Sila received her bachelor degree in Bilkent University, Ankara, Turkey. She went on to do her PhD at Columbia University in NYC, working in Dr Rafael Yuste’s laboratory. She investigated dendritic spine morphogenesis during development. As a postdoctoral fellow she studied the role of NMDA receptors in synaptogenesis in mouse models in Dr Anirvan Ghosh’s lab at UCSD (Ultanir et al, 2007, PNAS). She then did a second postdoc in Dr Yuh-Nung Jan’s lab at UCSF. Using chemical genetics methods She discovered roles NDR1/2 and MST3 kinases in brain development, which led to two publications in collaboration with Kevan Shokat at UCSF (Ultanir et al, 2012, Neuron & Ultanir et al 2014, Neuron). In 2013, she established her lab at the MRC funded National Institute for Medical Research (NIMR) at Mill Hill, London, UK, which later became part of the Francis Crick Institute in London. In her lab, Sila combines her expertise in neurodevelopment and kinase & mass spectrometry methods to study multiple brain disease-associated kinases. Her current projects center around deciphering the function of the kinase CDKL5, mutations of which cause a rare neurodevelopmental disorder (CDKL5 Deficiency Disorder). Her lab made pivotal discoveries on the set of substrates phosphorylated by CDKL5, and their biological functions in mouse models (Baltussen et al 2018, Sampedro-Castaneda et al 2023, Silvestre et al 2024). These roles include microtubule-based transport and voltage gated calcium channel function. Sila aims to bridge our understanding of CDKL5’s molecular functions with circuit formation utilizing paradigms of circuit development in visual cortex and expand molecular roles of how CDKL5’s regulation of substrates affects neuronal development. Sila uses CDKL5 as an entry point to reveal novel molecular mechanisms critical for brain development in humans. These mechanisms could have commonalities with other monogenic or more diverse neurodevelopmental disorders. In addition to CDKL5, Sila’s lab is interested in determining roles for disease-linked kinases including schizophrenia-associated TNIK, epilepsy linked mTOR, Parkinson’s associated GAK (Lin et al 2018) and NDR family of kinases NDR1/2 & LATS1/2 (Eder et al 2020, Rosianu et al 2022). Sila has substantial translational activities in her pursuit to help develop therapies for CDD. Sila’s discoveries led to a successful preclinical biomarker, EB2 phosphorylation, which is used in academia and biotech to report CDKL5 activity. The novel molecular link between Cav2.3 and CDD is being pursued in collaboration with a biotech company with funds from the Loulou foundation, a private organization dedicated to CDD research. The lab recently determined that CDKL2 phosphorylates CDKL5 substrates in mouse brain. This new finding opens a possibility that in enhancing CDKL2 function could be a new therapy avenue for CDD. In collaboration with university and biotech partners, Sila is pursuing CDKL2 as a target for CDD. Ultanir lab was selected for the “Lab of the year” award in 2018 and 2023 CDKL5 Forums.Sila have been awarded several grants from the Loulou foundation for CDKL5 research, Ultanir lab was selected as lab of the year award in 2018 and 2023 in CDKL5 Forums. Sila received grants from AstraZeneca, MSD and GSK in collaborative projects.