This massive endocytosis ("MEND") can be elicited in a variety of cell types with a range of different experimental manipulations, including internal calcium transients in the presence of ATP, membrane treatment with sphingomyelinase, and introduction of various amphiphiles into the membrane bilayer.
MEND does not employ the canonical endocytic mechanisms involving clathrin, the actin cytoskeleton or dynamins. MEND preferentially causes endocytosis of the low-ordered, cholesterol-containing membrane fraction. The mechanisms underlying MEND likely include the merger of nanoscopic low-ordered domains into larger domains with attendant changes in lipid line tension.
Application of MEND promises to serve as a valuable tool in determining which membrane proteins are associated with low- or high-ordered membrane fractions.
About The Journal of General Physiology Founded in 1918, The Journal of General Physiology (JGP) is published by The Rockefeller University Press. All editorial decisions on manuscripts submitted are made by active scientists. JGP content is posted to PubMed Central, where it is available to the public for free six months after publication. Authors retain copyright of their published works and third parties may reuse the content for non-commercial purposes under a creative commons license. For more information, please visit www.jgp.org.Fine, M., et al. 2011. J. Gen. Physiol. doi:10.1085/jgp.201010469
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