Wyniki wyszukiwania

1

W kwestii socjalizacji ustroju rolnego

100%

Blazejczyk M.

Wieś i Rolnictwo

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1987

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nr 1

2

Rodzinne gospodarstwa rolne i status prawny młodych rolników w doktrynie i ustawodawstwie hiszpańskim

100%

Blazejczyk M.

Wieś i Rolnictwo

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1983

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nr 1

3

Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik

Polskie gospodarstwa mleczne w rankingu efektywności technicznej gospodarstw unijnych z wykorzystaniem modelu SE-CCR

100%

Blazejczyk M.

Zeszyty Naukowe Szkoły Głównej Gospodarstwa Wiejskiego w Warszawie. Problemy Rolnictwa Światowego

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2016

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tom 16[31]

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nr 3

4

System ochrony gruntów rolnych w Bułgarskiej Republice Ludowej

100%

Blazejczyk M.

Postępy Nauk Rolniczych

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1966

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tom 13

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nr 6

5

Molecular basis of dendritic arborization

51%

Urbanska M., Blazejczyk M., Jaworski J.

Acta Neurobiologiae Experimentalis

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2008

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tom 68

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nr 2

The pattern of dendritic branching along with the receptor and channel composition and density of synapses regulate the electrical properties of neurons. Abnormalities in dendritic tree development lead to serious dysfunction of neuronal circuits and, consequently, the whole nervous system. Not surprisingly, the complicated and multi-step process of dendritic arbor development is highly regulated and controlled at every stage by both extrinsic signals and intrinsic molecular mechanisms. In this review, we analyze the molecular mechanisms that contribute to cellular processes that are crucial for the proper formation and stability of dendritic arbors, in such distant organisms as insects (e.g. Drosophila melanogaster), amphibians (Xenopus laevis), and mammals.

6

Regulation and cellular functions of mTORC1 in animal models of epilepsy

51%

Jaworski J., Macias M., Blazejczyk M., Urbanska M.

Acta Neurobiologiae Experimentalis

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2017

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tom 77

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nr Suppl.1

Introduction: Mammalian target of rapamycin (mTOR) is a protein kinase that regulates cellular metabolism. Adequate mTOR activity is needed for development as well as proper physiology of mature neurons. Changes in mTOR activity are often observed in neuropathology. Several groups reported that seizures increase mTOR activity, and mTOR contributes to spontaneous seizures. However, the current knowledge about 1) the spatiotemporal and 2) the subcellular pattern of mTOR activation as well as 3) mTOR downstream effectorsin epilepsy is limited. Effects of mTOR insufficiency in seizures also remain under investigated. Aim: The aim of my team is to understand regulation and contribution of mTOR to epilepsy and pinpointing cellular mechanisms downstream mTOR. Methods: To study a role of mTOR in epilepsy we used models of pharmacological treatment with kainic acid (KA). We performed analysis of status epilepticus (SE) severity and progression. We analyzed with quantitative Western-blot and microarrays changes in signaling pathways and gene expression. Subcellular distribution of mTOR and its activity was analyzed by live microscopy. Results: We showed that SE induces mTOR first in neurons and next in astrocytes. At early times post seizures mTOR translocates to the nucleus, where its activity increases gradually. We showed that mTOR is involved in KA-dependent gene expression and genes regulated by mTOR regulate cytoskeleton. One of them, Elmo-1 regulates axonal growth and dendritic spine changes. Our research shows also that insufficient mTOR activity lead to increased sensitivity to KA. Conclusions: mTOR is an important player in epilepsy. One of the processes likely controlled by mTOR in epilepsy is transcription of genes responsible for cytoskeleton rearrangement. On the other hand, insufficient mTOR activity decreases threshold for epileptic-like neuronal activity. FINANCIAL SUPPORT: The research was supported by Polish National Science Centre (grants no. 2012/05/B/ NZ3/00429; 2012/07/E/NZ3/00503), 7FP grant (no. 602391, “EPISTOP”) and the Polish Ministerial funds for science (years 2014–2018) for the implementation of international co‑financed project. JJ is a recipient of the Foundation for Polish Science “Mistrz” Professorial Subsidy.

