de la Luna Gargantilla, Susana
ICREA Research Professor at Centre de Regulació Genòmica (CRG).
Life & Medical Sciences
Short biography
I obtained a BsC in Biology in 1985 at Universidad Autónoma de Madrid. For my PhD studies, I joined Juan Ortín's lab at the CBMSO and worked on the biology of influenza virus, characterizing molecularly and functionally the viral polymerase. After getting the PhD in 1989 at UAM, I stayed in Ortín's lab at CNB until 1994 when I moved to London to the lab of Nick La Thangue at the National Institute for Medical Research. There, I worked on the G1/S transition in the mammalian cell cycle focusing in the transcription factor E2F, with fellowships from the HFSO (at NIMR) and EU-Marie Curie (at Glasgow University) Programs. In 1998, I returned to Spain with a reintegration contract to join the HSA21/Down syndrome Research group led by Xavier Estivill (IRO, Barcelona). In 2002, I joined ICREA and established my own research group working on the functional characterization of the family of kinases DYRK and their relationship with disease at the Centre for Genomic Regulation-CRG.
Research interests
Protein kinases are central to all cellular processes in eukaryotes, and often linked to disease when they are altered. My group works on a family of protein kinases known as DYRK (dual-specificity tyrosine-regulated kinases), whose members -DYRK1A, DYRK1B, DYRK2, DYRK3, DYRK4- participate in the regulation of processes critical for cell viability and homeostasis, and their dysregulation leads to disease in humans. Thus, mutations in one DYRK1A allele underlie a rare syndrome associated with general growth retardation and microcephaly. Moreover, DYRK1A overexpression in Down syndrome (DS) correlates with several DS pathological phenotypes. In general, alteration in DYRKs is linked to different cancer types. My group aims to dissect how DYRK activities are linked to human pathology. We are particularly interested on the DYRK-associated activities that impact on the regulation of expression programs either directly on chromatin or indirectly through modulation of signaling pathways.