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1

Zastosowanie spektrometrii mas w poszukiwaniach biomarkerow chorob nowotworowych

100%
Tarkowski B., Girstun A.
Kosmos
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2005
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tom 54
|
nr 4
331-343
2

Kainic acid causes mTOR activation and translocation from cytosol to the nucleus – Live imaging study

71%
Macias M., Janusz-Kaminska A., Tarkowski B., Gozdz A., Jaworski J.
Acta Neurobiologiae Experimentalis
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2017
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tom 77
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nr Suppl.1
INTRODUCTION: The mechanistic target of rapamycin (mTOR) is a protein kinase, which integrates eukaryotic cell growth, metabolism and external stimuli. Most research link mTOR with control of protein translation but recent studies revealed additional mTOR function in cell nucleus. Previously, we showed that phosphorylation of mTOR (Ser2448; P-mTOR) is upregulated in neuronal nucleus upon kainate (KA) induced status epilepticus. Whether other stimuli have the same effect on nuclear mTOR phosphorylation and if increased nuclear import of mTOR contributes to this phenomenon remained unknown. Also it was not known if nuclear transport of other proteins affects mTOR signaling. AIM(S): To analyze effects of neuronal activity on nuclear translocation of mTOR and its nuclear activity. To analyze importance of nuclear transport for mTOR signaling. METHOD(S): Cultured hippocampal neurons were treated with: KA, BDNF; NMDA and chemical LTP (cLTP) protocol or TTX. mTOR activity was measured with FRET method. mTOR nuclear translocation was assessed using FRAP. Nuclear import was blocked with importazole. Immunofluorescence of P-S6 protein was used as a marker of mTOR activity. RESULTS: We found that KA, BDNF, NMDA and cLTP caused nuclear upregulation of P-mTOR. However, TTX or cLTD had no effect. FRAP and FRET revealed that mTOR activity due to KA treatment is first observed in cytosol and then in nucleus, where mTOR is translocated upon treatment. Blocking nuclear import silenced mTOR activity in response to KA and inhibited P-mTOR upregulation in the nucleus. CONCLUSIONS: Our experiments showed that increased neuronal activity upregulates nuclear P-mTOR and increases nuclear activity of mTOR due to nuclear translocation of the kinase. FINANCIAL SUPPORT: The research was supported by PNSC grants no. 2012/05/B/NZ3/00429 and 2012/07/E/ NZ3/00503.
3

The role of adaptor complex AP2 in formation of dendritic arbors of hippocampal neurons

61%
Koscielny A., Malik A., Liszewska E., Zmorzynka J., Tempes A., Tarkowski B., Jaworski J.
Acta Neurobiologiae Experimentalis
|
2017
|
tom 77
|
nr Suppl.1
INTRODUCTION: The proper dendritic branching is a highly regulated process. Among its regulators are membrane proteins internalized via clathrin-mediated endocytosis. AP2 adaptor complex is a key player in this process, but its role in mammalian dendritogenesis has not yet been tested. AIM(S): The aim of this study was to find how AP2 complex contributes to shaping dendritic tree of developing hippocampal neurons. METHOD(S): To study role of AP2 complex in dendritic arborization we used primary hippocampal neurons expressing AP2b1 (b-adaptin) shRNA alone or in combination of functional rescue constructs (i.a. GluA2, S6K1ca). The effect was also tested in vivo by lentiviral injections to newborn rats. Upon b-adaptin knockdown, we tested GluA2 trafficking via internalization assay and GluA2 level by Western blot and immunochemistry. GluA2 degradation and mTOR dependent biosynthesis were investigated by e.g. cycloheximide or rapamycin treatment. RESULTS: We showed that knockdown of b-adaptin led to reduction in dendritic arbors of developing hippocampal neurons in vitro and in vivo. The knockdown of AP2 also led to decreased level of GluA2, what is a result of impaired mTOR dependent GluA2 biosynthesis. However, the overexpression of functional GluA2 or restoration of mTOR activity rescued this effect. CONCLUSIONS: AP2 adaptor complex regulates the dendritogenesis of mammalian neurons via mTOR dependent GluA2 biosynthesis. FINANCIAL SUPPORT: This work has been financed by National Research Centre grant no. 2011/03/B/NZ3/01970.
4

Spatiotemporal characterization of mTOR kinase activity following kainic acid induced status epilepticus and analysis of rat brain response to chronic rapamycin treatment

51%
Macias M., Blazejczyk M., Kazmierska P., Caban B., Skalecka A., Tarkowski B., Konopacki J., Jaworski J.
Acta Neurobiologiae Experimentalis
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2013
|
tom 73
|
nr Suppl.1
Mammalian target of rapamycin (mTOR) is a protein kinase that senses nutrient availability, trophic factors support, cellular energy level, cellular stress, neurotransmitters and adjusts cellular metabolism accordingly. Recently, several groups reported that seizures increase mTOR activity, and such increased activity in genetic models can contribute to spontaneous seizures. However, the current knowledge about the spatiotemporal pattern of mTOR activation induced by proconvulsive agents is rather rudimentary. Also consequences of insufficient mTOR activity on a status epilepticus are poorly understood. Here, we investigated these two issues. We showed that mTOR signaling was activated by kainic acid (KA)-induced status epilepticus through several brain areas as well as revealed two waves of mTOR activation: an early wave (2 h) that occurs in neurons and a late wave that predominantly occurs in astrocytes. Unexpectedly, we found that pretreatment with rapamycin, a potent mTOR inhibitor, gradually (1) sensitized animals to KA treatment and (2) induced gross anatomical changes in the brain. Supported by Polish National Science Center OPUS grant (2012/05/B/ NZ3/00429)
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