7

Zastosowanie bakterii kwasu mlekowego do produkcji probiotycznego soku warzywnego

51%

Sionek B., Kolozyn-Krajewska D., Jaworska D., Blazejczyk M.

Żywność Nauka Technologia Jakość

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2015

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tom 22

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nr 4

Celem pracy było zaprojektowanie i wytworzenie probiotycznego soku warzywnego o właściwej jakości mikrobiologicznej i sensorycznej. Użyto pięciu potencjalnie probiotycznych szczepów bakterii z gatunku Lactobacillus, tj. Lb. plantarum, Lb. rhamnosus (2 szczepy), Lb. brevis i Lb. pentosus do przeprowadzenia kontrolowanej fermentacji soku z kapusty oraz soku z kapusty z dodatkiem soku jabłkowego. W ocenie sensorycznej najwyżej oceniono sok fermentowany szczepem Lb. plantarum K1. Przez cały okres przechowywania liczba komórek bakterii utrzymywała się na poziomie 8,76 ÷ 9,17 log jtk/cm³. W zależności od temperatury przechowywania wartość pH soków stopniowo zmniejszała się z 4,17 do poziomu 3,61 ÷ 3,34. Po 16 dniach składowania nastąpiło obniżenie ogólnej jakości sensorycznej soków przechowywanych w temp. 4 i 8 ºC, co mogło być spowodowane znacznym stopniem ich zakwaszenia. W sokach przechowywanych w temp. 15 ºC po 8 dniach zaobserwowano obniżenie jakości ogólnej do poziomu poniżej 5 j.u. Potwierdzono możliwość zastosowania szczepu Lb. plantarum K1 do otrzymania fermentowanego soku z kapusty z dodatkiem soku jabłkowego o zadowalającej jakości sensorycznej, zawierającego odpowiednio dużą (10⁸ jtk/cm³) liczbę komórek bakterii.

8

Spatio-temporal characterization mTOR kinase activity induced by kainic acid evoked seizures

51%

Macias M., Blazejczyk M., Jaworski J.

Acta Neurobiologiae Experimentalis

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2009

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tom 69

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nr 3

The common effects of epileptic seizures are aberrant plastic changes in synaptic connectivity and morphological rearrangements in hippocampal mossy fi bers. This phenomenon is believed to be a basis of facilitation of further epileptic episodes, however its molecular mechanism remains elusive. mTOR kinase is crucial for rearrangements of neuronal morphology and for long term synaptic plasticity. Overactivation of mTOR was reported in brain pathologies associated with seizures (tuberous sclerosis, cortical dysplasia). Experimental evidence supports causative role of mTOR in these forms of epilepsy. So far, however, links of mTOR signaling pathway to other types of epilepsy are unknown. To address this issue we investigated activation of mTOR and its downstream effectors in rat brain after kainic acid (KA) induced epilepsy. Animals were sacrifi ced 2, 6, 12, 24 and 72 hours after KA administration and levels of phosphorylated mTOR and S6 has been examined. Both, biochemical methods and immunohistochemistry proved S6 activation in hippocampus and cerebral cortex at all time points after KA. Immunohistochemical analysis additionally revealed that 2 h after KA, activities of mTOR and S6 are upregulated mainly in neurons while after 6 h there was also enhancement of glial S6 immunoreactivity. Our data suggest that KA induced seizures activate mTOR signaling in various cell types with specifi c spatio-temporal pattern. This work has been fi nanced by PNRF-96-AI-1/07 grant.

9

CLIP-170 and IQGAP1 in dendritic arbor development

51%

Swiech L., Blazejczyk M., Jaworski J.

