Cited by 52

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Functional Dissection of an AP-2 β2 Appendage-binding Sequence within the Autosomal Recessive Hypercholesterolemia Protein

Mishra, Sanjay K., Keyel, Peter A., Edeling, Melissa A., Dupin, Amie L., Owen, David J., Traub, Linton M.·2005·Journal of Biological Chemistry

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Crossref · 10.1074/jbc.m501029200

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  • ARH-F259A, which is unable to bind AP2, exits the nucleus upon CD8/LDLR overexpression but is not recruited into CCPs.

    “Upon overexpression of CD8/LDLR, ARH-F259A exited the nucleus, but was not recruited into CCPs (Fig. 5 B).”

    From Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis (2010) · cites this paper as Mishra et al., 2005

    The Results and Discussion report that F259A abolishes ARH binding to AP-2 and that GFP-tagged ARH fragments bearing F259A lose colocalization with AP-2. This supports the AP-2-binding aspect and is consistent with impaired recruitment to coated regions, but our copy does not report ARH-F259A exiting the nucleus upon CD8/LDLR overexpression or directly test its recruitment to CCPs under that condition. (LLM, conf=0.86)

    Experimental — accuracy not yet measured
  • Residues 252-268 of ARH bind the β2-adaptin subunit of AP-2.

    “Following the clathrin box motif, the protein has a highly conserved amino acid sequence (residues 252-268) that binds the ␤2-adaptin subunit of the adaptor protein-2 (AP-2) (13,15).”
  • ARH can interact directly with both clathrin and AP2 complexes.

    “ARH can interact directly with both clathrin (He et al., 2002) and AP2 complexes (Mishra et al., 2005)”

    From Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis (2010) · cites this paper as Mishra et al., 2005

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Citations

Cites

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Metadata

Authors
Mishra, S. K., Keyel, P. A., Edeling, M. A., Dupin, A. L., Owen, D. J., & Traub, L. M.
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
2005-05
Volume
280
Issue
19
Pages
19270-19280
ISSN
0021-9258
Cited by
52
References
2
Language
en

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