Excellent Cell Video!

While red blood cells are carried away at a high velocity by a strong blood flow,leukocytes roll sowly on endothelial cells.P-selectins on endothelial cells interact with PSGL-1,aglycoprotein on leukocyte microvilli.Leukocytes pulled by the blood flow adhere and roll on endothelial cells because the existing interactions are broken while new ones are formed.These interaction are possible because the standard extracellular domains of both proteins immerge from extracellular matrix,which cover the surface of both cell types.
The outer leaflet of the lipid bilayer is rich in single lipids and phosphotidylcholine.Single lipid rich raft raised about the rest of the rafts recuse specified membrane proteins.Rafts rigidity caused by the tight parking of cholesterol molecules against the straight single lipid hydrocarbon chain.Outside the raft,kinks unsaturated chains and lower cholesterol concentration result in increase fluidity.At sights of information,secreted chemokines bind to heparan sulfate proteoglycan endothelial cells are presented to leukocyte's seven transmembrane receptors.The binding stimulates leukocytes and triggers an intraccllular cascade of signaling reactions.
The inner leaflet of the bilayer has very different composition than that of the outer leaflet.While some protein traverse the membrane,other are *rivet anchored into the inner leaflet by covalently attach fatty acid chains or a recruited through non-covalent interactions with membrane proteins.The membrane bond protein complexes are critical for the transmition of signal across the plasma membrane.The *leafy lipid bilayer,spectrin tetramers arranged into hexagonal network that are anchored by membrane proteins.This network forms the membrane skeleton that contributes to membrane stability and membrane protein distribution.
The cytososkelecton is comprised of networks of filamental protein that are responsible for the special organization of cytosoltic components.Inside the microvilli,actin filaments form type parallel bundles which are stabilized by cross -linking proteins.While deeper in the cytosome,the actin networks adapt jawlike structure stabilized by a variety of actin binding proteins.Filaments kep their minus-ends by protein complex,grow away from plasma membrane by the addition of actin polymers to the plus-end.The actin network is a very dynamic structure with continuous directional polymerization and disassembly.severing proteins induce kinks in the filaments and led to the formation of short filaments that rapidly depolymerize or give rise to new filaments.
The cytososkeleton includes a network of microtubules created by lateral association of protofilaments formed with the polymerization of tubulin dimers.While the plus-ends of some microtubule extend toward the plasma membrane,protein stabilizes the cure conformation of protofilaments from other microtubules,causing the rapidly plus-end depolymeriztion.
Microtubules provide tracts along which membrane bounded vesicles travel to and from the plasma membrane.The directional movement of these cargo vesicles is due to a family of motor proteins linking vesicles and microtubules.membrane bounded organelles like mitochondria are loosely trapped by the cytoskeleton.mitochondria change shape continuously and their orientation is partly *dicty by their interaction with microtubules.
Cell secreted proteins accumulate in the lumen of endoplasmic reticulum while integral membrane proteins become embedded in the endoplasmic reticulum membrane.Proteins are transport from the endoplasmic reticulum to the Golgi apparatus(GA) by vesicles travelling along the microtubules.Protein glycosylation initiated in the endplasmic reticulum is completed inside the lumen of Golgi apparatus.Fully glycosylation proteins are transport from the Golgi apparatus to the plasma membrane.
When the vesicle fuses with plasma membrane,proteins containing in the vesicle lumen are secreted and proteins embedded in the vesicle membrane diffuse in the cell membrane.At sights of information,chemokine secreted by the endothelial cells bind to the extracellular domains of G-protein coupled membrane receptors.This binding causes a conformational change in the cytosonic portion of the receptor,and consequential activation of the subunit of the G-protein.The activation of the G-protein subunit triggers a cascade of protein activation which in turn leads to the activation and plasterin of integrin inside lipid rafts.
A domatic conformation change occurs in the extracellular domain of activated integrins.These now allow for they interaction with I-cam proteins display in the surface of the endothelial cells.These strong interactions immobilize the rolling leukocyte at sight of information. Additional signaling events cause profound reorganization of the cytoskeleton,resulting in the spreading of one edge of the leukocyte.The leading edge of the leukocyte inserts itself between the endothelial cells,and leukocytes migrate through the blood vessel walls into the inflamed tissue.Rolling,activation,adhesion,and trans endothelial migration are the four steps of a proeess called leukocyte extradrivation.