Acta Neurobiologiae Experimentalis

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2009

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tom 69

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nr 3

The precise control of the microtubule polymerization dynamics as well as strict actin organization are both crucial for formation of neuronal dendritic arbor and require microtubule and actin binding proteins activity. Cytoplasmic linker protein 170 (CLIP-170), one of microtubule plus-end binding proteins, regulates microtubule dynamics at plus-end during polymerization, by promoting rescuephase in its phosphorylation status dependent manner. We show evidence that mammalian target of rapamycin (mTOR), is one of kinases capable of regulating CLIP-170 activity and both, mTOR and CLIP-170 are crucial for proper dendritic arbor development of hippocampal neurons. Furthermore, we identifi ed in neurons several proteins, which bound to CLIP-170 when mTOR is active, including IQGAP1, a known partner of CLIP-170 and regulator of the actin dynamics. Taken together our data strongly suggest that CLIP-170 activity during dendritogenesis can be regulated by mTOR at the level of CLIP-170 protein-protein interactions. Moreover, obtained results, showing mTOR dependent interaction of CLIP-170 with IQGAP imply that mTOR can coordinate tubulin and actin cytoskeleton organization. Supported by Polish Ministry of Science and Higher Education Research Grant 2P04A01530 and Polish-Norwegian Research Found grant PNRF-96-AI-1/07.

10

A comparison of the species composition of spider communities over sixty years in the vicinity of Krotoszyn

51%

Szymkowiak P., Wozny M., Blazejczyk M.

Fragmenta Faunistica

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1999

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tom 42

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nr 01-06

11

Brain expression and subcellular localization of Calmyrin 2, a novel Ca-binding protein

45%

Blazejczyk M., Sobczak A., Jaworski J., Kuznicki J., Wojda U.

Acta Neurobiologiae Experimentalis

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2007

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tom 67

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nr 3

12

Ca2plus-binding calmyrin is a monomeric protein highly expressed in motoneurons of rat spinał cord

39%

Blazejczyk M., Sobczak A., Piszczek G., Kreutz M. R., Kuznicki J., Wojda U.

Acta Neurobiologiae Experimentalis

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2005

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tom 65

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nr 3

13

Structural and biochemical properties of Calmyrin 2, a novel calcium binding protein in the brain

39%

Sobczak A., Blazejczyk M., Debowska K., Cymerman I., Kirilenko A., Pikula S., Wojda U.

Acta Neurobiologiae Experimentalis

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2007

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tom 67

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nr 3

14

Expression regulation of a novel Ca2+ binding protein Calmyrin 2 (Cih2) indicates its function in NMDA receptor mediated Ca2+signaling

39%

Debowska K., Blazejczyk M., Sobczak A., Jaworski J., Kuzmicki J., Wojda U.

Acta Neurobiologiae Experimentalis

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2009

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tom 69

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nr 3

Calmyrin 2 (CaMy2, Cib2) represents a novel calmyrin subfamily of Ca2+ binding proteins that coordinate Ca2+ in the EF-hand motives. CaMy2 mRNA was recently detected in brain, but nothing is known about CaMy2 protein localization and properties in the brain. We have cloned CaMy2 from rat brain, demonstrated CaMy2 Ca2+- sensor properties and determined its neuronal pattern of rat brain expression. CaMy2 protein is expressed mainly in hippocampal neurons and localizes together with Golgi apparatus and dendrite markers. Our studies in primary cultures of hippocampal neurons demonstrate that expression of CaMy2 protein is induced upon neuronal activation with pharmacological agents that stimulate Ca2+ infl ux through such types of Ca2+ channels as glutamate excitatory receptors and voltage-operated Ca2+ channels. In addition, increase in CaMy2 protein level was induced by soluble amyloid β and BDNF. However, most prominent increase in CaMy2 protein (7-fold), and mRNA (2-fold) occurs upon stimulation of NMDA receptor (NMDAR). The induction is blocked by translation inhibitors, specifi c antagonists of NMDAR, the Ca2+-chelator BAPTA, and inhibitors of ERK1/2 and PKC, kinases transmitting NMDAR-linked Ca2+ signal. Our results show that CaMy2 level is controlled by NMDAR and Ca2+ and suggest CaMy2 role in Ca2+ signaling underlying NMDAR activation. This work was supported by the Polish Ministerial Research grant N301 109 32/3854.

