to snoo-finity ... and beyond!
to snoo-finity ... and beyond!
basically glucose stimulates Beta cells to exocytos insulin. An process involving exocytosis involves fusion od an intracellular vesicle with the plasma membrane.
The β-cells have evolved a mechanism to detect the amount of insulin stored and secreted and adjust insulin synthesis accordingly. A granule transmembrane protein called islet cell autoantigen 512 (ICA512), is a crucial part of this feedback control. Insulin granules travel a long distance on tubulin tracks before arriving at the peripheral actin network [125]. Before becoming linked to the cytoskeleton, insulin granules are anchored to actin cortex via ICA512 and β2-synthrophin. Upon activation, the granule membrane fuses transiently to the cell membrane to release insulin. Elevated Ca2+ levels in the meantime activate the protease μ-calpain to cleave away a cytosolic fragment from ICA512. The free ICA512 cytosolic fragment then moves to the nucleus and binds to the tyrosine-phosphorylated transcriptional factor STAT5 to prevent STAT 5 from dephosphorylation, which in turn upregulates insulin transcription [127]. Nuclear free ICA512 cytosolic fragments also bind to sumoylating enzyme PIASγ. The sumoylation of ICA512 by PIAS γ reverses the binding of ICA512 to STAT5 [127]. Hence, the release of insulin from secretory granules is communicated to the nucleus, which serves as a positive feedback mechanism to initiate insulin translation for maintaining an adequate amount of stored insulin.
submitted by trichotillomaniac(13), 2019-06-30T16:44:12Z
basically glucose stimulates Beta cells to exocytose insulin. Any process involving exocytosis involves fusion of an intracellular vesicle with the plasma membrane.