Michaela Kilander, Ph.D.
Postdoctoral Research Scientist
2014- present Postdoctoral Research Scientist, Program in Neuroscience, Hussman Institute for Autism, Baltimore, MD
2014 Analyst, The Public Health Agency of Sweden, Stockholm, Sweden
2013 Ph.D. Medical Sciences and Pharmacology, Karolinska Institute, Stockholm, Sweden
2007 B.Sc. Molecular Biology, Stockholm University, Stockholm, Sweden
Drawing from my background in pharmacology, G-protein signal transduction and in the WNT cell communication pathways, I am interested in studying cell-to-cell communications in the autistic brain from a developmental point of view. To investigate and pinpoint the impact of mutations in genes participating in cell signaling events early in embryogenesis is something I strongly believe will reveal the critical factors involved in the dysregulation of nervous tissue patterning and organization, which ultimately leads to the progression of altered brain function later in life.
My research focus has been aimed at describing molecular interactions of proteins involved in the early events of WNT signaling pathways. To perform these studies I used pharmacological, biochemical and advanced imaging techniques and methods to investigate the G protein coupled receptor (GPCR) properties of the WNT receptor Frizzled as well as the dynamics of ligands and intracellular effector molecules at these receptors. The results of my research revealed that WNTs could function as endogenous biased agonists, a property otherwise commonly seen in synthetic pharmaceutical compounds. Furthermore, the data collected show evidence of a novel GPCR signaling mechanism involving the scaffold molecule Disheveled. WNT signaling is highly active during embryonic development and essential for the formation of neuronal tissue. Thus, investigating signaling events and molecules participating in these cellular pathways could contribute to the understanding of the mechanisms at play in autism spectrum conditions.
Kilander MB, Dahlström J, Schulte G. Assessment of Frizzled 6 membrane mobility by FRAP supports G protein coupling and reveals WNT-Frizzled selectivity. Cell Signal. 2014, 26:1943-9. PMID: 24873871.
Kilander MB, Petersen J, Andressen KW, Ganji RS, Levy FO, Schuster J, Dahl N, Bryja V, Schulte G. Disheveled regulates precoupling of heterotrimeric G proteins to Frizzled 6. FASEB J. 2014, 28:2293-305. PMID: 24500924.
Kilander MB, Halleskog C, Schulte G. Recombinant WNTs differentially activate β-catenin-dependent and -independent signalling in mouse microglia-like cells. Acta Physiol (Oxf). 2011, 203:363-72. PMID: 21557822.
Fröjmark AS, Schuster J, Sobol M, Entesarian M, Kilander MB, Gabrikova D, Nawaz S, Baig SM, Schulte G, Klar J, Dahl N. Mutations in Frizzled 6 cause isolated autosomal-recessive nail dysplasia. Am J Hum Genet. 2011, 88:852-60. PMID: 21665003.
Kilander MB, Dijksterhuis JP, Ganji RS, Bryja V, Schulte G. WNT-5A stimulates the GDP/GTP exchange at pertussis toxin-sensitive heterotrimeric G proteins. Cell Signal. 2011, 23:550-4. PMID: 21070854.