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Wyszukujesz frazę "Erk1/2" wg kryterium: Temat


Wyświetlanie 1-2 z 2
Tytuł:
Modulation of ERK1/2 activity is crucial for sphingosine-induced death of glioma C6 cells
Autorzy:
Krzemiński, Patryk
Powiązania:
https://bibliotekanauki.pl/articles/1041346.pdf
Data publikacji:
2005
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
glioma C6
ERK1/2
cytoskeleton
programmed cell death
Opis:
In this study the contribution of the ERK1/2 pathway to sphingosine-induced death and morphological changes of the actin cytoskeleton in glioma C6 cells was investigated. Surprisingly, the level of ERK1/2 phosphorylation does not change after incubation of cells with sphingosine. Despite this, sphingosine induces rounding and detachment of cells without formation of apoptotic bodies. To shed light on this process, a specific inhibitor of ERK1/2 phosphorylation, U0126, was used. Cells incubated simultaneously with sphingosine and U0126 not only detached, but also exhibited formation of apoptotic-like blebs. These data suggest that during sphingosine-induced glioma C6 cell death apoptotic blebbing is dependent on ERK1/2 signalling and occurs only when ERK1/2 activity is decreased or abolished.
Źródło:
Acta Biochimica Polonica; 2005, 52, 4; 927-930
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Crosstalk between the TGF-β and WNT signalling pathways during cardiac fibrogenesis
Autorzy:
Działo, Edyta
Tkacz, Karolina
Błyszczuk, Przemysław
Powiązania:
https://bibliotekanauki.pl/articles/1038355.pdf
Data publikacji:
2018
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
TGF-beta
Smad
WNT
beta-catenin
RhoA-ROCK
p38
JNK
Erk1/2
MAPK
cardiac fibrosis
tissue remodelling
cardiac fibroblasts
heart
Opis:
Cardiac fibrosis is referred to as an excessive accumulation of stromal cells and extracellular matrix proteins in the myocardium. Progressive fibrosis causes stiffening of the cardiac tissue and affects conduction of electrical impulses, leading to heart failures in a broad range of cardiac conditions. At the cellular level, activation of the cardiac stromal cells and myofibroblast formation are considered as hallmarks of fibrogenesis. At the molecular level, transforming growth factor β (TGF-β) is traditionally considered as a master regulator of the profibrotic processes. More recently, the WNT signalling pathway has also been found to be implicated in the development of myocardial fibrosis. In this review, we summarize current knowledge on the involvement of TGF-β and WNT downstream molecular pathways to cardiac fibrogenesis and describe a crosstalk between these two profibrotic pathways. TGF-β and WNT ligands bind to different receptors and trigger various outputs. However, a growing body of evidence points to cross-regulation between these two pathways. It has been recognized that in cardiac pathologies TGF-β activates WNT/β-catenin signalling, which in turn stabilizes the TGF-β/Smad response. Furthermore both, the non-canonical TGF-β and non-canonical WNT signalling pathways, activate the same mitogen-activated protein kinases (MAPKs): the extracellular signal-regulated kinase (Erk), the c-Jun N-terminal kinases (JNKs) and p38. The crosstalk between TGF-β and WNT pathways seems to play an essential role in switching on the genetic machinery initiating profibrotic changes in the heart. Better understanding of these mechanisms will open new opportunities for development of targeted therapeutic approaches against cardiac fibrosis in the future.
Źródło:
Acta Biochimica Polonica; 2018, 65, 3; 341-349
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
    Wyświetlanie 1-2 z 2

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