, Alejandro; Cano, Amparo; Nieto, M. Ángela
    The epithelial-mesenchymal transition (EMT) is required in the embryo for the formation of tissues for which cells originate far from their final destination. Carcinoma cells hijack this program for tumor dissemination. The relevance of the EMT in cancer is still debated because it is unclear how these migratory cells colonize distant tissues to form macrometastases. We show that the homeobox factor Prrx1 is an EMT inducer conferring migratory and invasive properties. The loss of Prrx1 is required for cancer cells to metastasize in vivo, which revert to the epithelial phenotype concomitant with the acquisition of stem cell properties. Thus, unlike...

  7. Lats2 kinase potentiates Snail1 activity by promoting nuclear retention upon phosphorylation

    Zhang, Kun; Rodríguez-Aznar, E.; Yabuta, Norikazu; Owen, R. J.; Mingot, José Manuel; Nojima, Hiroshi; Nieto, M. Ángela; Longmore, Gregory D.
    Snail1 is a central regulator of epithelial cell adhesion and movement in epithelial-to-mesenchymal transitions (EMTs) during embryo development; a process reactivated during cancer metastasis. While induction of Snail1 transcription precedes EMT induction, post-translational regulation of Snail1 is also critical for determining Snail1's protein level, subcellular localization, and capacity to induce EMT. To identify novel post-translational regulators of Snail1, we developed a live cell, bioluminescence-based screen. From a human kinome RNAi screen, we have identified Lats2 kinase as a novel regulator of Snail1 protein level, subcellular localization, and thus, activity. We show that Lats2 interacts with Snail1 and directly phosphorylates Snail1...

  8. Reciprocal repression between Sox3 and Snail transcription factors defines embryonic territories at gastrulation

    Acloque, Hervé; Ocaña, Oscar H.; Matheu, Ander; Rizzoti, Karine; Wise, Clare; Lovell-Badge, Robin; Nieto, M. Ángela
    13 p., 8 figures and references.

  9. The endogenous retrovirus ENS-1 provides active binding sites for transcription factors in embryonic stem cells that specify extra embryonic tissue

    Mey, Anne; Acloque, Hervé; Lerat, Emmanuelle; Gounel, Sebastien; Tribollet, Violaine; Blanc, Sophie; Curton, Damien; Birot, Anne-Marie; Nieto, M. Ángela; Samarut, Jacques
    Abstract Background Long terminal repeats (LTR) from endogenous retroviruses (ERV) are source of binding sites for transcription factors which affect the host regulatory networks in different cell types, including pluripotent cells. The embryonic epiblast is made of pluripotent cells that are subjected to opposite transcriptional regulatory networks to give rise to distinct embryonic and extraembryonic lineages. To assess the transcriptional contribution of ERV to early developmental processes, we have characterized in vitro and in vivo the regulation of ENS-1, a host adopted and developmentally regulated ERV that is expressed in chick embryonic stem cells. Results We show that Ens-1 LTR...

  10. An epigenetic mark that protects the epithelial phenotype in health and disease

    Heredia, Fabiana; Nieto, M. Ángela
    Epithelial plasticity is crucial during embryonic development and progression of carcinomas. In this issue, Abell et al. (2011) show that acetylation on histones H2A/H2B prevents epithelial cells from undergoing epithelial-to-mesenchymal transition (EMT). Their findings also suggest that under conditions where EMT and stemness coexist, they can be independently regulated. © 2011 Elsevier Inc.

  11. Repression of Puma by Scratch2 is required for neuronal survival during embryonic development

    Rodríguez-Aznar, E.; Nieto, M. Ángela
    Although Snail factors promote cell survival in development and cancer, the tumor-suppressor p53 promotes apoptosis in response to stress. p53 and Snail2 act antagonistically to regulate p53 upregulated modulator of apoptosis (Puma) and cell death in hematopoietic progenitors following DNA damage. Here, we show that this relationship is conserved in the developing nervous system in which Snail genes are excluded from vertebrate neurons and they are substituted by Scratch, a related but independent neural-specific factor. The transcription of scratch2 is induced directly by p53 after DNA damage to repress puma, thereby antagonizing p53-mediated apoptosis. In addition, we show that scratch2...

  12. Thanatophoric dysplasia type II with encephalocele and semilobar holoprosencephaly: Insights into its pathogenesis

    Martínez-Frías, María Luisa; Egüés, X.; Puras, A.; Hualde, J.; Frutos, Cristina A. de; Bermejo, Eva; Nieto, M. Ángela; Martínez, Salvador
    6 páginas, 3 figuras.

  13. Epithelial plasticity, stemness and pluripotency

    Ocaña, Oscar H.; Nieto, M. Ángela
    3 páginas, 1 figura.

  14. Snail1 suppresses TGF-β-induced apoptosis and is sufficient to trigger EMT in hepatocytes

    Franco, D. Lorena; Mainez, Jèssica; Vega, Sonia; Sancho, Patricia; Murillo, Miguel M.; Frutos, Cristina A. de; Castillo, Gael del; López-Blau, Cristina; Fabregat, Isabel; Nieto, M. Ángela
    11 páginas.

  15. Deletion of H-Ras decreases renal fibrosis and myofibroblast activation following ureteral obstruction in mice

    Grande, M. Teresa; Fuentes-Calvo, Isabel; Arévalo, Miguel; Heredia, Fabiana; Santos de Dios, Eugenio; Martínez-Salgado, Carlos; Rodríguez-Puyol, Diego; Nieto, M. Ángela; López-Novoa, José M.
    10 páginas.

  16. Review of the recently defined molecular mechanisms underlying thanatophoric dysplasia and their potential therapeutic implications for achondroplasia

    Martínez-Frías, María Luisa; Frutos, Cristina A. de; Bermejo, Eva; Nieto, M. Ángela
    11 páginas, 5 figuras, 1 tabla.

  17. Epithelial-Mesenchymal Transitions in Development and Disease

    Thiery, Jean Paul; Acloque, Hervé; Huang, Ruby Y. J.; Nieto, M. Ángela
    20 páginas, 7 figuras.

  18. Inflammation and EMT: an alliance towards organ fibrosis and cancer progression

    López-Novoa, José M.; Nieto, M. Ángela
    12 páginas, 3 figuras, 1 cuadro.

  19. Non-coding RNAs take centre stage in epithelial-to-mesenchymal transition

    Cano, Amparo; Nieto, M. Ángela
    3 páginas, 1 figura.

  20. A new regulatory loop in cancer-cell invasion

    Ocaña, Oscar H.; Nieto, M. Ángela
    2 páginas, 1 figura.

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