15

Serum response factor (SRF) regulates matrix metalloproteinase-9 (MMP-9) transcription in neurons

39%

Kuzniewska B., Blazejczyk M., Malik A., Jaworski J., Kaczmarek L., Kalita-Bykowska K.

Acta Neurobiologiae Experimentalis

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2011

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tom 71

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nr S

MMP-9 is an endopeptidase playing important role in neuronal plasticity. Although multiple factors regulating MMP-9 expression have been described in different cell types, the molecular mechanism directly controlling its transcription in neurons remains poorly understood. The aim of the current study was to determine, whether SRF/c-Fos pathway is involved in the transcriptional regulation of MMP-9 in neurons. Real-Time PCR analysis revealed strong upregulation of MMP-9 mRNA levels after stimulation of rat primary cortical neurons with BDNF. Additionally, elevated MMP-9 gelatinolytic activity was observed. To investigate mechanism of MMP-9 promoter regulation, we used luciferase gene reporter assay system in which luciferase gene is controlled by MMP-9 promoter fragment (-1369/+35). Treatment of neurons with BDNF led to MMP-9 promoter activation, that was dependent on ERK1/2 actvity, as demonstrated using selective inhibitor or overexpressing constitutively active MKK1. As in MMP-9 promoter there are two AP-1 binding sites, we investigated whether AP-1 contributes to the BDNF-mediated MMP-9 transcription in neurons. MMP-9 reporter construct was induced upon overexpression of different AP-1 dimers in neurons, the most potent being those containing c-Fos. Moreover, BDNFinduced activation of the MMP-9 reporter construct was reduced if proximal, but not distal, AP-1 binding site was mutated. Furthermore knocking-down c-Fos expression in neurons by shRNA decreased MMP-9 gene activation in response to BDNF. As c-fos gene is a known target of SRF, we tested whether SRF can contribute to MMP-9 transcription. Inhibition of SRF by the overexpression of dominant-negative mutant of SRF or using shRNA targeting SRF, abolished BDNF-induced activation of MMP-9 promoter. Our data indicate that MMP-9 expression in neurons can be induced by BDNF. The signal propagation could involve ERK1/2 pathway and SRF-mediated transcription of c-fos gene resulting in activation of MMP-9 promoter.

16

Calcium-binding calmyrin forms stable covalent dimers in vitro, but in vivo is found in monomeric form

39%

Sobczak A., Blazejczyk M., Piszczek G., Zhao G., Kuznicki J., Wojda U.

Acta Biochimica Polonica

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2005

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tom 52

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nr 2

The EF-hand Ca2+-binding protein calmyrin is expressed in many tissues and can interact with multiple effector proteins, probably as a sensor transferring Ca2+ signals. As oligomerization may represent one of Ca2+-signal transduction mechanisms, we characterised recombinant calmyrin forms using non-reducing SDS/PAGE, analytical ultracentrifugation and gel filtration. We also aimed at identification of biologically active calmyrin forms. Non-reducing SDS/PAGE showed that in vitro apo- and Ca2+-bound calmyrin oligomerizes forming stable intermolecular disulfide bridges. Ultracentrifugation indicated that at a 220 μM initial protein concentration apo-calmyrin existed in an equilibrium of a 21.9 kDa monomer and a 43.8 kDa dimer (trimeric or tetrameric species were not detected). The dimerization constant was calculated as Ka = 1.78 × 103 M–1 at 6oC. Gel filtration of apo- and Ca2+-bound calmyrin at a 100 μM protein concentration confirmed an equilibrium of a monomer and a covalent dimer state. Importantly, both monomer and dimer underwent significant conformational changes in response to binding of Ca2+. However, when calmyrin forms were analyzed under non-reducing conditions in cell extracts by Western blotting, only monomeric calmyrin was detected in human platelets and lymphocytes, and in rat brain. Moreover, in contrast to recombinant calmyrin, crosslinking did not preserve any dimeric species of calmyrin regardless of Ca2+ concentrations. In summary, our data indicate that although calmyrin forms stable covalent dimers in vitro, it most probably functions as a monomer in vivo.

