Disabled-2 (Dab2) is required for transforming growth factor beta-induced epithelial to mesenchymal transition (EMT) (Q24296708)

negative regulation of apoptotic process

GOA release 2020-03-11

1 reference

Disabled 2, mitogen-responsive phosphoprotein

GOA release 2020-03-11

1 reference

Journal of Biological Chemistry

GOA release 2020-03-11

author name string

Céline Prunier

series ordinal

1

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Philip H Howe

series ordinal

2

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language of work or name

English

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publication date

29 April 2005

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published in

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volume

280

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issue

17

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page(s)

17540-8

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Disabled-2 colocalizes with the LDLR in clathrin-coated pits and interacts with AP-2

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Myosin VI binds to and localises with Dab2, potentially linking receptor-mediated endocytosis and the actin cytoskeleton

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Disabled-2 exhibits the properties of a cargo-selective endocytic clathrin adaptor

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Cytosolic adaptor protein Dab2 is an intracellular ligand of endocytic receptor gp600/megalin

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Dab2 links CIN85 with clathrin-mediated receptor internalization

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DOC-2/DAB2 is the binding partner of myosin VI.

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Disabled-2 mediates c-Fos suppression and the cell growth regulatory activity of retinoic acid in embryonic carcinoma cells

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The adaptor molecule Disabled-2 links the transforming growth factor beta receptors to the Smad pathway

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C-terminal-binding protein corepresses epithelial and proapoptotic gene expression programs

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Disabled-2 inactivation is an early step in ovarian tumorigenicity

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Smad3 potentiates transforming growth factor beta (TGFbeta )-induced apoptosis and expression of the BH3-only protein Bim in WEHI 231 B lymphocytes

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Down-Regulation of DOC-2 in Colorectal Cancer Points to Its Role as a Tumor Suppressor in This Malignancy

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