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Using the 3’UTR to control gene function and develop targeted therapies

Our laboratory’s long-term goal is to understand gene regulation and develop novel therapeutic approaches by fine-tuning the expression of a gene selectively in cells in which the gene is normally expressed. This innovative approach is complementary to—and in some respects, superior to—current gene deletion and gene over-expression methods.

A gene’s 3’UTR regulates its expression at the post-transcriptional level. Therefore, we explore new methods for manipulating the 3’UTR of target genes. This approach enables us to control endogenous gene expression specifically in cells that naturally express the gene of interest.

In our laboratory, we use state-of-the-art cellular and molecular biology tools to identify molecules that regulate gene expression by interacting with the target gene’s 3’UTR, including microRNAs (miRNAs) and RNA-binding proteins.

To understand the functional role of a gene’s 3’UTR, we generate and analyze mouse models in which the 3’UTR has been targeted, providing constitutive or conditional control over the endogenous gene’s expression.

Our current research focuses on the biology of brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF). Both BDNF and GDNF modulate the growth and function of a variety of cell types throughout the body, including the central nervous system. We hypothesize that the ability to conditionally upregulate the endogenous expression of BDNF and/or GDNF in mouse models will help establish novel methods for treating a wide range of neurodegenerative disease, including Parkinson’s disease, Alzheimer’s disease, and amyotrophic lateral sclerosis. We also use these powerful models to discover new functions for GDNF and BDNF in peripheral tissues, including the urogenital tract and the enteric nervous system.
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PublikatsioonAutoridAastaVäljaande pealkiriKlassifikaatorFailAsutused
Correction: GDNF Overexpression from the Native Locus Reveals its Role in the Nigrostriatal Dopaminergic System Function.Kumar, A.; Kopra, J.; Varendi, K.; Porokuokka, LL.; Panhelainen, A.; Kuure, S.; Marshall, P.; Karalija, N.; Härma, MA.; Vilenius, C.; Lilleväli, K.; Tekko, T.; Mijatovic, J.; Pulkkinen, N.; Jakobson, M.; Jakobson, M.; Ola, R.; Palm, E.; Lindahl, M.; Stromberg, I. ... Andressoo, JO.2016PLOS Genetics1.1.Tartu Ülikool
GDNF is not required for catecholaminergic neuron survival in vivo.Kopra, Jaakko; Vilenius, Carolina; Grealish, Shane; Härma, Mari-Anne; Varendi, Kärt; Lindholm, Jesse; Castrén, Eero; Võikar, Vootele; Björklund, Anders; Piepponen, T Petteri; Saarma, Mart; Andressoo, Jaan-Olle2015Nature Neuroscience1.1.
GDNF Overexpression from the Native Locus Reveals its Role in the Nigrostriatal Dopaminergic System Function.Kumar,Anmol; Kopra, Jaakko; Varendi, Kärt; Porokuokka, Lauriina L; Panhelainen, Anne; Kuure, Satu; Marshall, Pepin; Karalija, Nina; Härma, Mari-Anne; Vilenius, Carolina; Lilleväli, Kersti; Tekko, Triin; Mijatovic, Jelena; Pulkkinen, Nita; Jakobson, Madis; Jakobson, Maili; Ola, Roxana; Palm, Erik; Lindahl, Maria; Strömberg, Ingrid ... Andressoo, Jaan-Olle2015PLOS Genetics1.1.Tartu Ülikool
miR-1, miR-10b, miR-155, and miR-191 are novel regulators of BDNF.Varendi, Kärt; Kumar, Anmol; Härma, Mari-Anne; Andressoo, Jaan-Olle2014Cellular and molecular life sciences : CMLS1.1.