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    Wyświetlanie 1-9 z 9
    Tytuł:
    Expression of soluble recombinant TGF-β type II receptor fused with the Fc portion of human IgG1 (sTβRII-Fc) in NS0 cells
    Autorzy:
    Kwiatkowska, Eliza
    Kazimierczak, Urszula
    Mackiewicz, Andrzej
    Kowalczyk, Dariusz
    Powiązania:
    https://bibliotekanauki.pl/articles/1041250.pdf
    Data publikacji:
    2006
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    GS-NS0 expression system
    chimeric receptor
    TGF-β
    TGF-βreceptor
    TGF antagonist
    Opis:
    We have constructed and expressed recombinant chimeric soluble TGF-β type II receptor fused with the Fc portion of human IgG1 (sTβRII-Fc) in NS0 mouse myeloma cells and isolated cell lines constitutively secreting very high levels of biologically active protein. The GS-NS0 expression system takes advantage of the strong human cytomegalovirus immediate early promoter expression vector and glutamine synthetase as a selectable marker. The recombinant chimeric receptor could be produced in high amounts and efficiently purified by one step chromatography on a protein A column. Biochemical studies revealed that recombinant sTβRII-Fc binds native TGF-β1 and TGF-β3 isoforms and neutralizes their activity in vitro.
    Źródło:
    Acta Biochimica Polonica; 2006, 53, 2; 361-369
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Assessment of the frequency of the transforming growth factor beta-1 sequence polymorphisms in patients with alcohol dependence syndrome
    Autorzy:
    Augustyńska, Beata
    Araszkiewicz, Aleksander
    Woźniak, Marcin
    Grzybowski, Tomasz
    Skonieczna, Katarzyna
    Woźniak, Alina
    Żyła, Magdalena
    Powiązania:
    https://bibliotekanauki.pl/articles/1039134.pdf
    Data publikacji:
    2015
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    transforming growth factor TGFβ-1
    alcohol dependence syndrome
    TGF-β1 gene
    Opis:
    Alcohol abuse is one of the most significant factors in the development of liver fibrosis. The pathomechanism of liver fibrosis is the same regardless of its etiology. Fibrosis is a sign of an imbalance between the synthesis of the extracellular matrix components and their degradation. Among the many cytokines that affect hepatic stellate cell activation it seems that transforming growth factor beta (TGF-β) is the most significant, either as the direct factor stimulating polymerase chain reaction (HSC) proliferation and transformation into myofibroblasts, or as the direct factor causing an increase in the activity of genes responsible for the synthesis of extracellular matrix components. The aim of the study was to reveal possible dependencies and differences between the presence of certain alleles of the TGF-β1 gene and its blood level in the study and control group. Blood samples were obtained from 39 patients, the control group consisted of 21 patients. The results obtained in the course of this study showed no statistically significant differences between the frequencies of particular polymorphisms. In the case of haplotype frequencies, insignificant differences were found for the algorithm Excoffier-Laval-Balding predicted haplotypes while one significant difference between the study and control groups was detected in case of the TC haplotype frequency predicted using the Expectation-Maximization algorithm. However, the difference in frequency of TC haplotype predicted by both algorithms was not significant. Genetic analysis of two single nucleotide polymorphisms (SNPs) in exon I of the TGF-β1 gene did not show significant differences between the occurrence of particular polymorphisms and haplotypes in the populations under study.
    Źródło:
    Acta Biochimica Polonica; 2015, 62, 1; 63-67
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Inhibition of CYP17 expression by adrenal androgens and transforming growth factor β in adrenocortical cells.
