PhD Student at University of Salamanca. Currently working on lipid metabolism and NADPH oxidases (NOXs) in the context of acute myeloid leukemia (AML)
EDUCATION
PhD Student (Bioquemistry and Molecular Biology). University of Salamanca
MSc Molecular Cell Biology graduate. University of Salamanca
BSc Biotechnology graduate . University of Salamanca
RESEARCH, TEACHING, or OTHER INTERESTS
Cancer Research, Cell Biology, Biochemistry, Genetics and Molecular Biology, Hematology
2
Scopus Publications
Scopus Publications
Altered PTPN13–β-catenin interaction by pathogenic mutations and involvement of this axis in B-cell receptor signalling David A. Cabrera-Riofrío, Hongbing Li, Clara García-Calvo, Carmen Sánchez-Bernal, Jesús Sánchez-Yagüe, Yigal Dror, Rubén M. Buey, Ángel Hernández-Hernández Scientific Reports, 2026 Protein tyrosine phosphatase non-receptor type 13 (PTPN13) is a non-receptor protein tyrosine phosphatase with context-dependent roles as tumour suppressor or promoter. Its modular structure supports multiple molecular interactions, including a critical one with β-catenin, a regulator of the haematopoietic system. We previously identified three pathogenic PTPN13 mutations in families with acute lymphoblastic leukaemia (ALL), anaemia, and/or inherited bone marrow failure (IBMF). Our current findings reveal that these mutations impair the PTPN13-β-catenin interaction. β-catenin and PTPN13 are stabilised upon B-cell receptor (BCR) activation, while PTPN13 silencing reduces Bruton's tyrosine kinase (BTK) activation and β-catenin levels, indicating that PTPN13 modulates BCR signalling at multiple points. Together with prior evidence showing that PTPN13 mutations compromise protein stability and decrease β-catenin levels, these data support a role for disrupted lymphoid signalling. Altered expression of key surface markers (CD25 and CD38) upon silencing of either PTPN13 or β-catenin further supports this interpretation. In conclusion, our study identifies the PTPN13-β-catenin axis as a critical regulator of lymphoid cell homeostasis and highlights its disruption as a potential driver of haematological abnormalities in patients carrying PTPN13 mutations.
NOX2 control over energy metabolism plays a role in acute myeloid leukaemia prognosis and survival Carla Ijurko, Marta Romo-González, Clara García-Calvo, José Luis Sardina, Carmen Sánchez-Bernal, Jesús Sánchez-Yagüe, Bénédicte Elena-Herrmann, Joran Villaret, Catherine Garrel, Julie Mondet, Pascal Mossuz, Ángel Hernández-Hernández Free Radical Biology and Medicine, 2023 Acute myeloid leukaemia (AML) is a highly heterogeneous disease, however the therapeutic approaches have hardly changed in the last decades. Metabolism rewiring and the enhanced production of reactive oxygen species (ROS) are hallmarks of cancer. A deeper understanding of these features could be instrumental for the development of specific AML-subtypes treatments. NADPH oxidases (NOX), the only cellular system specialised in ROS production, are also involved in leukemic metabolism control. NOX2 shows a variable expression in AML patients, so patients can be classified based on such difference. Here we have analysed whether NOX2 levels are important for AML metabolism control. The lack of NOX2 in AML cells slowdowns basal glycolysis and oxidative phosphorylation (OXPHOS), along with the accumulation of metabolites that feed such routes, and a sharp decrease of glutathione. In addition, we found changes in the expression of 725 genes. Among them, we have discovered a panel of 30 differentially expressed metabolic genes, whose relevance was validated in patients. This panel can segregate AML patients according to CYBB expression, and it can predict patient prognosis and survival. In summary, our data strongly support the relevance of NOX2 for AML metabolism, and highlights the potential of our discoveries in AML prognosis.
