In mice, Th17 cells require transforming growth factor-β and IL-6 for their differentiation from naïve T cells, and their maintenance and expansion is controlled by IL-23, a cytokine that is produced by DCs.
Understanding how progenitor cell maintenance and homeostasis is controlled over developmental time is crucial for understanding normal cellular and tissue dynamics, especially in the context of ageing or disease.
Homeostatic maintenance of T cells is controlled by tonic signaling through T cell antigen receptors and common γ chain cytokine receptors.
Active maintenance of MII arrest is controlled by the oocyte-specific Cytostatic Factor (CSF), which requires activity of the mitogen-activated protein kinase (MAPK) pathway of the oocyte [14], [15].
In our model, protein autophosphorylation, leading to the maintenance of long-term plasticity, is controlled by Ca2+ entry through the NMDA receptor channels.
The onset of the instabilities is primarily controlled by the diffusional-thermal instability, while characteristics of the subsequent transition to and maintenance of the saturated state is controlled by the hydrodynamic instability.
In turn, maintenance of these collinear patterns is controlled, at least in part, by Shh [26].
The maintenance of stem cell pluripotency is controlled by a core cluster of transcription factors, including NANOG, OCT4 and SOX2.
The maintenance of stem cell pluripotency is controlled by a core cluster of transcription factors, NANOG, OCT4 and SOX2 – genes that jointly regulate each other's expression.
Gastrointestinal (GI) function (motility, secretion, and maintenance of fluid and electrolyte homeostasis) is controlled by three branches of the autonomic nervous system the sympathetic, parasympathetic, and the enteric nerves.
