Resultados totales (Incluyendo duplicados): 35683
Encontrada(s) 3569 página(s)
Encontrada(s) 3569 página(s)
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354267
Dataset. 2023
IMAGE2_EVC-EVC2 COMPLEX STABILITY AND CILIARY TARGETING ARE REGULATED BY MODIFICATION WITH UBIQUITIN AND SUMO.TIF [DATASET]
- Barbeito, Pablo
- Martin-Morales, Raquel
- Palencia-Campos, Adrián
- Cerrolaza, Juan
- Rivas-Santos, Celia
- Gallego-Colastra, Leticia
- Caparrós-Martín, José A.
- Martín Bravo, Carolina
- Martín-Hurtado, Ana
- Sánchez-Bellver, Laura
- Marfany, Gemma
- Ruiz-Pérez, Victor L.
- Garcia-Gonzalo, Francesc R.
Ellis van Creveld syndrome and Weyers acrofacial dysostosis are two rare genetic diseases affecting skeletal development. They are both ciliopathies, as they are due to malfunction of primary cilia, microtubule-based plasma membrane protrusions that function as cellular antennae and are required for Hedgehog signaling, a key pathway during skeletal morphogenesis. These ciliopathies are caused by mutations affecting the EVC-EVC2 complex, a transmembrane protein heterodimer that regulates Hedgehog signaling from inside primary cilia. Despite the importance of this complex, the mechanisms underlying its stability, targeting and function are poorly understood. To address this, we characterized the endogenous EVC protein interactome in control and Evc-null cells. This proteomic screen confirmed EVC’s main known interactors (EVC2, IQCE, EFCAB7), while revealing new ones, including USP7, a deubiquitinating enzyme involved in Hedgehog signaling. We therefore looked at EVC-EVC2 complex ubiquitination. Such ubiquitination exists but is independent of USP7 (and of USP48, also involved in Hh signaling). We did find, however, that monoubiquitination of EVC-EVC2 cytosolic tails greatly reduces their protein levels. On the other hand, modification of EVC-EVC2 cytosolic tails with the small ubiquitin-related modifier SUMO3 has a different effect, enhancing complex accumulation at the EvC zone, immediately distal to the ciliary transition zone, possibly via increased binding to the EFCAB7-IQCE complex. Lastly, we find that EvC zone targeting of EVC-EVC2 depends on two separate EFCAB7-binding motifs within EVC2’s Weyers-deleted peptide. Only one of these motifs had been characterized previously, so we have mapped the second herein. Altogether, our data shed light on EVC-EVC2 complex regulatory mechanisms, with implications for ciliopathies., Peer reviewed
Proyecto: //
DOI: http://hdl.handle.net/10261/354267
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354267
HANDLE: http://hdl.handle.net/10261/354267
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354267
PMID: http://hdl.handle.net/10261/354267
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354267
Ver en: http://hdl.handle.net/10261/354267
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354267
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354271
Dataset. 2023
IMAGE3_EVC-EVC2 COMPLEX STABILITY AND CILIARY TARGETING ARE REGULATED BY MODIFICATION WITH UBIQUITIN AND SUMO.TIF [DATASET]
- Barbeito, Pablo
- Martin-Morales, Raquel
- Palencia-Campos, Adrián
- Cerrolaza, Juan
- Rivas-Santos, Celia
- Gallego-Colastra, Leticia
- Caparrós-Martín, José A.
- Martín Bravo, Carolina
- Martín-Hurtado, Ana
- Sánchez-Bellver, Laura
- Marfany, Gemma
- Ruiz-Pérez, Victor L.
- Garcia-Gonzalo, Francesc R.
