contact inhibition การใช้

• This natural cell process is known as " contact inhibition ."
• Thus, contact inhibition of proliferation may be viewed as a reversible form of cell cycle arrest.
• The transformed cells will form raised, dense spots on the sample as they grow without contact inhibition.
• In fact, YAP overexpression antagonizes contact inhibition.
• Many different stimuli apply checkpoint controls including TGFb, DNA damage, contact inhibition, replicative senescence, and growth factor withdrawal.
• Cancer cells do not have contact inhibition, and so will continue to grow and divide, regardless of their surroundings.
• Migration of keratinocytes over the wound site is stimulated by lack of contact inhibition and by chemicals such as nitric oxide.
• Their recent studies have shown that regulation of YAP by the Hippo pathway plays a critical role in cell contact inhibition.
• Some immortalised cell lines, despite being able to proliferate indefinitely, still experience contact inhibition, though generally to a lesser extent than normal cell lines.
• In the past, cells were thought to enter G 0 by default simply because of proliferation limits such as nutrient deprivation or contact inhibition.
• Thus, it may be reasonably concluded that cell-cell contact is an essential condition for contact inhibition of proliferation, but is by itself insufficient for mitotic inhibition.
• Some cell types are not limited by contact inhibition, such as immortalized cells, may continue to divide and form layers on top of the parent cells.
• Any changes in cytoskeletal organization and adhesion can lead to altered signaling, migration and a loss of contact inhibition that can promote cancer development and tumor formation.
• On the other hand, some treatment concepts involve upregulating the E-cadherin / catenin adhesion system to prevent disruptions in adhesions and contact inhibition from promoting cancer metastasis.
• Presumably, T-cadherin could play a navigating role in the growing tumor vessels, which in the absence of contact inhibition from the stromal cells, grow into the surrounding tumor tissue.
• Another way cells prevent over-division is that normal cells will also stop dividing when the cells fill up the space they are in and touch other cells; known as contact inhibition.
• Mutations in genes encoding these proteins can lead to inactivation of cadherin cell adhesions and elimination of contact inhibition, allowing cells to proliferate and migrate, thus promoting tumorigenesis and cancer development.
• The mechanism of T-cadherin mediated negative guidance in nervous system involves homophilic interaction and contact inhibition; in vascular system it is supposed that " -cadherin expressing blood vessels would avoid " -cadherin expressing tissues.
• First of all, by binding to cadherin receptor intracellular cytoplasmic tail domains, it can act as an integral component of a protein complex in adherens junctions that helps cells maintain epithelial layers . ?-catenin acts by anchoring the actin cytoskeleton to the junctions, and may possibly aid in contact inhibition signaling within the cell.
• They lose the property called contact inhibition ( cells arrest their growth in the case when more cells come into contact with each other ), and they also lose the growth dependency on adhesive surfaces; both these phenomena contribute to the increase in the number of fibroblast-like synoviocytes in the inflammatory tissue and are also typical for example for the growth of cancerous cells.