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Michaela Kilander, Ph.D.

Postdoctoral Research Scientist


Laboratory of Neuronal Connectivity
Program in Neuroscience
Hussman Institute for Autism
801 W. Baltimore Street
Suite 301
Baltimore, MD 21201
443.860.2580 ext.740
mkilander@hussmanautism.org

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  • Education & Experience
  • Research Interests
  • Research Background
  • Selected Publications

Education & Experience

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

 

Research Interests

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.

Research Background

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.

Selected Publications

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.

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Recent Activity:
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  • Parental optimism, school inclusion may affect long-term progress of individuals with autism
    April 12, 2016
  • Young adults with autism increase empathic communication with training
    March 24, 2016
  • Seeing things differently: Altered GABA signaling at play in autistic visual perception
    March 10, 2016

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Program on Neuroscience
Hussman Institute for Autism
801 W. Baltimore Street, Third Floor
Baltimore, MD 21201
Phone 443-860-2580 | Email info@hussmanautism.org

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