ArticleThe Journal of cell biology2020
Stress-induced phosphorylation of CLIP-170 by JNK promotes microtubule rescue.
Article in The Journal of cell biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- CLASP2 promotes repair of kinesin-1 damage to the microtubule lattice.bioRxiv : the preprint server for biology · 2026Article
- Article
- Phase separation of +TIP networks regulates microtubule dynamics.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- The autophagy inducer SMER28 attenuates microtubule dynamics mediating neuroprotection.Scientific reports · 2022Article
- Tension of plus-end tracking protein Clip170 confers directionality and aggressiveness during breast cancer migration.Cell death & disease · 2022Article
- A kinesin-1 variant reveals motor-induced microtubule damage in cells.Current biology : CB · 2022Article
- Cytoskeleton and Associated Proteins: Pleiotropic JNK Substrates and Regulators.International journal of molecular sciences · 2021Review
- α-tubulin tail modifications regulate microtubule stability through selective effector recruitment, not changes in intrinsic polymer dynamics.Developmental cell · 2021Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The stress-induced c-Jun N-terminal kinase (JNK) controls microtubule dynamics by enhancing both microtubule growth and rescues. Here, we show that upon cell stress, JNK directly phosphorylates the microtubule rescue factor CLIP-170 in its microtubule-binding domain to increase its rescue-promoting activity. Phosphomimetic versions of CLIP-170 enhance its ability to promote rescue events in vitro and in cells. Furthermore, while phosphomimetic mutations do not alter CLIP-170's capability to form comets at growing microtubule ends, both phosphomimetic mutations and JNK activation increase the occurrence of CLIP-170 remnants on the microtubule lattice at the rear of comets. As the CLIP-170 remnants, which are potential sites of microtubule rescue, display a shorter lifetime when CLIP-170 is phosphorylated, we propose that instead of acting at the time of rescue occurrence, CLIP-170 would rather contribute in preparing the microtubule lattice for future rescues at these predetermined sites.
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