Ellis van Creveld syndrome and Weyers acrofacial dysostosis are two rare genetic diseases affecting skeletal development. They are both ciliopathies, as they are due to malfunction of primary cilia, microtubule-based plasma membrane protrusions that function as cellular antennae and are required for Hedgehog signaling, a key pathway during skeletal morphogenesis. These ciliopathies are caused by mutations affecting the EVC-EVC2 complex, a transmembrane protein heterodimer that regulates Hedgehog signaling from inside primary cilia. Despite the importance of this complex, the mechanisms underlying its stability, targeting and function are poorly understood. To address this, we characterized the endogenous EVC protein interactome in control and Evc-null cells. This proteomic screen confirmed EVC’s main known interactors (EVC2, IQCE, EFCAB7), while revealing new ones, including USP7, a deubiquitinating enzyme involved in Hedgehog signaling. We therefore looked at EVC-EVC2 complex ubiquitination. Such ubiquitination exists but is independent of USP7 (and of USP48, also involved in Hh signaling). We did find, however, that monoubiquitination of EVC-EVC2 cytosolic tails greatly reduces their protein levels. On the other hand, modification of EVC-EVC2 cytosolic tails with the small ubiquitin-related modifier SUMO3 has a different effect, enhancing complex accumulation at the EvC zone, immediately distal to the ciliary transition zone, possibly via increased binding to the EFCAB7-IQCE complex. Lastly, we find that EvC zone targeting of EVC-EVC2 depends on two separate EFCAB7-binding motifs within EVC2’s Weyers-deleted peptide. Only one of these motifs had been characterized previously, so we have mapped the second herein. Altogether, our data shed light on EVC-EVC2 complex regulatory mechanisms, with implications for ciliopathies., Peer reviewed
Proyecto: //
DOI: http://hdl.handle.net/10261/354271
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354271
HANDLE: http://hdl.handle.net/10261/354271
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354271
PMID: http://hdl.handle.net/10261/354271
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354271
Ver en: http://hdl.handle.net/10261/354271
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354271
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354290
Dataset. 2024
PHENOTYPING DATA OF LEGUMES-CEREALS INTERCROPPING DATA
- Villegas-Fernández, Ángel M.
- Rubiales, Diego
Phenotyping data of legumes-cereals intercrops under field conditions at Córdob-Spain during two consecutive seasons 2021-2022 and 2022-2023., PROYECTO P20_00986 PAIDI2020 Junta Andalucía., Peer reviewed
Proyecto: //
DOI: http://hdl.handle.net/10261/354290, https://doi.org/10.20350/digitalCSIC/16224
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354290
HANDLE: http://hdl.handle.net/10261/354290, https://doi.org/10.20350/digitalCSIC/16224
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354290
PMID: http://hdl.handle.net/10261/354290, https://doi.org/10.20350/digitalCSIC/16224
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354290
Ver en: http://hdl.handle.net/10261/354290, https://doi.org/10.20350/digitalCSIC/16224
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354290
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354292
Dataset. 2023
DECADAL TRENDS IN THE OCEANIC STORAGE OF ANTHROPOGENIC CARBON FROM 1994 TO 2014 [DATASET]
- Müller, Jens Daniel
- Gruber, Nicolas
- Carter, Brendan R.
- Feely, Richard A.
- Ishii, Masao
- Lange, Nico
- Lauvset, Siv K.
- Murata, Akihiko
- Olsen, Are
- Pérez, Fiz F.
- Sabine, Christopher L.