    Autorzy:
    Biernacka-Łukanty, Justyna
    Lehmann, Tomasz
    Trzeciak, Wiesław
    Powiązania:
    https://bibliotekanauki.pl/articles/1041500.pdf
    Data publikacji:
    2004
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    CYP17
    adrenocortical cells
    TGF-β
    androgens
    expression
    Opis:
    Cytochrome P450c17, encoded by the CYP17 gene, is a component of the 17a-hydroxylase/17,20-lyase enzyme complex essential for production of adrenal glucocorticoids and androgens as well as gonadal androgens. The expression of CYP17 in adrenocortical cells is stimulated by corticotropin (ACTH) via the signal transduction pathway involving cAMP and protein kinase A (PKA). Thus, in addition to glucocorticoids, ACTH stimulates formation of adrenal androgens, which are known to induce transforming growth factor β (TGF-β) secretion. TGF-β in turn inhibits steroid hormone output by attenuating both basal and ACTH-dependent expression of CYP17. The present study revealed that treatment of bovine and human H295R adrenocortical cells with androgens resulted in a decrease in the basal level of CYP17 transcript and cortisol secretion, without affecting forskolin-stimulated levels. We also demonstrated that in H295R cells TGF-β inhibited both basal and forskolin-stimulated accumulation of CYP17 mRNA. Determination of promoter activity, directing luciferase reporter gene expression in H295R cells transfected with deletion fragments of bovine CYP17 promoter, indicated that the -483 to -433 bp fragment of the promoter was necessary for the inhibitory action of TGF-β on CYP17 expression. It is concluded that in bovine and human adrenocortical cells, androgens inhibit basal CYP17 expression probably at the transcriptional level and independently of the effect of TGF-β.
    Źródło:
    Acta Biochimica Polonica; 2004, 51, 4; 907-917
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Peripheral regulatory T cells and anti-inflammatory cytokines in children with juvenile idiopathic arthritis
    Autorzy:
    Sznurkowska, Katarzyna
    Boćkowska, Małgorzata
    Zieliński, Maciej
    Plata-Nazar, Katarzyna
    Trzonkowski, Piotr
    Liberek, Anna
    Kamińska, Barbara
    Szlagatys-Sidorkiewicz, Agnieszka
    Powiązania:
    https://bibliotekanauki.pl/articles/1038532.pdf
    Data publikacji:
    2018
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    Tregs
    IL-10
    TGF-β1
    juvenile idiopathic arthritis
    Opis:
    Background: Juvenile idiopathic arthritis (JIA) is a chronic, heterogenous inflammatory disease of unclear pathogenesis. JIA is hypothesized to be linked to a defective immune regulation. Anti-inflammatory cytokines belong to the best known regulatory factors. T-regulatory cells are a crucial cellular component of immune tolerance. One of their functions is synthesis of interleukin 10 (IL-10) and transforming growth factor beta1 (TGF-β1). The aim of this study was to determine the proportion of T-regulatory cells (CD4+CD25highFOXP3+) in peripheral blood, and serum levels of TGF-β1 and IL-10 in patients with JIA. Methods: The study included 25 patients with newly diagnosed JIA: oligoarthritis (n=17) and polyarthritis (n=8). The control group was comprised of 17 healthy children. CD4+CD25highFOXP3+ T cells in peripheral blood were quantified by means of three-color flow cytometry. Serum concentrations of TGF-β1 and IL-10 were estimated with ELISA. Results: The proportion of peripheral CD4+CD25highFOXP3+ cells in patients with JIA was significantly higher than in the controls (p=0.04). The two groups did not differ significantly in terms of their TGF-β1 and IL-10 concentrations. Conclusions: At the time of diagnosis, children with JIA presented with an elevated proportion of T-regulatory cells (CD4+CD25highFOXP3+) in peripheral blood. Anti-inflammatory cytokines, IL-10 and TGF-β1, are not upregulated in the serum of patients with JIA, and therefore should not be considered as biomarkers of this condition.
    Źródło:
    Acta Biochimica Polonica; 2018, 65, 1; 119-123
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    TGF-β1, IL-10 and IL-4 in colostrum of allergic and nonallergic mothers
    Autorzy:
    Marek, Andrzej
    Zagierski, Maciej
    Liberek, Anna
    Aleksandrowicz, Ewa
    Korzon, Michał
    Krzykowski, Grzegorz
    Kamińska, Barbara
    Szlagatys-Sidorkiewicz, Agnieszka
    Powiązania:
    https://bibliotekanauki.pl/articles/1040529.pdf
    Data publikacji:
    2009
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    IL-10
    allergy
    IL-4
    human milk
    TGF-β1
    Opis:
    Objective: To determine transforming growth factor (TGF) β1, interleukin (IL) 4, and IL-10 concentrations in human milk and to assess the relationship between allergic disorders in mothers and the content of the interleukins in their milk. Material and methods: Thirty allergic and 46 healthy mothers were included in the study. Colostrum was collected 2-3 days after delivery. Cytokine concentrations were determined with commercial enzyme-linked immunosorbent systems. Results: TGF-β1was found in milk from 23 women in the control group (53.49%) and 11 in the allergy group (37.93%). When TGF-β1 was present, the median concentration was higher in the allergy group than in the control (61.5 and 30.4 pg/mL, respectively; P < 0.004). IL-10 was present in the colostrum of all the women and the median IL-10 concentration did not differ between the allergy (50.5 pg/mL) and control (51.5 pg/mL) groups. The probability of occurrence of a positive IL-4 value in the allergy group was greater than in the control group (chi-squared [df=1] = 2.60, P < 0.053). Median IL-4 level did not differ significantly between the two groups (0.5 and 0.5 pg/mL respectively). Conclusions: TGF-β1 was detected less often in the colostrum of allergic mothers than in that of mothers without allergy (but the difference was not statistically significant). IL-4 was found more often in the colostrum of allergic mothers than nonallergic ones. The allergy status did not correlate with IL-10 concentration.
