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Wyszukujesz frazę "Wesoly, Joanna" wg kryterium: Autor


Wyświetlanie 1-3 z 3
Tytuł:
STAT activation and differential complex formation dictate selectivity of interferon responses
Autorzy:
Wesoly, Joanna
Szweykowska-Kulinska, Zofia
Bluyssen, Hans
Powiązania:
https://bibliotekanauki.pl/articles/1041103.pdf
Data publikacji:
2007
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
transcription factor complexes
gene regulation
IRFs
JAK/STAT pathway
IFNs
Opis:
Interferons (IFNs) induce gene expression by phosphorylating latent transcription factors belonging to the signal transducer and activator of transcription (STAT) family, mediated by janus kinases (Jaks). STAT dimers directly activate genes containing the IFNγ activation site (GAS) DNA element, with different STAT proteins displaying slightly different intrinsic DNA binding specificities. The combinatorial association of STATs with the additional DNA binding adaptor protein interferon regulatory factor (IRF)9 expands the range of enhancer elements that can be targeted by the JAK-STAT pathway to interferon-stimulated response element (ISRE) and IRF response element (IRE). Based on the amino-acid sequence similarity within the IRF family and functional overlap with the STAT family, in this paper we hypothesize that other IRF members could serve as adapter proteins for the STATs during IFN responses to redirect them to subsets of ISRE, GAS and/or IRE-containing IFN-stimulated genes (ISGs). In addition, the fact that STAT2 homodimers are not capable of binding consensus GAS sites leaves the possibility for a novel type of DNA-binding site bound by STAT2 homodimers and potentially other STAT complexes.
Źródło:
Acta Biochimica Polonica; 2007, 54, 1; 27-38
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Suppressor of cytokine signaling and accelerated atherosclerosis in kidney disease
Autorzy:
Wesoly, Joanna
Sikorski, Krzysztof
Lee, Chien-Kuo
Bluyssen, Hans
Powiązania:
https://bibliotekanauki.pl/articles/1040361.pdf
Data publikacji:
2010
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
inflammation
atherosclerosis
SOCS
kidney disease
Opis:
The prevalence of cardiovascular disease in patients with renal failure is extremely high and accounts for a large part of the morbidity and mortality. Inflammation participates importantly in host defense against infectious agents and injury, but also contributes to the pathophysiology of many diseases, including cardiovascular atherosclerosis, which is a main problem in patients with renal failure. Recruitment of blood leukocytes to the injured vascular endothelium characterizes the initiation and progression of atherosclerosis and involves many inflammatory mediators, modulated by cells of both innate and adaptive immunity. Excessive inflammatory and immune responses, communicated by these different cell types, are driven by inflammatory cytokines that promote associated tissue damage if cytokine signaling pathways remain unregulated. Thus, pathways capable of suppressing proinflammatory cytokine signaling hold the potential to limit life-threatening cardiovascular events caused by atherogenesis. Suppressor of cytokine signaling (SOCS) are a family of intracellular proteins, several of which have emerged as key physiological regulators of cytokine-mediated homeostasis, including innate and adaptive immunity. Accumulating evidence supports the idea that dysregulation of cytokine signaling by differential SOCS expression is involved in the pathogenesis of various inflammatory, and immunological diseases, including atherosclerosis. Based on recent observations, in which SOCS expression levels are profoundly altered in kidney disease, we discuss the possibilities of SOCS as new intracellular markers of inflammation as well as their potential atherogenic properties in renal failure related cardiovascular disease.
Źródło:
Acta Biochimica Polonica; 2010, 57, 3; 251-260
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Consequences of the loss of the Grainyhead-like 1 gene for renal gene expression, regulation of blood pressure and heart rate in a mouse model
Autorzy:
Pawlak, Magdalena
Walkowska, Agnieszka
Mlącki, Michał
Pistolic, Jelena
Wrzesiński, Tomasz
Benes, Vladimir
Jane, Stephen
Wesoły, Joanna
Kompanowska-Jezierska, Elżbieta
Wilanowski, Tomasz
Powiązania:
https://bibliotekanauki.pl/articles/1039106.pdf
Data publikacji:
2015
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
blood pressure
genetics
grainy head
heart rate
kidney
transcription factor
Opis:
Aim: The Grainyhead-like 1 (GRHL1) transcription factor is tissue-specific and is very highly expressed in the kidney. In humans the GRHL1 gene is located at the chromosomal position 2p25. A locus conferring increased susceptibility to essential hypertension has been mapped to 2p25 in two independent studies, but the causative gene has never been identified. Furthermore, a statistically significant association has been found between a polymorphism in the GRHL1 gene and heart rate regulation. The aim of our study was to investigate the physiological consequences of Grhl1 loss in a mouse model and ascertain whether Grhl1 may be involved in the regulation of blood pressure and heart rate. Experimental approach: In our research we employed the Grhl1 "knock-out" mouse strain. We analyzed renal gene expression, blood pressure and heart rate in the Grhl1-null mice in comparison with their "wild-type" littermate controls. Most important results: The expression of many genes is altered in the Grhl1-/- kidneys. Some of these genes have previously been linked to blood pressure regulation. Despite this, the Grhl1-null mice have normal blood pressure and interestingly, increased heart rate. Conclusions: Our work did not discover any new evidence to suggest any involvement of Grhl1 in blood pressure regulation. However, we determined that the loss of Grhl1 influences the regulation of heart rate in a mouse model.
Źródło:
Acta Biochimica Polonica; 2015, 62, 2; 287-296
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
    Wyświetlanie 1-3 z 3

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