- Tanhua, Toste
- Wanninkhof, Rik
- Zhu, Donghe
6 files, This dataset consists of the estimated decadal changes in the oceanic content of anthropogenic CO2 (∆Cant) between 1994, 2004 and 2014 as described in detail in Müller et al. (2023, in press, AGU Advances). These estimates have been derived from the GLODAPv2.2021 product (Lauvset et al., 2021) using the eMLR(C*) method developed by Clement & Gruber (2018). The datasets contain in addition to the standard estimate also 10 sensitivity cases, which are intended to assess the robustness of the standard estimates to different changes in the estimation procedure. All estimates are provided on a horizontal grid with 1° x 1° resolution. Two primary files are provided: one containing the full three-dimensional distribution of ∆Cant and one containing the vertically integrated values, i.e., the column inventories, 821003 - Climate-Carbon Interactions in the Coming Century (EC); 821001 - Southern Ocean Carbon and Heat Impact on Climate (EC), Peer reviewed
Proyecto: EC, EC/H2020, H2020/821003, 821001
DOI: http://hdl.handle.net/10261/354292
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354292
HANDLE: http://hdl.handle.net/10261/354292
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354292
PMID: http://hdl.handle.net/10261/354292
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354292
Ver en: http://hdl.handle.net/10261/354292
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354292
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354316
Dataset. 2023
IMAGE5_EVC-EVC2 COMPLEX STABILITY AND CILIARY TARGETING ARE REGULATED BY MODIFICATION WITH UBIQUITIN AND SUMO.TIF [DATASET]
- Barbeito, Pablo
- Martin-Morales, Raquel
- Palencia-Campos, Adrián
- Cerrolaza, Juan
- Rivas-Santos, Celia
- Gallego-Colastra, Leticia
- Caparrós-Martín, José A.
- Martín Bravo, Carolina
- Martín-Hurtado, Ana
- Sánchez-Bellver, Laura
- Marfany, Gemma
- Ruiz-Pérez, Victor L.
- Garcia-Gonzalo, Francesc R.
Ellis van Creveld syndrome and Weyers acrofacial dysostosis are two rare genetic diseases affecting skeletal development. They are both ciliopathies, as they are due to malfunction of primary cilia, microtubule-based plasma membrane protrusions that function as cellular antennae and are required for Hedgehog signaling, a key pathway during skeletal morphogenesis. These ciliopathies are caused by mutations affecting the EVC-EVC2 complex, a transmembrane protein heterodimer that regulates Hedgehog signaling from inside primary cilia. Despite the importance of this complex, the mechanisms underlying its stability, targeting and function are poorly understood. To address this, we characterized the endogenous EVC protein interactome in control and Evc-null cells. This proteomic screen confirmed EVC’s main known interactors (EVC2, IQCE, EFCAB7), while revealing new ones, including USP7, a deubiquitinating enzyme involved in Hedgehog signaling. We therefore looked at EVC-EVC2 complex ubiquitination. Such ubiquitination exists but is independent of USP7 (and of USP48, also involved in Hh signaling). We did find, however, that monoubiquitination of EVC-EVC2 cytosolic tails greatly reduces their protein levels. On the other hand, modification of EVC-EVC2 cytosolic tails with the small ubiquitin-related modifier SUMO3 has a different effect, enhancing complex accumulation at the EvC zone, immediately distal to the ciliary transition zone, possibly via increased binding to the EFCAB7-IQCE complex. Lastly, we find that EvC zone targeting of EVC-EVC2 depends on two separate EFCAB7-binding motifs within EVC2’s Weyers-deleted peptide. Only one of these motifs had been characterized previously, so we have mapped the second herein. Altogether, our data shed light on EVC-EVC2 complex regulatory mechanisms, with implications for ciliopathies., Peer reviewed
Proyecto: //
DOI: http://hdl.handle.net/10261/354316
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354316
HANDLE: http://hdl.handle.net/10261/354316
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354316
PMID: http://hdl.handle.net/10261/354316
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354316
Ver en: http://hdl.handle.net/10261/354316
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354316
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354317
Dataset. 2023
IMAGE6_EVC-EVC2 COMPLEX STABILITY AND CILIARY TARGETING ARE REGULATED BY MODIFICATION WITH UBIQUITIN AND SUMO.TIF [DATASET]
- Barbeito, Pablo
- Martin-Morales, Raquel
- Palencia-Campos, Adrián
- Cerrolaza, Juan
- Rivas-Santos, Celia
- Gallego-Colastra, Leticia
- Caparrós-Martín, José A.
