David Partida
Scripps Research Institute
8 Papers
9 Citations
David Partida is an academic researcher from Scripps Research Institute. The author has contributed to research in topics: Cell cycle & Mitosis. The author has an hindex of 7, co-authored 8 publications.
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Papers
AMPK and PFKFB3 mediate glycolysis and survival in response to mitophagy during mitotic arrest
Elena Doménech,Carolina Maestre,Lorena Esteban-Martínez,David Partida,Rosa Pascual,Gonzalo Fernández-Miranda,Esther Seco,Ramón Campos-Olivas,Manuel Pérez,Diego Megías,Katherine Allen,Miguel López,Asish K. Saha,Guillermo Velasco,Eduardo Rial,Raúl Méndez,Patricia Boya,María Salazar-Roa,Marcos Malumbres +18 more
TL;DR: It is shown here that survival during mitotic arrest is affected by the special energetic requirements of mitotic cells, which results in mitophagy-dependent loss of mitochondria, accompanied by reduced ATP levels and the activation of AMPK.
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Aurora B overexpression causes aneuploidy and p21Cip1 repression during tumor development
Alejandra González-Loyola,Gonzalo Fernández-Miranda,Marianna Trakala,David Partida,Kumiko Samejima,Hiromi Ogawa,Marta Cañamero,Alba de Martino,Ángel Martínez-Ramírez,Guillermo de Cárcer,Ignacio Pérez de Castro,William C. Earnshaw,Marcos Malumbres +12 more
TL;DR: A new mouse model is reported in which expression of the endogenous Aurkb locus can be induced in vitro and in vivo, and overexpression of Aurora B may contribute to tumor formation not only by inducing chromosomal instability but also by suppressing the function of the cell cycle inhibitor p21Cip1.
Identification of regulatory elements that control PPARγ expression in adipocyte progenitors.
TL;DR: Characterization of 5 highly conserved non-coding sequences from the PPARγ locus may enable isolation of the transcription factors that bind these cis elements and provide insight into the molecular regulation of adipose tissue expansion in normal and pathological states.
Activation of the endomitotic spindle assembly checkpoint and thrombocytopenia in Plk1-deficient mice
Marianna Trakala,David Partida,María Salazar-Roa,María Maroto,Paulina Wachowicz,Guillermo de Cárcer,Marcos Malumbres +6 more
TL;DR: It is shown here that Polo-like kinase 1 (Plk1) is required for endomitosis, and ablation of the Plk1 gene in megakaryocytes results in defective polyploidization accompanied by mitotic arrest and cell death, raising a note of caution in the use of PlK1 inhibitors in therapeutic strategies based on polyploidsization regulators.
Therapeutic relevance of the PP2A-B55 inhibitory kinase MASTL/Greatwall in breast cancer
Mónica Álvarez-Fernández,María Sanz-Flores,Belén Sanz-Castillo,María Salazar-Roa,David Partida,Elisabet Zapatero-Solana,H. Raza Ali,Eusebio Manchado,Scott W. Lowe,Todd VanArsdale,David Shields,Carlos Caldas,Miguel Quintela-Fandino,Marcos Malumbres +13 more
TL;DR: It is shown that MASTL overexpression predicts poor survival and shows prognostic value in breast cancer patients and that genetic ablation of MastL displays a significant therapeutic effect in vivo, suggesting that the PP2A inhibitory kinase MASTl may have both prognostic and therapeutic value in human breast cancer.