The demonstration that leptin-dependent central control of bone mass, appetite and energy expenditure occurs through its ability to inhibit serotonin production raised questions about the location and identity of serotonin receptors on hypothalamic neurons mediating these function.
The molecular mechanisms by which CDKs mediate these functions are unknown.
Despite growing evidence of the diverse functions of Bergmann glia, the molecular mechanisms that mediate these functions have remained largely unknown.
DCC and CEACAM1 contribute to the adhesive, migratory, or invasive properties of several types of solid tumor cells [13] [16] including neuroblastoma [17], but the molecular interactions that mediate these functions have been difficult to identify.
These results suggested that leptin acts first elsewhere in the brain to mediate these functions.
Therefore, we hypothesized that RBPs may, as a group, be extensively regulated to mediate these functions.
It mediates these functions via binding to its unique receptor c-Met, a receptor tyrosine kinase.
To mediate these functions, the p53 protein must be activated by posttranslational modifications, which modulate p53 activity and interactions.
During evolution, functions (and the receptors that mediate these functions) develop for the intermediate products of the pathway, and structural diversity involving intermediates in the pathway can increase over time.
In yeast, the class III phosphatidylinositol 3‐kinase (PtdIns3K) complex that includes Vps34 (vacuolar protein sorting 34) functions in both autophagy and the sorting of vacuolar proteins, and 2 separate Vps34-containing subcomplexes (complex I and II) have been identified to mediate these functions.
