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A canaliculus is an adaptation found on gastric parietal cells. It is a deep infolding, or little channel, which serves to increase the surface area, e.g. for secretion. The parietal cell membrane is dynamic; the numbers of canaliculi rise and fall according to secretory n
The eukaryotic cell cycle consists of four distinct phases: G 1 phase, S phase (synthesis), G 2 phase (collectively known as interphase) and M phase (mitosis and cytokinesis). M phase is itself composed of two tightly coupled processes: mitosis, in which the cell's nucleus divides, and cytokinesis, in which the cell's cytoplasm and cell membrane divides forming two daughter cells.
Gastrin is a hormone produced by enteroendocrine G cells in the pyloric glands. [1] All three of these stimulate parietal cells to secrete hydrochloric acid and intrinsic factor. The chief cells secrete pepsinogen in response to gastrin and especially Ach, and ACh also stimulates mucus secretion. [1]
The hydrogen potassium ATPase is activated indirectly by gastrin that causes ECL cells to release histamine. [11] The histamine binds to H2 receptors on the parietal cell, activating a cAMP-dependent pathway which causes the enzyme to move from the cytoplasmic tubular membranes to deeply folded canaliculi of the stimulated parietal cell. [2]
As the eukaryotic cell cycle is a complex process, eukaryotes have evolved a network of regulatory proteins, known as the cell cycle control system, which monitors and dictates the progression of the cell through the cell cycle. [5]
Parietal cells produce potent hydrochloric acid, which damages cells. Gastric chief cells produce pepsinogen, which is activated by the acid to form pepsin. Pepsin is a protease that can digest and damage stomach cells. To prevent these disastrous effects, mucus and bicarbonate ions (HCO 3 −) are secreted by the foveolar cells.
Within the cell cycle, there is a stringent set of regulations known as the cell cycle control system that controls the timing and coordination of the phases to ensure a correct order of events. Biochemical triggers known as cyclin-dependent kinases (Cdks) switch on cell cycles events at the corrected time and in the correct order to prevent ...
An early observation that loss of Rb promoted cell cycle re-entry in G 0 cells suggested that Rb is also essential in regulating the G 0 to G 1 transition in quiescent cells. [20] Further observations revealed that levels of cyclin C mRNA are highest when human cells exit G 0 , suggesting that cyclin C may be involved in Rb phosphorylation to ...