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1

Role of mTOR regulated proteins in dendritic branching

100%
Jaworski J., Swiech L.
Acta Neurobiologiae Experimentalis
|
2007
|
tom 67
|
nr 3
2

CLIP17O role in dendritic arbor development

81%
Swiech L., Dortland B., Hoogenraad C. C., Jaworski J.
Acta Neurobiologiae Experimentalis
|
2007
|
tom 67
|
nr 3
3

CLIP-170 and IQGAP1 in dendritic arbor development

81%
Swiech L., Blazejczyk M., Jaworski J.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
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.
4

mTOR w fizjologii i patologii ukladu nerwowego

81%
Perycz M., Swiech L., Malik A., Jaworski J.
Postępy Biologii Komórki
|
2007
|
tom 34
|
nr 3
511-525
5

The role of adhesion protein CD44 in the shape changes of astrocytes

71%
Konopka A., Swiech L., Jaworski J., Wilczynski G. M., Dzwonek J.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr Suppl.1
CD44 is a widely distributed type I transmembrane glycoprotein and functions as the major hyaluronan receptor on most cell types. CD44 through interaction with actin cytoskeleton affects the transmission of signals from the outside to the inside of the cell in many tissues and organs. Primary cultures of astrocyte are diverse in their morphology and many factors can influence on it. In vivo astrocyte also are able to change their shape in response to various stimuli. The appearance of reactive astrocytes in vivo with thicker and longer processes and increased cellular content of glial fibrillary acidic protein (GFAP) has been observed in the CNS after various types of injury caused by physical, chemical, and pathological trauma. Furthermore, it has been showed that CD44 expression increases after brain injury. In our study we investigated the influence of knock down of CD44 by specific shRNA and CD44 overexpression on the astrocytes shape changes. Our results indicate that knock down of CD44 in astrocytes results in more regular and flat shape. In contrast the overexpression of CD44 promotes more irregular, radial-like shape of astrocyte. Our data support the hypothesis that CD44 plays role in morphological changes of astrocyte and give the opportunity to investigate its role in pathological processes such as brain injury.
6

The role of adhesion molecule CD44 in dendritic tree arborization

61%
Dzwonek J., Gorlewicz A., Konopka A., Swiech L., Jaworski J., Wilczynski G.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr S
Dendritic arborization patterns define neuronal subtypes, and have important functional implications, determining how signals coming from individual synapses are integrated. Developing dendrites of neurons are responsive to extrinsic signals. Although several secreted proteins, cell surface receptors and adhesion molecules have been recently shown to be involved in dendrite morphogenesis, the role of extracellular matrix (ECM) components and molecular mechanisms of signal transduction from ECM to the neuronal cells involved in these processes are still poorly understood. The main component of the ECM in the brain is hyaluronan (HA). The major receptor for hyaluronan is CD44 adhesion molecule which mediates the response of cells to their extracellular microenvironment. The aim of this study was to investigate the role of CD44 in regulation of dendritic tree arborization. First, we examined the expression pattern of CD44 at the protein and RNA level in the rat brain by immunohistochemical, in situ hybridization and in situ PCR assays. All our experimental approaches clearly point to the neuronal localization of CD44, in addition to widely accepted presence in glia. Next, we investigated the role of CD44 in the hippocampal neurons cultured in vitro using the shRNA technology and anti-CD44 function-blocking antibody. The morphometric analysis show that cells with diminished expression of CD44 have more complex dendritic tree then control cells. Moreover, we have shown that treatment of neuronal cells with CD44 blocking antibody caused activation of small Rho GTPases (Cdc42, Rac1 and RhoA), which were previously shown to regulate dendritic tree arborization. These observations indicate that the members of small Rho GTPase family can be downstream effectors of CD44 in neuronal cells. The results of our experiments point to the importance of CD44 protein for the development of dendritic tree.
7

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

42%
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
|
2009
|
tom 69
|
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.
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