ArticleScience signaling2018
The depalmitoylase APT1 directs the asymmetric partitioning of Notch and Wnt signaling during cell division.
Article in Science signaling, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- Protein lipidation in cardiovascular homeostasis, development, and disease.Clinical science (London, England : 1979) · 2026Review
- Inhibition of BRD4 sensitizes NSCLC cells to osimertinib by suppressing APT1 and promoting MST1 palmitoylation.Cell death discovery · 2025Article
- Palmitoylation in cancer: decoding its roles in signal transduction, tumor immunity, and emerging therapeutic opportunities.Frontiers in immunology · 2025Review
- Protein palmitoylation in cancer: molecular functions and therapeutic potential.Molecular oncology · 2023Review
- FASN-dependent de novo lipogenesis is required for brain development.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Asymmetric Cell Division and Tumor Heterogeneity.Frontiers in cell and developmental biology · 2022Review
- Protein Palmitoylation Modification During Viral Infection and Detection Methods of Palmitoylated Proteins.Frontiers in cellular and infection microbiology · 2022Review
- Lipidation of small GTPase Cdc42 as regulator of its physiological and pathophysiological functions.Frontiers in physiology · 2022Review
- A Not-So-Ancient Grease History: Click Chemistry and Protein Lipid Modifications.Chemical reviews · 2021Review
- Regulation of Wnt Signaling Pathways at the Plasma Membrane and Their Misregulation in Cancer.Frontiers in cell and developmental biology · 2021Review
- Article
- Palmitoylated Proteins in Dendritic Spine Remodeling.Frontiers in synaptic neuroscience · 2020Article
- Temporal Profiling Establishes a Dynamic S-Palmitoylation Cycle.ACS chemical biology · 2018Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Asymmetric cell division results in two distinctly fated daughter cells. A molecular hallmark of asymmetric division is the unequal partitioning of cell fate determinants. We have previously established that growth factor signaling promotes protein depalmitoylation to foster polarized protein localization, which, in turn, drives migration and metastasis. We report protein palmitoylation as a key mechanism for the asymmetric partitioning of the cell fate determinants Numb and β-catenin through the activity of the depalmitoylating enzyme APT1. Using point mutations, we showed that specific palmitoylated residues on Numb were required for its asymmetric localization. By live-cell imaging, we showed that reciprocal interactions between APT1 and the Rho family GTPase CDC42 promoted the asymmetric localization of Numb and β-catenin to the plasma membrane. This, in turn, restricted Notch- or Wnt-responsive transcriptional activity to one daughter cell. Moreover, we showed that altering APT1 abundance changed the transcriptional signatures of MDA-MB-231 triple receptor-negative breast cancer cells, similar to changes in Notch and β-catenin-mediated Wnt signaling. We also showed that loss of APT1 depleted a specific subpopulation of tumorigenic cells in colony formation assays. Together, our findings suggest that APT1-mediated depalmitoylation is a major mechanism of asymmetric cell division that maintains Notch- and Wnt-associated protein dynamics, gene expression, and cellular functions.
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