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Cited by 200

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

Focal adhesion disassembly requires clathrin-dependent endocytosis of integrins

Chao, Wei-Ting, Kunz, Jeannette·2009·FEBS Letters
DOI 10.1016/j.febslet.2009.03.037PMC PMC2801759
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Abstract

Cell migration requires the controlled disassembly of focal adhesions, but the underlying mechanisms remain poorly understood. Here, we show that adhesion turnover is mediated through dynamin‐ and clathrin‐dependent endocytosis of activated β1 integrins. Consistent with this, clathrin and the clathrin adaptors AP‐2 and disabled‐2 (DAB2) distribute along with dynamin 2 to adhesion sites prior to adhesion disassembly. Moreover, knockdown of either dynamin 2 or both clathrin adaptors blocks β1 integrin internalization, leading to impaired focal adhesion disassembly and cell migration. Together, these results provide important insight into the mechanisms underlying adhesion disassembly and identify novel components of the disassembly pathway.

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Crossref · 10.1016/j.febslet.2009.03.037

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  • Dab2 tumor suppressor function is attributed to cell adhesion/migration.

    “and cell adhesion/migration (Chetrit et al., 2009; Chao and Kunz, 2009; Chetrit et al., 2009; Teckchandani et al., 2009; Xie et al., 2015).”

    From Endocytosis and Physiology: Insights from Disabled-2 Deficient Mice (2016) · cites this paper as Chao and Kunz, 2009

    The Results (§3.3; page not provided) show that DAB2 helps regulate focal adhesion disassembly and that combined DAB2/AP-2 knockdown inhibits cell migration. The paper does not attribute DAB2’s tumor-suppressor function to its role in adhesion or migration. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • Studies in cultured cells suggested a role of Dab2 in endocytic recycling and trafficking of integrins and thus impact cell mobility.

    “Studies in cultured cells suggested a role of Dab2 in endocytic recycling and trafficking of integrins and thus impact cell mobility”

    From Endocytosis and Physiology: Insights from Disabled-2 Deficient Mice (2016) · cites this paper as Chao and Kunz, 2009

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Research works printed but not linked: 24

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  2. 10.1016/j.ceb.2007.10.009 · DOI
  3. 10.1038/ncb1094 · DOI
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  7. 10.1073/pnas.0510306103 · DOI · Paper page
  8. 10.1016/S1097-2765(00)80398-6 · DOI
  9. 10.1242/jcs.03383 · DOI
  10. 10.1016/j.devcel.2007.05.003 · DOI
  11. 10.1091/mbc.E03-01-0046 · DOI
  12. 10.1007/978-1-59745-178-9_2 · DOI
  13. 10.1152/ajpcell.00160.2006 · DOI
  14. 10.1083/jcb.200309175 · DOI
  15. 10.1083/jcb.150.5.1137 · DOI
  16. 10.1016/j.tcb.2008.03.004 · DOI
  17. 10.1042/BJ20081288 · DOI · Paper page
  18. 10.1126/science.7569928 · DOI
  19. 10.1146/annurev.biochem.72.121801.161800 · DOI · Paper page
  20. 10.1034/j.1600-0854.2001.020206.x · DOI · Paper page
  21. 10.1002/j.1460-2075.1996.tb00965.x · DOI · Paper page
  22. 10.1083/jcb.117.6.1321 · DOI
  23. 10.1083/jcb.141.2.527 · DOI
  24. 10.1006/bbrc.1994.1271 · DOI

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Metadata

Authors
Chao, W.-T., & Kunz, J.
Venue
FEBS Letters
Publisher
Wiley
Published
2009-03-21
Volume
583
Issue
8
Pages
1337-1343
ISSN
  • 0014-5793
  • 1873-3468
DOI
10.1016/j.febslet.2009.03.037
PMC
PMC2801759
Cited by
200
References
2
Language
en
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor)

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