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The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.

Clathrin-mediated endocytosis in AP-2–depleted cells

Open access
Motley, Alison, Bright, Nicholas A., Seaman, Matthew N.J., Robinson, Margaret S.·2003·The Journal of Cell Biology

Abstract

We have used RNA interference to knock down the AP-2 μ2 subunit and clathrin heavy chain to undetectable levels in HeLaM cells. Clathrin-coated pits associated with the plasma membrane were still present in the AP-2–depleted cells, but they were 12-fold less abundant than in control cells. No clathrin-coated pits or vesicles could be detected in the clathrin-depleted cells, and post-Golgi membrane compartments were swollen. Receptor-mediated endocytosis of transferrin was severely inhibited in both clathrin- and AP-2–depleted cells. Endocytosis of EGF, and of an LDL receptor chimera, were also inhibited in the clathrin-depleted cells; however, both were internalized as efficiently in the AP-2–depleted cells as in control cells. These results indicate that AP-2 is not essential for clathrin-coated vesicle formation at the plasma membrane, but that it is one of several endocytic adaptors required for the uptake of certain cargo proteins including the transferrin receptor. Uptake of the EGF and LDL receptors may be facilitated by alternative adaptors.

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Metadata

Authors
Motley, A., Bright, N. A., Seaman, M. N. J., & Robinson, M. S.
Venue
The Journal of Cell Biology
Published
2003-09-01
Volume
162
Issue
5
Pages
909-918
ISSN
  • 0021-9525 (ISSN-L)
  • 1540-8140
OpenAlex
W2032444338
Cited by
697
References
2
FWCI
15.63
Type
journal article
Language
en
Open access
bronze

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