ArticleMolecular biology of the cell2015
Preventing farnesylation of the dynein adaptor Spindly contributes to the mitotic defects caused by farnesyltransferase inhibitors.
Article in Molecular biology of the cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 47 citations in OpenAlex.
- Structure and function of the outer kinetochore.Nature reviews. Molecular cell biology · 2026Review
- From molecular pathogenesis to novel Therapeutic approaches - a review of recent advances in the treatment of peripheral T cell Lymphomas.Biomarker research · 2026Review
- Protein lipidation in the tumor microenvironment: enzymology, signaling pathways, and therapeutics.Molecular cancer · 2025Review
- Functional-proteomics-based investigation of the cellular response to farnesyltransferase inhibition in lung cancer.iScience · 2025Article
- A farnesyl-dependent structural role for CENP-E in expansion of the fibrous corona.The Journal of cell biology · 2024Article
- HPV16 E6 induces chromosomal instability due to polar chromosomes caused by E6AP-dependent degradation of the mitotic kinesin CENP-E.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Kinetochore-catalyzed MCC formation: A structural perspective.IUBMB life · 2023Article
- Conformational transitions of the Spindly adaptor underlie its interaction with Dynein and Dynactin.The Journal of cell biology · 2022Article
- Structure of the RZZ complex and molecular basis of Spindly-driven corona assembly at human kinetochores.The EMBO journal · 2022Article
- Mevalonate Pathway-mediated ER Homeostasis Is Required for Haploid Stability in Human Somatic Cells.Cell structure and function · 2021Article
- The Disordered Spindly C-terminus Interacts with RZZ Subunits ROD-1 and ZWL-1 in the Kinetochore through the Same Sites in C. Elegans.Journal of molecular biology · 2021Article
- Leaving no-one behind: how CENP-E facilitates chromosome alignment.Essays in biochemistry · 2020Review
- Dynamics of kinetochore structure and its regulations during mitotic progression.Cellular and molecular life sciences : CMLS · 2020Review
- RZZ-SPINDLY-DYNEIN: you got to keep 'em separated.Cell cycle (Georgetown, Tex.) · 2020Review
- Kinetochore protein Spindly controls microtubule polarity inProceedings of the National Academy of Sciences of the United States of America · 2020Article
- Article
- Miro-dependent mitochondrial pool of CENP-F and its farnesylated C-terminal domain are dispensable for normal development in mice.PLoS genetics · 2019Article
- Distinct Roles of RZZ and Bub1-KNL1 in Mitotic Checkpoint Signaling and Kinetochore Expansion.Current biology : CB · 2018Article
- USP45 and Spindly are part of the same complex implicated in cell migration.Scientific reports · 2018Article
- Dynamic kinetochore size regulation promotes microtubule capture and chromosome biorientation in mitosis.Nature cell biology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
The clinical interest in farnesyltransferase inhibitors (FTIs) makes it important to understand how these compounds affect cellular processes involving farnesylated proteins. Mitotic abnormalities observed after treatment with FTIs have so far been attributed to defects in the farnesylation of the outer kinetochore proteins CENP-E and CENP-F, which are involved in chromosome congression and spindle assembly checkpoint signaling. Here we identify the cytoplasmic dynein adaptor Spindly as an additional component of the outer kinetochore that is modified by farnesyltransferase (FTase). We show that farnesylation of Spindly is essential for its localization, and thus for the proper localization of dynein and its cofactor dynactin, to prometaphase kinetochores and that Spindly kinetochore recruitment is more severely affected by FTase inhibition than kinetochore recruitment of CENP-E and CENP-F. Molecular replacement experiments show that both Spindly and CENP-E farnesylation are required for efficient chromosome congression. The identification of Spindly as a new mitotic substrate of FTase provides insight into the causes of the mitotic phenotypes observed with FTase inhibitors.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.