17

Role of Arc phosphorylation in structural plasticity

33%

Gozdz A., Nikolaienko O., Urbanska M., Cymerman I., Sitkiewicz E., Blazejczyk M., Dadlez M., Bramham C., Jaworski J.

Acta Neurobiologiae Experimentalis

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2019

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tom 79

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nr Suppl.1

Arc protein was shown to control synaptic AMPA receptor content, dendritic spine maintenance, and structure. Given its importance for neuronal function, Arc protein expression has to be tightly regulated and it occurs via ubiquitination and proteasomal degradation. Glycogen synthase kinases α and β (GSK3α/β) are serine‑threonine kinases abundantly expressed in neuronal cells, crucial for neuronal plasticity. GSK3α/β phosphorylate and prime numerous proteins for ubiquitination and degradation, however until now no interaction between Arc and GSK3α/β has been reported. The present study aims to address if and how GSK3α/β affects Arc protein expression, and whether their interaction plays a role in the regulation of dendritic spine morphology. GSK3-dependent Arc protein degradation and the effects of this process on dendritic spine morphology were studied in cultured embryonic cortical and hippocampal murine neurons upon NMDA receptors stimulation. Arc protein residues modified in GSK3‑dependent manner were identified by mass spectrometry. Obtained results were confirmed by in vitro kinase assays and the use of anti‑phospho‑Arc antibodies. We observed higher Arc levels in neurons exposed to NMDA upon GSK3α/β inhibition. In vitro kinase assays revealed that Arc is a substrate for GSK3α and β. Further analysis identified four residues phosphorylated by GSK3α/β (S170, T175, T368, T380) and one ubiquitinated in GSK3‑dependent manner (K136). Finally, we demonstrated that quadruple phosphodeficient mutant of Arc, as well as ubiquitination‑resistant Arc, were more stable in neurons upon NMDAR stimulation, and produced significant thinning of dendritic spine head. Our results identify GSK3α/β‑catalyzed Arc phosphorylation and degradation as a novel mechanism for controlling the duration of Arc expression and its effect on dendritic spine structure.

18

Sound frequency discrimination: functional role of c-FOS in auditory cortex

33%

Gierej D., Lioudyno V., Mikosz M., Nowak A., Blazejczyk M., Filipkowski R. K., Jaworski J., Kaczmarek L., Knapska E.

Acta Neurobiologiae Experimentalis

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2011

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tom 71

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nr S

Immediate-early genes, c-fos in particular, are expressed in the brain upon neuronal activation. c-Fos expression is thought to reflect novelty detection and propensity for a plastic change as its levels decrease when the animal fully acquire a new task. However, its functional role in the brain remains largely unknown. In the present study, we used c-Fos immmunolabeling to identify the cortical network components within auditory and motor cortices that subserve sound frequency discrimination in a behavioral context. We designed a protocol in a fully automated cage for mice (IntelliCage), in which animals were supposed to discriminate between two sounds of different frequencies, one signaling safe access to water and another signaling punishment (air puff). c-Fos expression was analyzed at different stages of the training. Within the anterior parts of ventral and dorsal auditory cortices significant changes in c-Fos levels were observed that correlated with the discrimination learning. On the other hand, c-Fos expression in the motor cortex correlated only with motor activity. In order to address questions concerning the role of c-Fos in learning discrimination of sounds, associated with a particular behavioral meaning, RNA interference was used. c-Fos expression in the auditory cortex was blocked using short hairpin RNA (shRNA) delivered by lentiviral vectors. Mice were bilaterally injected with control vectors and harboring shRNA for c-fos (experimental). Then, the animals were subjected to sound discrimination training. Both the control and the experimental animals were responsive to the aversive cues, but the experimental group learnt much more slowly and showed faster extinction of the learned behavior than the control group. These results show the functional involvement of c-Fos within the auditory cortex in sound discrimination learning. More generally, they also support the idea that c-Fos marks neuronal plasticity rather than simple activation.

