Publications by authors named "Tereza Holotnakova"

Carbonic anhydrase IX (CA IX) belongs to the physiologically important enzymes which contribute to tumor physiology. Tumor-associated expression of CA IX is induced mainly due to its strong transcriptional activation via hypoxia-inducible factor 1 (HIF-1). Therefore, CA IX can serve as a surrogate marker of hypoxia and a prognostic indicator.

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Carbonic anhydrase 9 (CA9), as one of the most hypoxia-responsive genes, has been associated almost exclusively with hypoxic tumors. Its principal role is in pH regulation which helps tumor cells overcome intracellular acidosis and survive extended periods of time with low oxygen. Hypoxia-inducible factor 1 (HIF-1) is the main transcriptional activator of CA9.

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Tumour-associated expression of CA IX (carbonic anhydrase IX) is to a major extent regulated by HIF-1 (hypoxia-inducible factor-1) which is important for transcriptional activation and consists of the oxygen-regulated subunit HIF-1alpha and the partner factor ARNT [AhR (aryl hydrocarbon receptor) nuclear translocator]. We have previously observed that HIF-1alpha competes with the AhR for interaction with ARNT under conditions when both conditionally regulated factors are activated. We have therefore investigated whether TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin)-induced activation of the AhR pathway might interfere with CA IX expression.

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Type 1 and 2 inositol 1,4,5-trisphosphate (IP3) receptors have been found in cardiac tissue, although they are localized in different types of cells. While the type 1 predominates in neuronal cells and cardiac ganglia, type 2 IP3 receptor is localized mainly in cardiomyocytes. In the heart, gene expression of the type 1 IP3 receptor is modulated by catecholamines, while type 2 is not affected.

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CA IX is an active transmembrane carbonic anhydrase isoform functionally implicated in cell adhesion and pH control. Human CA IX is strongly induced by hypoxia and frequently associated with various tumors. In this study, we investigated the expression of the rat CA IX in response to chronic hypoxia and to treatment with chemical compounds that disrupt oxygen sensing, including dimethyloxalylglycine, dimethylester succinate, diazoxide, and tempol.

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