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International Journal of Physiology and Pathophysiology
SJR: 0.116

ISSN 印刷: 2155-014X
ISSN オンライン: 2155-0158

Archives: Volume 1, 2010 to Volume 9, 2018

International Journal of Physiology and Pathophysiology

DOI: 10.1615/IntJPhysPathophys.v5.i1.10
pages 1-22

Molecular Mechanisms of ERN1-Mediated Angiogenesis

Oleksandr H. Minchenko
Department of Molecular Biology, Palladin Institute of Biochemistry National Academy of Sciences of Ukraine, Kyiv, Ukraine
Kateryna I. Kubaichuk
Department of Molecular Biology, Palladin Institute of Biochemistry National Academy of Sciences of Ukraine, Kyiv, Ukraine
Dmytro O. Minchenko
Department of Molecular Biology, Palladin Institute of Biochemistry National Academy of Sciences of Ukraine, Kyiv, Ukraine; Bogomolets National Medical University, Kyiv, Ukraine
Olena V. Kovalevska
Department of Molecular Biology, Palladin Institute of Biochemistry National Academy of Sciences of Ukraine, Kyiv, Ukraine
Anna O. Kulinich
Department of Molecular Biology, Palladin Institute of Biochemistry National Academy of Sciences of Ukraine, Kyiv, Ukraine
Nadia M. Lypova
Department of Molecular Biology, Palladin Institute of Biochemistry National Academy of Sciences of Ukraine, Kyiv, Ukraine

要約

The endoplasmic reticulum is a dynamic intracellular organelle with exquisite sensitivity to alterations in homeostasis, and provides stringent quality control systems to ensure that only correctly folded proteins transit to the Golgi and unfolded or misfolded proteins are retained and ultimately degraded. The endoplasmic reticulum stress represents the unfolded protein response to cope with the accumulation of unfolded or misfolded proteins and is required to maintain the functional integrity of the endoplasmic reticulum. This stress is a fundamental phenomenon which provides a secure protection of the cells from different factors. The endoplasmic reticulum stress provides a wide spectrum of physiological roles in diverse developmental and metabolic processes, especially for professional secretory cells with high-level secretory protein synthesis, such as pancreatic beta cells, hepatocytes and osteoblasts and is required throughout the entire life. The endoplasmic reticulum stress and hypoxia are obligate components of malignant tumor growth, are interconnected and activate angiogenesis via growth and metabolism control. The endoplasmic reticulum stress is mediated by three sensor and signaling pathways (PERK, ATF6 and ERN1), besides that a blockade of one of them (ERN1) leads to a decrease of tumor growth through suppression of the angiogenesis and pro-liferation processes. Data concerning the interaction of signaling enzyme ERN1 and pro- and anti-angiogenic gene expressions is analyzed.


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