mitogenesis


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mitogenesis

[‚mīd·ə′jen·ə·səs]
(cell and molecular biology)
Induction of mitosis.
Formation as a result of mitosis.
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References in periodicals archive ?
Cyclooxygenase-2 (COX-2) is transiently induced by pro-inflammatory cytokines and growth factors, and is involved in inflammation and mitogenesis.
The level of glucose is high in cancer cells and free of insulin binding to its receptor; the effects of the insulin receptor activation on cancer cells may stimulate cell mitogenesis and survival, proliferation, protection from apoptotic stimuli, invasion and metastasis [7].
In addition, some events during bovine oocyte maturation including mitogenesis and metabolism are regulated by cytosolic kinase activity such as MAPK also called "extracellular signal-regulated kinase" (ERK) and maturation promoting factor (MPF).
Moreover, it induces human chorionic gonadotrophin production in trophoblast cells, regulates placental growth, enhances mitogenesis and stimulates amino acid uptake (17, 13).
Davidai et al27 and Sandy et al28 with different experiments proposed this pathway to be important in mitogenesis in bone cells.
Overwhelming data demonstrate that FGF/FGFR signaling cascades play an important role in many cellular processes including mitogenesis, differentiation, migration, survival and polarity (1-4).
Many of these growth factors are over expressed in leiomyomas and either increase smooth muscle proliferation (TGF-transforming growth factor, FGF-Fibroblast growth factors) or DNA synthesis (EGF, PDGF), stimulate synthesis of extracellular matrix (TGF-b), and promote mitogenesis (TGFB,EGF,IGF, Prolactin) or angiogenesis (FGF,VEGF) (10).
Compelling evidence has shown that FGF signaling pathways are implicated in cancer progression by inducing mitogenesis, cell migration, and tumor angiogenesis (16, 17).
Inhibition of mitogen-activated protein kinase and phosphatidylinositol 3-kinase activity in MCF-7 cells prevents estrogen-induced mitogenesis.
Neuregulin-1 isoform induces mitogenesis, KCa and Ca2+ currents in PC12 cells.
La enfermedad periodontal podria constituirse en un factor de riesgo para la disfuncion endotelial, dado que las citocinas proinflamatorias producidas por monocitos (IL-1, IL-6 y factor de necrosis tumoral [FNT]), como consecuencia de la infeccion periodontal, inhiben las lipasas lipoproteinas, por lo que la lipidemia es un factor prominente de las infecciones cronicas, a la vez que sobrerregula la expresion de la adhesion molecular sobre las celulas endoteliales y pueden estimular la mitogenesis y la produccion de fibrinogeno.

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