19

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

33%

Macias M., Blazejczyk M., Kazmierska P., Caban B., Skalecka A., Tarkowski B., Konopacki J., Jaworski J.

Acta Neurobiologiae Experimentalis

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2013

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tom 73

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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)

20

How neurons become giant-identification of proteins regulated by mTOR kinase in etiopathology of tuberous sclerosis

27%

Malik A., Swiech L., Perycz M., Urbanska M., Blazejczyk M., Wulf P., Parobczak K., Pietruszka P., Zarebska M., Rutowicz K., Jaworski J.

Acta Neurobiologiae Experimentalis

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2009

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tom 69

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nr 3

mTOR is a serine-threonine protein kinase for several aspects of neuronal function. Increased mTOR signaling has been implicated in tuberous sclerosis (TS), a multiorgan disease affecting brain. TS is caused by mutations in genes encoding for hamartin and tuberin that lead to increase of the mTOR activity and subsequent abnormal cell growth and proliferation, leading to brain lesions containing giant cells. It is unclear how mTOR contributes to observed changes. Our aim was to identify downstream mTOR effectors important for the disease related abnormal cell growth. To model TS giant cells, rat cortical neurons cultured in vitro were transfected with short interfering RNA (siRNA) targeting tuberin that caused a Rapamycin-sensitive increase of neuron soma size. Next, we designed a siRNA library directed against 140 mRNAs encoding potential mTOR targets, selected based on published data. To select siRNAs decreasing soma size of enlarged cells, cortical neurons were contransfected with tuberin siRNA together with siRNAs from the library. Our screen revealed over 20 genes, whose expression downregulation reversed the giant-cell like phenotype and 6 siRNAs that further increased size of cells with tuberin knockdown. Among proteins contributing to abnormal neuron growth upon mTOR overactivation, we identifi ed those involved in actin cytoskeleton dynamics, vesicular transport and cellular signaling. This work has been fi nanced by PBZ-MNiI-2/1/2005 and PNRF-96- AI-1/07 grants.

Ograniczanie wyników

W kwestii socjalizacji ustroju rolnego

Rodzinne gospodarstwa rolne i status prawny młodych rolników w doktrynie i ustawodawstwie hiszpańskim

Polskie gospodarstwa mleczne w rankingu efektywności technicznej gospodarstw unijnych z wykorzystaniem modelu SE-CCR

System ochrony gruntów rolnych w Bułgarskiej Republice Ludowej

Molecular basis of dendritic arborization

Regulation and cellular functions of mTORC1 in animal models of epilepsy

Zastosowanie bakterii kwasu mlekowego do produkcji probiotycznego soku warzywnego

Spatio-temporal characterization mTOR kinase activity induced by kainic acid evoked seizures

CLIP-170 and IQGAP1 in dendritic arbor development

A comparison of the species composition of spider communities over sixty years in the vicinity of Krotoszyn

Brain expression and subcellular localization of Calmyrin 2, a novel Ca-binding protein

Ca2plus-binding calmyrin is a monomeric protein highly expressed in motoneurons of rat spinał cord

Structural and biochemical properties of Calmyrin 2, a novel calcium binding protein in the brain

Expression regulation of a novel Ca2+ binding protein Calmyrin 2 (Cih2) indicates its function in NMDA receptor mediated Ca2+signaling

Serum response factor (SRF) regulates matrix metalloproteinase-9 (MMP-9) transcription in neurons

Calcium-binding calmyrin forms stable covalent dimers in vitro, but in vivo is found in monomeric form

Role of Arc phosphorylation in structural plasticity

Sound frequency discrimination: functional role of c-FOS in auditory cortex

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

How neurons become giant-identification of proteins regulated by mTOR kinase in etiopathology of tuberous sclerosis