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Tytuł:
Cloning of the lymphoid enhancer binding factor-1 (Lef-1) cDNA from rat kidney: Homology to the mouse sequence
Autorzy:
Kobielak, Krzysztof
Kobielak, Agnieszka
Trzeciak, Wiesław
Powiązania:
https://bibliotekanauki.pl/articles/1044445.pdf
Data publikacji:
1999
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
sequencing
predicted protein product
cDNA cloning
rat Lef-1
Opis:
We have cloned and sequenced rat cDNA that encodes the Lef-1 protein. The cDNA, containing 1194 nt exhibits 94% similarity to the mouse Lef-1 cDNA. The deduced amino-acids sequence of rat Lef-1 protein, consisting of 397 amino acids, exhibited 98% homology with the known sequence of mouse Lef-1 protein.
Źródło:
Acta Biochimica Polonica; 1999, 46, 4; 885-888
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
A novel isoform of human lymphoid enhancer-binding factor-1 (LEF-1) gene transcript encodes a protein devoid of HMG domain and nuclear localization signal.
Autorzy:
Kobielak, Agnieszka
Kobielak, Krzysztof
Trzeciak, Wieslaw
Powiązania:
https://bibliotekanauki.pl/articles/1044190.pdf
Data publikacji:
2001
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
human LEF-1
novel transcript isoform
HMG domain
Opis:
Lymphoid enhancer-binding factor-1 (LEF-1), a member of the high mobility group (HMG) family of proteins, regulates expression of T-cell receptor-α gene and is one of the key regulatory molecules in the epithelial-mesenchymal interactions during embryonic development. Among others, LEF-1 regulates expression of cytokeratin genes involved in formation of hair follicles and the gene encoding the cell-adhesion molecule E-cadherin. Transcription factor LEF-1, which acts as a dimer, binds β-catenin and is involved in signal transduction by the wnt pathway. We have cloned and sequenced a novel isoform of human LEF-1 gene transcript. This isoform encodes a truncated protein devoid of HMG domain and nuclear localization signal but retaining β-catenin binding domain. This isoform might either act in a dominant-negative manner by interfering with native LEF-1, or might bind β-catenin in the cytosol, which would result in attenuation of the signals transmitted by theLEF-b-catenin pathway.
Źródło:
Acta Biochimica Polonica; 2001, 48, 1; 221-226
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:
Mutation in the regulatory region of the EDA gene coincides with the symptoms of anhidrotic ectodermal dysplasia
Autorzy:
Kobielak, Krzysztof
Kobielak, Agnieszka
Limon, Janusz
Trzeciak, Wiesław
Powiązania:
https://bibliotekanauki.pl/articles/1044878.pdf
Data publikacji:
1998
Wydawca:
Polskie Towarzystwo Biochemiczne
Źródło:
Acta Biochimica Polonica; 1998, 45, 1; 245-250
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Screening of chromosomal region 21q22.3 for mutations in genes associated with neuronal Ca2+ signalling in bipolar affective disorder
Autorzy:
Kostyrko, Andrzej
Hauser, Joanna
Rybakowski, Janusz
Trzeciak, Wiesław
Powiązania:
https://bibliotekanauki.pl/articles/1041245.pdf
Data publikacji:
2006
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
TRPM2 protein
AMPA glutamate receptor B
bipolar affective disorder
Opis:
The therapeutic effect of lithium in bipolar affective disorder may be connected with decreasing intracellular Ca2+ concentrations. Several linkage studies have identified a potential bipolar affective disorder susceptibility locus within chromosomal region 21q22.3. This locus contains two genes expressed in the brain - ADARB1 and TRPM2 - involved in regulating intracellular Ca2+ concentrations. The aim of this study was an identification of mutations in the coding sequences of ADARB1 and TRPM2 and their association with bipolar affective disorder. For that purpose we screened 60 patients with bipolar affective disorder and a control group of 66 subjects using single strand conformation polymorphism and sequence analysis. For rapid screening we performed restriction fragment length polymorphism analysis. Screening of bipolar affective disorder patients for mutations in TRPM2 led to identification of three novel and four known transitions. Two transitions resulted in the substitutions: R755C and A890V. Screening of the coding sequence of ADARB1 did not reveal any mutations except one already known transition. A comparison of the transition frequency in patients and controls does not support association of the detected mutations with bipolar affective disorder. According to our results, bipolar affective disorder may not be caused by mutations in ADARB1. However, this study does not exclude TRPM2 as a candidate gene since we have screened only about 30 per cent of the entire coding sequence of this large gene.
Źródło:
Acta Biochimica Polonica; 2006, 53, 2; 317-320
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
A novel mutation A1270G of the EDA1 gene causing Tyr343Cys substitution in ectodysplasin-A in a family with anhidrotic ectodermal dysplasia.
Autorzy:
Kobielak, Agnieszka
Kobielak, Krzysztof
Biedziak, Barbara
Trzeciak, Wieslaw
Powiązania:
https://bibliotekanauki.pl/articles/1043673.pdf
Data publikacji:
2003
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
ectodysplasin-A
EDA1 gene
A1270G
Tyr336Cys
Opis:
The structure of the EDA1 gene was investigated in a patient with anhidrotic ectodermal dysplasia. Sequence analysis revealed a novel A1270G transition in exon 9 of the EDA1 gene in the patient and his uncle, whereas the patient's mother and grandmother were heterozygotes. This mutation resulted in Tyr343Cys substitution in the extracellular domain of the EDA1 gene product - ectodysplasin-A. The additional Cys343 was located between Cys332 and Cys346 and formed with Cys352 a cluster of four closely situated residues that could potentially form disulfide bonds. This mutation might affect the tertiary structure of the receptor-binding domain of ectodysplasin-A and precipitate the clinical symptoms of anhidrotic ectodermal dysplasia.
Źródło:
Acta Biochimica Polonica; 2003, 50, 1; 255-258
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
The effect of indole-3-carbinol on the expression of CYP1A1, CYP1B1 and AhR genes and proliferation of MCF-7 cells
Autorzy:
Ociepa-Zawal, Marta
Rubiś, Błażej
Łaciński, Mariusz
Trzeciak, Wiesław
Powiązania:
https://bibliotekanauki.pl/articles/1041121.pdf
Data publikacji:
2007
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
p21
AhR
CYP
cell proliferation
estrone hydroxylation
xenoestrogens
Opis:
The influence of an antiestrogen, indole-3-carbinol (I3C) on the expression of CYP1A1, CYP1B1 and AhR genes was investigated in an attempt to establish whether I3C could increase the expression of genes involved in estrone metabolism. Another purpose was to examine the proliferation of an estrogen-dependent breast cancer cell (MCF-7 line) under the influence of I3C and both I3C and DDT. In MCF-7 cells incubated with I3C or I3C and DDT combined, quantitative RT-PCR analysis revealed a significant increase in the level of CYP1A1, AhR, and CYP1B1 transcripts. The proliferation rate of MCF-7 cells was increased by treatment with DDT or estradiol (E2), whereas I3C did not affect the proliferation of MCF-7 cells but greatly reduced the stimulatory effect of DDT, and abolished the effect of E2. The level of p21 transcript, encoding p21 protein involved in the cell cycle, was increased several-fold by I3C comparing to its level in cells incubated with estradiol or DDT. The results suggest that the proliferation of MCF-7 cells is accompanied not only by expression of genes encoding cytochromes involved in estrogen metabolism, but also by changes in the expression of other genes including that encoding p21 protein involved in the cell cycle.
Źródło:
Acta Biochimica Polonica; 2007, 54, 1; 113-117
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł

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