- Martín Bravo, Carolina
- Martín-Hurtado, Ana
- Sánchez-Bellver, Laura
- Marfany, Gemma
- Ruiz-Pérez, Victor L.
- Garcia-Gonzalo, Francesc R.
Ellis van Creveld syndrome and Weyers acrofacial dysostosis are two rare genetic diseases affecting skeletal development. They are both ciliopathies, as they are due to malfunction of primary cilia, microtubule-based plasma membrane protrusions that function as cellular antennae and are required for Hedgehog signaling, a key pathway during skeletal morphogenesis. These ciliopathies are caused by mutations affecting the EVC-EVC2 complex, a transmembrane protein heterodimer that regulates Hedgehog signaling from inside primary cilia. Despite the importance of this complex, the mechanisms underlying its stability, targeting and function are poorly understood. To address this, we characterized the endogenous EVC protein interactome in control and Evc-null cells. This proteomic screen confirmed EVC’s main known interactors (EVC2, IQCE, EFCAB7), while revealing new ones, including USP7, a deubiquitinating enzyme involved in Hedgehog signaling. We therefore looked at EVC-EVC2 complex ubiquitination. Such ubiquitination exists but is independent of USP7 (and of USP48, also involved in Hh signaling). We did find, however, that monoubiquitination of EVC-EVC2 cytosolic tails greatly reduces their protein levels. On the other hand, modification of EVC-EVC2 cytosolic tails with the small ubiquitin-related modifier SUMO3 has a different effect, enhancing complex accumulation at the EvC zone, immediately distal to the ciliary transition zone, possibly via increased binding to the EFCAB7-IQCE complex. Lastly, we find that EvC zone targeting of EVC-EVC2 depends on two separate EFCAB7-binding motifs within EVC2’s Weyers-deleted peptide. Only one of these motifs had been characterized previously, so we have mapped the second herein. Altogether, our data shed light on EVC-EVC2 complex regulatory mechanisms, with implications for ciliopathies., Peer reviewed
Proyecto: //
DOI: http://hdl.handle.net/10261/354317
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354317
HANDLE: http://hdl.handle.net/10261/354317
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354317
PMID: http://hdl.handle.net/10261/354317
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354317
Ver en: http://hdl.handle.net/10261/354317
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354317
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354320
Dataset. 2023
IMAGE7_EVC-EVC2 COMPLEX STABILITY AND CILIARY TARGETING ARE REGULATED BY MODIFICATION WITH UBIQUITIN AND SUMO.TIF [DATASET]
- Barbeito, Pablo
- Martin-Morales, Raquel
- Palencia-Campos, Adrián
- Cerrolaza, Juan
- Rivas-Santos, Celia
- Gallego-Colastra, Leticia
- Caparrós-Martín, José A.
- Martín Bravo, Carolina
- Martín-Hurtado, Ana
- Sánchez-Bellver, Laura
- Marfany, Gemma
- Ruiz-Pérez, Victor L.
- Garcia-Gonzalo, Francesc R.