    Źródło:
    Acta Biochimica Polonica; 2009, 56, 3; 411-414
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Can transforming growth factor-β1 and retinoids modify the activity of estradiol and antiestrogens in MCF-7 breast cancer cells?
    Autorzy:
    Czeczuga-Semeniuk, Ewa
    Anchim, Tomasz
    Dzięcioł, Janusz
    Dąbrowska, Milena
    Wołczyński, Sławomir
    Powiązania:
    https://bibliotekanauki.pl/articles/1041552.pdf
    Data publikacji:
    2004
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    estradiol
    apoptotic index
    tamoxifen
    TGF-β1
    proliferation
    MCF-7
    retinoids
    Opis:
    Retinoic acid and transforming growth factor-β (TGF-β) affect differentiation, proliferation and carcinogenesis of epithelial cells. The effect of both compounds on the proliferation of cells of the hormone sensitive human breast cancer cell line (ER+) MCF-7 was assessed in the presence of estradiol and tamoxifen. The assay was based on [3H]thymidine incorporation and the proliferative activity of PCNA- and Ki 67-positive cells. The apoptotic index and expression of the Bcl-2 and p53 antigens in MCF-7 cells were also determined. Exogenous TGF-β1 added to the cell culture showed antiproliferative activity within the concentration range of 0.003-30 ng/ml. Irrespective of TGF-β1 concentrations, a marked reduction in the stimulatory action of estradiol (10-9 and 10-8 M) was observed whereas in combination with tamoxifen (10-7 and 10-6 M) only 30 ng/ml TGF-β1 caused a statistically significant reduction to aproximately 30% of the proliferative cells. In further experiments we examined the effect of exposure of breast cancer cells to retinoids in combination with TGF-β1. The incorporation of [3H]thymidine into MCF-7 cells was inhibited to 52 ± 19% (control =100%) by 3 ng/ml TGF-β1, and this dose was used throughout. It was found that addition of TGF-β1 and isotretinoin to the culture did not decrease proliferation, while TGF-β1 and tretinoin at low concentrations (3 × 10-8 and 3 × 10-7 M) reduced the percentage of proliferating cells by aproximately 30% (67±8% and 67±5%, P <0.05 compared to values in the tretinoin group). Both retinoids also led to a statistically significant decrease in the stimulatory effect of 10-9 M estradiol, attenuated by TGF-β1. In addition, the retinoids in combination with TGF-β1 and tamoxifen (10-6 M) caused a further reduction in the percentage of proliferating cells. Immunocytochemical analysis showed that all the examined compounds gave a statistically significant reduction in the percentage of cells with a positive reaction to PCNA and Ki 67 antigen. TGF-β1, isotretinoin and tretinoin added to the culture resulted in the lowest percentage of PCNA positive cells. However, the lowest fraction of Ki 67 positive cells was observed after addition of isotretinoin. The obtained results also confirm the fact that the well-known regulatory proteins Bcl-2 and p53 play an important role in the regulation of apoptosis in the MCF-7 cell line, with lowered Bcl-2 expression accompanying easier apoptotic induction. The majority of the examined compounds act via the p53 pathway although some bypass this important proapoptotic factor.
    Źródło:
    Acta Biochimica Polonica; 2004, 51, 3; 733-745
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    TGF beta signalling and its role in tumour pathogenesis.
    Autorzy:
    Kaminska, Bozena
    Wesolowska, Aleksandra
    Danilkiewicz, Malgorzata
    Powiązania:
    https://bibliotekanauki.pl/articles/1041410.pdf
    Data publikacji:
    2005
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    Smad propteins
    RNA interference.
