S
Servando Giráldez
Researcher at University of Seville
Publications - 13
Citations - 205
Servando Giráldez is an academic researcher from University of Seville. The author has contributed to research in topics: Ubiquitin ligase & Cell cycle. The author has an hindex of 8, co-authored 13 publications receiving 146 citations. Previous affiliations of Servando Giráldez include Salk Institute for Biological Studies & Scripps Research Institute.
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Journal ArticleDOI
Both p62/SQSTM1-HDAC6-dependent autophagy and the aggresome pathway mediate CDK1 degradation in human breast cancer
María Galindo-Moreno,Servando Giráldez,Carmen Sáez,Miguel A. Japón,María Tortolero,Francisco Romero +5 more
TL;DR: It is determined that both chemotherapeutic agents and proteolytic stress induce CDK1 degradation in human breast cancer MCF7 cells through p62/HDAC6-mediated selective autophagy and is proposed as a potential predictive biomarker of antitumor treatment efficacy.
Journal ArticleDOI
Loss of FBXW7 and accumulation of MCL1 and PLK1 promote paclitaxel resistance in breast cancer
Jessica Gasca,Maria Luz Flores,Servando Giráldez,Manuel Ruiz-Borrego,María Tortolero,Francisco Romero,Miguel A. Japón,Carmen Sáez +7 more
TL;DR: It is concluded that FBXW7 regulates the response to pac litaxel by targeting MCL1 and PLK1 in breast cancer cells and thus targeting these substrates may be a valuable adjunct for paclitaxel treatment.
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A single mutation in Securin induces chromosomal instability and enhances cell invasion
Mar Mora-Santos,Carolina Castilla,Joaquín Herrero-Ruiz,Servando Giráldez,M. Cristina Limón-Mortés,Carmen Sáez,Miguel A. Japón,María Tortolero,Francisco Romero +8 more
TL;DR: For the first time, a single mutation in pttg1 is sufficient to trigger the oncogenic properties of Securin and the finding of this point mutation in patients might be used as an effective strategy for early detection of cancer.
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Breast cancer cell line MCF7 escapes from G1/S arrest induced by proteasome inhibition through a GSK-3β dependent mechanism
TL;DR: The results support the relevance of GSK-3β and autophagy as two targets for controlling cell cycle progression and proliferative capacity in MCF7, highlighting the co-treatment of breast cancer cells with 3-MA to synergize the effect of the proteasome inhibition.
Journal ArticleDOI
βTrCP controls the lysosome-mediated degradation of CDK1, whose accumulation correlates with tumor malignancy.
Joaquín Herrero-Ruiz,Mar Mora-Santos,Servando Giráldez,Carmen Sáez,Miguel A. Japón,María Tortolero,F J Romero +6 more
TL;DR: The finding that treatment with the chemotherapeutic agent doxorubicin in certain cell lines provokes CDK1 degradation and induces apoptosis, whereas in others it inhibits destruction of the protein raises the possibility that different tumor types, depending on their pathogenic spectrum mutations, may display different sensitivity to βTrCP-induced CDK 1 degradation after DNA damage.