Ellis van Creveld syndrome and Weyers acrofacial dysostosis are two rare genetic diseases affecting skeletal development. They are both ciliopathies, as they are due to malfunction of primary cilia, microtubule-based plasma membrane protrusions that function as cellular antennae and are required for Hedgehog signaling, a key pathway during skeletal morphogenesis. These ciliopathies are caused by mutations affecting the EVC-EVC2 complex, a transmembrane protein heterodimer that regulates Hedgehog signaling from inside primary cilia. Despite the importance of this complex, the mechanisms underlying its stability, targeting and function are poorly understood. To address this, we characterized the endogenous EVC protein interactome in control and Evc-null cells. This proteomic screen confirmed EVC’s main known interactors (EVC2, IQCE, EFCAB7), while revealing new ones, including USP7, a deubiquitinating enzyme involved in Hedgehog signaling. We therefore looked at EVC-EVC2 complex ubiquitination. Such ubiquitination exists but is independent of USP7 (and of USP48, also involved in Hh signaling). We did find, however, that monoubiquitination of EVC-EVC2 cytosolic tails greatly reduces their protein levels. On the other hand, modification of EVC-EVC2 cytosolic tails with the small ubiquitin-related modifier SUMO3 has a different effect, enhancing complex accumulation at the EvC zone, immediately distal to the ciliary transition zone, possibly via increased binding to the EFCAB7-IQCE complex. Lastly, we find that EvC zone targeting of EVC-EVC2 depends on two separate EFCAB7-binding motifs within EVC2’s Weyers-deleted peptide. Only one of these motifs had been characterized previously, so we have mapped the second herein. Altogether, our data shed light on EVC-EVC2 complex regulatory mechanisms, with implications for ciliopathies., Peer reviewed
Proyecto: //
DOI: http://hdl.handle.net/10261/354320
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354320
HANDLE: http://hdl.handle.net/10261/354320
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354320
PMID: http://hdl.handle.net/10261/354320
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354320
Ver en: http://hdl.handle.net/10261/354320
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354320
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354321
Dataset. 2023
IMAGE8_EVC-EVC2 COMPLEX STABILITY AND CILIARY TARGETING ARE REGULATED BY MODIFICATION WITH UBIQUITIN AND SUMO.TIF [DATASET]
- Barbeito, Pablo
- Martin-Morales, Raquel
- Palencia-Campos, Adrián
- Cerrolaza, Juan
- Rivas-Santos, Celia
- Gallego-Colastra, Leticia
- Caparrós-Martín, José A.
- Martín Bravo, Carolina
- Martín-Hurtado, Ana
- Sánchez-Bellver, Laura
- Marfany, Gemma
- Ruiz-Pérez, Victor L.
- Garcia-Gonzalo, Francesc R.
Ellis van Creveld syndrome and Weyers acrofacial dysostosis are two rare genetic diseases affecting skeletal development. They are both ciliopathies, as they are due to malfunction of primary cilia, microtubule-based plasma membrane protrusions that function as cellular antennae and are required for Hedgehog signaling, a key pathway during skeletal morphogenesis. These ciliopathies are caused by mutations affecting the EVC-EVC2 complex, a transmembrane protein heterodimer that regulates Hedgehog signaling from inside primary cilia. Despite the importance of this complex, the mechanisms underlying its stability, targeting and function are poorly understood. To address this, we characterized the endogenous EVC protein interactome in control and Evc-null cells. This proteomic screen confirmed EVC’s main known interactors (EVC2, IQCE, EFCAB7), while revealing new ones, including USP7, a deubiquitinating enzyme involved in Hedgehog signaling. We therefore looked at EVC-EVC2 complex ubiquitination. Such ubiquitination exists but is independent of USP7 (and of USP48, also involved in Hh signaling). We did find, however, that monoubiquitination of EVC-EVC2 cytosolic tails greatly reduces their protein levels. On the other hand, modification of EVC-EVC2 cytosolic tails with the small ubiquitin-related modifier SUMO3 has a different effect, enhancing complex accumulation at the EvC zone, immediately distal to the ciliary transition zone, possibly via increased binding to the EFCAB7-IQCE complex. Lastly, we find that EvC zone targeting of EVC-EVC2 depends on two separate EFCAB7-binding motifs within EVC2’s Weyers-deleted peptide. Only one of these motifs had been characterized previously, so we have mapped the second herein. Altogether, our data shed light on EVC-EVC2 complex regulatory mechanisms, with implications for ciliopathies., Peer reviewed
Proyecto: //
DOI: http://hdl.handle.net/10261/354321
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354321
HANDLE: http://hdl.handle.net/10261/354321
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354321
PMID: http://hdl.handle.net/10261/354321
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354321
Ver en: http://hdl.handle.net/10261/354321
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354321
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354322
Dataset. 2023
TABLE1_EVC-EVC2 COMPLEX STABILITY AND CILIARY TARGETING ARE REGULATED BY MODIFICATION WITH UBIQUITIN AND SUMO.XLSX [DATASET]
- Barbeito, Pablo
- Martin-Morales, Raquel
- Palencia-Campos, Adrián
- Cerrolaza, Juan
- Rivas-Santos, Celia
- Gallego-Colastra, Leticia
- Caparrós-Martín, José A.
