79 research outputs found

    ΠŸΠΎΡΡ‚Π°Π½ΠΎΠ²ΠΊΠ° Π·Π°Π΄Π°Ρ‡ΠΈ для Ρ€Π°Π·Ρ€Π°Π±ΠΎΡ‚ΠΊΠΈ ИБ ΡƒΡ‡Π΅Ρ‚Π° ΠΈΠ³Ρ€ΠΎΠ²Ρ‹Ρ… ΠΏΠΎΠ΄Ρ…ΠΎΠ΄ΠΎΠ² Π² ΠΎΠ±ΡƒΡ‡Π΅Π½ΠΈΠΈ

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    РассмотрСны ΠΏΠΎΠ»ΠΎΠΆΠΈΡ‚Π΅Π»ΡŒΠ½Ρ‹Π΅ ΠΈ ΠΎΡ‚Ρ€ΠΈΡ†Π°Ρ‚Π΅Π»ΡŒΠ½Ρ‹Π΅ аспСкты обучСния Ρ‡Π΅Ρ€Π΅Π· ΠΎΠ½Π»Π°ΠΉΠ½-срСды с ΠΏΡ€ΠΈΠΌΠ΅Π½Π΅Π½ΠΈΠ΅ΠΌ ΠΈΠ³Ρ€ΠΎΠ²Ρ‹Ρ… ΠΌΠ΅Ρ‚ΠΎΠ΄ΠΎΠ² обучСния, поставлСна Π·Π°Π΄Π°Ρ‡Π° Ρ€Π°Π·Ρ€Π°Π±ΠΎΡ‚ΠΊΠΈ

    ITIH5 mediates epigenetic reprogramming of breast cancer cells

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    Extracellular matrix (ECM) is known to maintain epithelial integrity. In carcinogenesis ECM degradation triggers metastasis by controlling migration and differentiation including cancer stem cell (CSC) characteristics. The ECM-modulator inter- Ξ±-trypsin inhibitor heavy chain family member five (ITIH5) was recently identified as tumor suppressor potentially involved in impairing breast cancer progression but molecular mechanisms underlying its function are still elusive

    Endoglin: An β€˜Accessory’ Receptor Regulating Blood Cell Development and Inflammation

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    Transforming growth factor-β1 (TGF-β1) is a pleiotropic factor sensed by most cells. It regulates a broad spectrum of cellular responses including hematopoiesis. In order to process TGF-β1-responses in time and space in an appropriate manner, there is a tight regulation of its signaling at diverse steps. The downstream signaling is mediated by type I and type II receptors and modulated by the ‘accessory’ receptor Endoglin also termed cluster of differentiation 105 (CD105). Endoglin was initially identified on pre-B leukemia cells but has received most attention due to its high expression on activated endothelial cells. In turn, Endoglin has been figured out as the causative factor for diseases associated with vascular dysfunction like hereditary hemorrhagic telangiectasia-1 (HHT-1), pre-eclampsia, and intrauterine growth restriction (IUPR). Because HHT patients often show signs of inflammation at vascular lesions, and loss of Endoglin in the myeloid lineage leads to spontaneous inflammation, it is speculated that Endoglin impacts inflammatory processes. In line, Endoglin is expressed on progenitor/precursor cells during hematopoiesis as well as on mature, differentiated cells of the innate and adaptive immune system. However, so far only pro-monocytes and macrophages have been in the focus of research, although Endoglin has been identified in many other immune system cell subsets. These findings imply a functional role of Endoglin in the maturation and function of immune cells. Aside the functional relevance of Endoglin in endothelial cells, CD105 is differentially expressed during hematopoiesis, arguing for a role of this receptor in the development of individual cell lineages. In addition, Endoglin expression is present on mature immune cells of the innate (i.e., macrophages and mast cells) and the adaptive (i.e., T-cells) immune system, further suggesting Endoglin as a factor that shapes immune responses. In this review, we summarize current knowledge on Endoglin expression and function in hematopoietic precursors and mature hematopoietic cells of different lineages

    Usage of Mitogen-Activated Protein Kinase Small Molecule Inhibitors: More Than Just Inhibition!

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    We have identified a phenomenon occurring in the usage of proposed β€œspecific” Mitogen-activated protein kinase (MAPK) inhibitors. We found that especially inhibitors of p38 potentiate the activation of other MAPKs in various cell types. This finding will have tremendous impact on the interpretation of all former studies using MAPK inhibitors
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