Functional properties of the Su(Hw) complex are determined by its regulatory environment and multiple interactions on the Su(Hw) protein platform

The Su(Hw) protein was first identified as a DNA-binding component of an insulator complex in Drosophila. Insulators are regulatory elements that can block the enhancer-promoter communication and exhibit boundary activity. Some insulator complexes contribute to the higher-order organization of chromatin in topologically associated domains that are fundamental elements of the eukaryotic genomic structure. The Su(Hw)-dependent protein complex is a unique model for studying the insulator, since its basic structural components affecting its activity are already known. However, the mechanisms involving this complex in various regulatory processes and the precise interaction between the components of the Su(Hw) insulators remain poorly understood. Our recent studies reveal the fine mechanism of formation and function of the Su(Hw) insulator. Our results provide, for the first time, an example of a high complexity of interactions between the insulator proteins that are required to form the (Su(Hw)/Mod(mdg4)-67.2/CP190) complex. All interactions between the proteins are to a greater or lesser extent redundant, which increases the reliability of the complex formation. We conclude that both association with CP190 and Mod(mdg4)-67.2 partners and the proper organization of the DNA binding site are essential for the efficient recruitment of the Su(Hw) complex to chromatin insulators. In this review, we demonstrate the role of multiple interactions between the major components of the Su(Hw) insulator complex (Su(Hw)/Mod(mdg4)-67.2/CP190) in its activity. It was shown that Su(Hw) may regulate the enhancer–promoter communication via the newly described insulator neutralization mechanism. Moreover, Su(Hw) participates in direct regulation of activity of vicinity promoters. Finally, we demonstrate the mechanism of organization of “insulator bodies” and suggest a model describing their role in proper binding of the Su(Hw) complex to chromatin

Мономолекулярные пленки для модифицирования поверхности мембран

It was shown the possibility to modificate membranes with different hydrophilic properties by LB-films with hydrophilic and hydrophobic monomolecular layers. The most thermostabile is a PS membrane modified with nafion film. Modification of latex particles raise a thermostability properties of PAN membranes. So, we can determine a polymer flux on initially stage and prevent soiling filtration liquid by substances of fabricated membranes by application AFM method.Изучена возможность выделения мономолекулярных пленок на различные типы мембран, а также оценено влияние воздействия температуры на исходные и модифицированные мембраны. Показано, что наиболее термически стабильной является ПС-мембрана, модифицированная пленкой нафиона. Использование метода АСМ позволяет определить расплав полимера на начальных стадиях и таким образом избежать загрязнения фильтруемого раствора веществом, из которого получена мембрана

CREB Inhibits AP-2α Expression to Regulate the Malignant Phenotype of Melanoma

The loss of AP-2alpha and increased activity of cAMP-responsive element binding (CREB) protein are two hallmarks of malignant progression of cutaneous melanoma. However, the molecular mechanism responsible for the loss of AP-2alpha during melanoma progression remains unknown.Herein, we demonstrate that both inhibition of PKA-dependent CREB phosphorylation, as well as silencing of CREB expression by shRNA, restored AP-2alpha protein expression in two metastatic melanoma cell lines. Moreover, rescue of CREB expression in CREB-silenced cell lines downregulates expression of AP-2alpha. Loss of AP-2alpha expression in metastatic melanoma occurs via a dual mechanism involving binding of CREB to the AP-2alpha promoter and CREB-induced overexpression of another oncogenic transcription factor, E2F-1. Upregulation of AP-2alpha expression following CREB silencing increases endogenous p21(Waf1) and decreases MCAM/MUC18, both known to be downstream target genes of AP-2alpha involved in melanoma progression.Since AP-2alpha regulates several genes associated with the metastatic potential of melanoma including c-KIT, VEGF, PAR-1, MCAM/MUC18, and p21(Waf1), our data identified CREB as a major regulator of the malignant melanoma phenotype