Author

J. Gonzalez-Martinez

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Cell Biology· 2 Bioengineering· 1

Signature Assays, Organisms & Methods

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Research Focus:cell type annotation· 3 Research Focus:cell signaling & trafficking· 2 Organism:human· 2 Organism:mouse· 2 Research Focus:chromatin & epigenetic regulation· 1 Research Focus:development & morphogenesis· 1 Assay:electrophysiology· 1 Approach:experimental assay· 1

Frequent Co-Authors

D. Martinez-Alonso· 2 shared M. Malumbres· 2 shared A. Behrens· 1 shared A. Cwersch· 1 shared A. El Bakkali· 1 shared A. G. Rouse· 1 shared A. Kanner· 1 shared A. Korzeniewska· 1 shared

Activity by Year

2020-2021 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 18 mutual co-author links

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2 shared papersCell Biology

D. Martinez-Alonso

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Source-sink connectivity: A novel interictal EEG marker for seizure localization

K. M. Gunnarsdottir, A. Li, R. J. Smith, J.-Y. Kang, A. Korzeniewska, N. Crone, A. G. Rouse, J. J. Cheng, M. J. Kinsman, P. Landazuri, U. Uysal, C. M. Ulloa, N. Cameron, I. Cajigas, J. R. Jagid, , S. V. Sarma

This paper develops a network-based interictal EEG marker to identify the epileptogenic zone, achieving 79% accuracy in predicting surgical outcomes compared to 43% for clinicians.

bioRxiv · Oct 15, 2021Bioengineering

A cell cycle kinase-phosphatase module restrains PI3K-Akt activity in an mTORC1-dependent manner

B. Sanz-Castillo, B. Hurtado, A. El Bakkali, D. Hermida, B. Salvador-Barbero, D. Martinez-Alonso, J. Gonzalez-Martinez, C. Santiveri, R. Campos-Oliva, P. Ximenez, J. Munoz, M. Alvarez-Fernandez, M. Malumbres

This study identifies a cell cycle kinase-phosphatase module that restrains PI3K-Akt activity through mTORC1-dependent phosphorylation of IRS1 and GRB10.

bioRxiv · Nov 26, 2020 · PreprintCell Biology

Lack of adaptation to centriolar defects leads to p53-independent microcephaly in the absence of Cep135

J. Gonzalez-Martinez, A. Cwersch, D. Martinez-Alonso, L. R. Lopez, J. Almagro, D. Megias, J. Boskovic, J. Gilabert, O. Grana Castro, A. Pierani, A. Behrens, S. Ortega, M. Malumbres

This study shows that Cep135 loss causes microcephaly in mice through p53-independent mechanisms due to neural progenitor adaptation failure to centriole defects.

bioRxiv · May 7, 2020 · PreprintCell Biology