Search results
Results from the WOW.Com Content Network
Grafting these cells into different parts of rats generates motor neurons regardless of the transplanted cells' microenvironment. [5] Following injury, neural stem cells enter a repair phase and express high levels of PI3K to enhance proliferation. This is better for survival of the neurons as a whole but is at the expense of generating motor ...
Cell division can occur without cell growth, producing many progressively smaller cells (as in cleavage of the zygote), while cell growth can occur without cell division to produce a single larger cell (as in growth of neurons). Thus, cell proliferation is not synonymous with either cell growth or cell division, despite these terms sometimes ...
Hyperplasia (from ancient Greek ὑπέρ huper 'over' + πλάσις plasis 'formation'), or hypergenesis, is an enlargement of an organ or tissue caused by an increase in the amount of organic tissue that results from cell proliferation. [4]
In cancer cells, both the heparan sulfate chains [42] [43] and the core protein [44] [45] of GPC3 are involved in regulating Wnt binding and activation for cell proliferation. [ 46 ] [ 47 ] Wnt recognizes a heparan sulfate structure on GPC3, which contains IdoA2S and GlcNS6S, and the 3-O-sulfation in GlcNS6S3S enhances the binding of Wnt to the ...
Unfortunately, regenerative potential of the adult heart is limited. The Hippo pathway is a recently identified signaling cascade that plays an evolutionarily conserved role in organ size control by inhibiting cell proliferation, promoting apoptosis, regulating fates of stem/progenitor cells, and in some circumstances, limiting cell size.
Also, STAT4 is able to activate NK cells (natural killer cells), and STAT5 can drive the formation of white blood cells. [2] [23] In response to cytokines, such as IL-4, JAK-STAT signalling is also able to stimulate STAT6, which can promote B-cell proliferation, immune cell survival, and the production of an antibody called IgE. [2]
These cell-cell interactions are mediated mainly by a group of Cell Adhesion Molecules (CAMs) called selectins. [1] T helper cells, central to the immune system, interact with other leukocytes by releasing signals known as cytokines which activate and stimulate the proliferation of B cells and killer T cells.
This delay between cell-cell contact and onset of proliferation inhibition is shortened as the culture becomes more confluent. 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.