- Martín Bravo, Carolina
- Martín-Hurtado, Ana
- Sánchez-Bellver, Laura
- Marfany, Gemma
- Ruiz-Pérez, Victor L.
- Garcia-Gonzalo, Francesc R.
Ellis van Creveld syndrome and Weyers acrofacial dysostosis are two rare genetic diseases affecting skeletal development. They are both ciliopathies, as they are due to malfunction of primary cilia, microtubule-based plasma membrane protrusions that function as cellular antennae and are required for Hedgehog signaling, a key pathway during skeletal morphogenesis. These ciliopathies are caused by mutations affecting the EVC-EVC2 complex, a transmembrane protein heterodimer that regulates Hedgehog signaling from inside primary cilia. Despite the importance of this complex, the mechanisms underlying its stability, targeting and function are poorly understood. To address this, we characterized the endogenous EVC protein interactome in control and Evc-null cells. This proteomic screen confirmed EVC’s main known interactors (EVC2, IQCE, EFCAB7), while revealing new ones, including USP7, a deubiquitinating enzyme involved in Hedgehog signaling. We therefore looked at EVC-EVC2 complex ubiquitination. Such ubiquitination exists but is independent of USP7 (and of USP48, also involved in Hh signaling). We did find, however, that monoubiquitination of EVC-EVC2 cytosolic tails greatly reduces their protein levels. On the other hand, modification of EVC-EVC2 cytosolic tails with the small ubiquitin-related modifier SUMO3 has a different effect, enhancing complex accumulation at the EvC zone, immediately distal to the ciliary transition zone, possibly via increased binding to the EFCAB7-IQCE complex. Lastly, we find that EvC zone targeting of EVC-EVC2 depends on two separate EFCAB7-binding motifs within EVC2’s Weyers-deleted peptide. Only one of these motifs had been characterized previously, so we have mapped the second herein. Altogether, our data shed light on EVC-EVC2 complex regulatory mechanisms, with implications for ciliopathies., Peer reviewed
Proyecto: //
DOI: http://hdl.handle.net/10261/354322
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354322
HANDLE: http://hdl.handle.net/10261/354322
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354322
PMID: http://hdl.handle.net/10261/354322
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354322
Ver en: http://hdl.handle.net/10261/354322
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354322
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354339
Dataset. 2023
CONSTRAINED TRAIT VARIATION BY WATER AVAILABILITY MODULATES RADIAL GROWTH IN EVERGREEN AND DECIDUOUS MEDITERRANEAN OAKS [DATASET]
- González de Andrés, Ester
- Serra-Maluquer, Xavier
- Gazol Burgos, Antonio
- Olano Mendoza, José Miguel
- García-Plazaola, José Ignacio
- Fernández-Marín, Beatriz
- Imbert, Juan Bosco
- Coll, Lluís
- Ameztegui, Aitor
- Espelta, Josep María
- Alla, A. Q.
- Camarero, Jesús Julio
Data supporting the findings of the study "Constrained trait variation by water availability modulates radial growth in two coexisting Mediterranean oaks", Peer reviewed
Proyecto: //
DOI: http://hdl.handle.net/10261/354339
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354339
HANDLE: http://hdl.handle.net/10261/354339
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354339
PMID: http://hdl.handle.net/10261/354339
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354339
Ver en: http://hdl.handle.net/10261/354339
Digital.CSIC. Repositorio Institucional del CSIC
oai:digital.csic.es:10261/354339
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