ArticleeLife2020
Splicing variation of BMP2K balances abundance of COPII assemblies and autophagic degradation in erythroid cells.
Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- AAK1-mediated phosphorylation of PDLIM5 and Talin1 promotes focal adhesion disassembly to accelerate cell migration.Nature communications · 2026Article
- The functional landscape of alternative splicing in hematopoietic lineage commitment.Nature communications · 2026Article
- Endoplasmic reticulum exit sites are segregated for secretion based on cargo size.Developmental cell · 2024Article
- Article
- ACKR3 Proximity Labeling Identifies Novel G protein- and β-arrestin-independent GPCR Interacting Proteins.bioRxiv : the preprint server for biology · 2024Article
- ER exit in physiology and disease.Frontiers in molecular biosciences · 2024Review
- Quantitative Analysis of Isoform Switching in Cancer.International journal of molecular sciences · 2023Article
- Splicing variants of an endocytic regulator, BMP2K, differentially control autophagic degradation in erythroid cells.Autophagy · 2020Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Intracellular transport undergoes remodeling upon cell differentiation, which involves cell type-specific regulators. Bone morphogenetic protein 2-inducible kinase (BMP2K) has been potentially implicated in endocytosis and cell differentiation but its molecular functions remained unknown. We discovered that its longer (L) and shorter (S) splicing variants regulate erythroid differentiation in a manner unexplainable by their involvement in AP-2 adaptor phosphorylation and endocytosis. However, both variants interact with SEC16A and could localize to the juxtanuclear secretory compartment. Variant-specific depletion approach showed that BMP2K isoforms constitute a BMP2K-L/S regulatory system that controls the distribution of SEC16A and SEC24B as well as SEC31A abundance at COPII assemblies. Finally, we found L to promote and S to restrict autophagic degradation and erythroid differentiation. Hence, we propose that BMP2K-L and BMP2K-S differentially regulate abundance and distribution of COPII assemblies as well as autophagy, possibly thereby fine-tuning erythroid differentiation.
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Registered trials
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