    TGF beta signal transduction
    tumour invasion
    cancer therapy
    MAP kinases
    Opis:
    Transforming growth factor beta (TGF-β) is a multifunctional cytokine involved in the regulation of cell proliferation, differentiation and survival/or apoptosis of many cells. Knock-out experiments in mice for the three isoforms of TGF-β have demonstrated their importance in regulating inflammation and tissue repair. TGF-β is implicated in the pathogenesis of human diseases, including tissue fibrosis and carcinogenesis. TGF-β receptors act through multiple intracellular pathways. Upon binding of TGF-β with its receptor, receptor-regulated Smad2/3 proteins become phosphorylated and associate with Smad4. Such complex translocates to the nucleus, binds to DNA and regulates transcription of specific genes. Negative regulation of TGF-β/Smad signalling may occur through the inhibitory Smad6/7. Furthermore, TGF-β-activated kinase-1 (TAK1) is a component of TGF-β signalling and activates stress-activated kinases: p38 through MKK6 or MKK3 and c-Jun N-terminal kinases (JNKs) via MKK4. In the brain TGF-β, normally expressed at the very low level, increases dramatically after injury. Increased mRNA levels of the three TGF-β isoforms correlate with the degree of malignancy of human gliomas. TGF-βs are secreted as latent precursors requiring activation into the mature form. TGF-β may contribute to tumour pathogenesis by direct support of tumour growth and influence on local microenvironment, resulting in immunosuppression, induction of angiogenesis, and modification of the extracellular matrix. TGF-β1,2 may stimulate production of vascular endothelial growth factor (VEGF) as well as plasminogen activator inhibitor (PAI-I), that are involved in vascular remodelling occurring during angiogenesis. Blocking of TGF-β action inhibits tumour viability, migration, metastases in mammary cancer, melanoma and prostate cancer model. Reduction of TGF-β production and activity may be a promising target of therapeutic strategies to control tumour growth.
    Źródło:
    Acta Biochimica Polonica; 2005, 52, 2; 329-337
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Transforming growth factor β1 protein and mRNA levels in inflammatory bowel diseases: towards solving the contradictions by longitudinal assessment of the protein and mRNA amounts
    Autorzy:
    Liberek, Anna
    Kmieć, Zbigniew
    Wierzbicki, Piotr
    Jakóbkiewicz-Banecka, Joanna
    Liberek, Tomasz
    Łuczak, Grażyna
    Plata-Nazar, Katarzyna
    Słomińska-Frączek, Magdalena
    Kaszubowska, Lucyna
    Gabig-Cimińska, Magdalena
    Węgrzyn, Alicja
    Powiązania:
    https://bibliotekanauki.pl/articles/1039466.pdf
    Data publikacji:
    2013
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    Crohn's disease
    ulcerative colitis
    Transforming Growth Factor-β1
    longitudinal assessment of TGF-β1 level
    Opis:
    Previously published studies on levels of the transforming growth factor-β1 (TGF-β1) protein and mRNA of the corresponding gene in patients suffering from inflammatory bowel diseases (IBD) gave varying results, leading to contradictory conclusions. To solve the contradictions, we aimed to assess longitudinally TGF-β1 protein and mRNA levels at different stages of the disease in children suffering from IBD. The study group consisted of 19 pediatric patients with IBD at the age between 3.5 and 18.4 years. The control group consisted of 42 children aged between 2.0 and 18.0 years. The plasma TGF-β1 concentration was measured with ELISA. mRNA levels of the TGF-β1 gene isolated from samples of the intestinal tissue were assessed by reverse transcription and real-time PCR. Levels of TGF-β1 protein in plasma and corresponding mRNA in intestinal tissue were significantly higher in IBD patients than in controls. TGF-β1 and corresponding transcripts were also more abundant in plasma and intestinal tissue, respectively, in patients at the active stage of the disease than during remission. In every single IBD patient, plasma TGF-β1 level and mRNA level in intestinal tissue was higher at the active stage of the disease than during remission. Levels of TGF-β1 and corresponding mRNA are elevated during the active stage of IBD but not during the remission. Longitudinal assessment of this cytokine in a single patient may help to monitor the clinical course of IBD.
    Źródło:
    Acta Biochimica Polonica; 2013, 60, 4; 683-688
    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 1-9 z 9

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