ArticleThe Journal of biological chemistry2020
Alternative splicing reverses the cell-intrinsic and cell-extrinsic pro-oncogenic potentials of YAP1.
Article in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- The role of splicing factor SRSF3 in cancer progression: Mechanisms, biomarkers, and therapeutic implications.Translational oncology · 2026Review
- Flow-Induced Yap/Taz Signaling Balances Endothelial and Hematopoietic Stem Cell Fates.bioRxiv : the preprint server for biology · 2026Article
- Succinate drives breast cancer bone metastasis by activating the HIF1α/YTHDF1/YAP signaling axis to upregulate chemokine CXCL5 and disrupt the bone microenvironment.Apoptosis : an international journal on programmed cell death · 2026Article
- YAP1 in control: how RNA networks and protein modifications shape its function and therapeutic targetability.Molecular cancer · 2026Review
- Optogenetic control of YAP can enhance the rate of wound healing.Cellular & molecular biology letters · 2023Article
- Oncogenic SRSF3 in health and diseases.International journal of biological sciences · 2023Review
- YAP/TAZ as master regulators in cancer: modulation, function and therapeutic approaches.Nature cancer · 2023Review
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Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In addition to acting as a transcriptional co-activator, YAP1 directly mediates translocalization of the pro-oncogenic phosphatase SHP2 from the cytoplasm to nucleus. In the cytoplasm, SHP2 potentiates RAS-ERK signaling, which promotes cell proliferation and cell motility, whereas in the nucleus, it mediates gene regulation. As a result, elucidating the details of SHP2 trafficking is important for understanding its biological roles, including in cancer. YAP1 comprises multiple splicing isoforms defined in part by the presence (as in YAP1-2γ) or absence (as in YAP1-2α) of a γ-segment encoded by exon 6 that disrupts a critical leucine zipper. Although the disruptive segment is known to reduce co-activator function, it is unclear how this element impacts the physical and functional relationships between YAP1 and SHP2. To explore this question, we first demonstrated that YAP1-2γ cannot bind SHP2. Nevertheless, YAP1-2γ exhibits stronger mitogenic and motogenic activities than does YAP1-2α because the YAP1-2α-mediated delivery of SHP2 to the nucleus weakens cytoplasmic RAS-ERK signaling. However, YAP1-2γ confers less
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Registered trials
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