Target intelligence / Profile preview

Disabled homolog 2 (DAB2)

Target
DAB2
Molecular classification
Clathrin adaptor protein, Endocytic adaptor protein, Scaffold protein, Other (Tumor suppressor)
01

Overview

Disabled homolog 2 (DAB2) is a cytosolic adaptor protein primarily known for its role as a clathrin-associated sorting protein (CLASP) essential for clathrin-mediated endocytosis of selected cargo proteins, including the LDL receptor, integrin β1, and others[2][3][4][5]. DAB2 contains an N-terminal phosphotyrosine-binding (PTB) domain that recognizes NPXY internalization motifs in receptor cargo, mediating the recruitment and assembly of clathrin-coated pits and vesicle trafficking. It interacts with multiple signaling molecules, including transforming growth factor-beta (TGF-β) receptors, Smad proteins, and components of the Wnt signaling pathway, and is involved in the regulation of cell adhesion, differentiation, and immune responses. DAB2 acts as a tumor suppressor, and its loss is correlated with various cancers, particularly ovarian carcinoma. Although no drugs target DAB2 directly, dysregulation of its expression or function impacts pathways relevant to cancer biology, lipid metabolism, and immune modulation[1][2][4][5][6].

Other names
DOC2DOC-2Differentially expressed in ovarian carcinoma 2Differentially-expressed protein 2Clathrin adaptor proteinDabMitogen-responsive phosphoproteinDAB adaptor protein 2Disabled (Drosophila) homolog 2Disabled homolog 2, mitogen-responsive phosphoprotein
02

Mechanism of action

Not directly targeted by drugs; molecular function primarily as an adaptor in endocytosis and signaling[4][5]

03

Biological functions

Clathrin-mediated endocytosisSignal transductionCell differentiationCell adhesionRegulation of Wnt/beta-catenin signalingTGF-beta receptor signalingImmune regulationCellular transportRegulation of receptor internalization
04

Disease associations

Cancer (specifically ovarian carcinoma, but also other epithelial cancers)TeratocarcinomaHypercholesterolemia, familial type 4Inflammation
05

Safety considerations

Therapeutic manipulation may disrupt normal endocytosis and signal transduction, potentially affecting essential cellular functions such as growth factor, lipoprotein, and immune signaling[2][4][5]No direct therapeutic targeting established; thus, clinical safety concerns are speculative
06

Interacting drugs

None identified as direct pharmacological interactors in current literature and databases[4][5]
07

Biomarkers

Downregulation associated with ovarian and several epithelial cancers[1][5]Loss of expression may serve as a tumor suppressor biomarker

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