Data · dataset · 2015
Gamma-actin is involved in regulating centrosome function and mitotic progression in cancer cells
Listed in DataCite
Reorganization of the actin cytoskeleton during mitosis is crucial for regulating cell division.
Description
A functional role for γ-actin in mitotic arrest induced by the microtubule-targeted agent, paclitaxel, has recently been demonstrated. We hypothesized that γ-actin plays a role in mitosis.
Herein, we investigated the effect of γ-actin in mitosis and demonstrated that γ-actin is important in the distribution of β-actin and formation of actin-rich retraction fibers during mitosis. The reduced ability of paclitaxel to induce mitotic arrest as a result of γ-actin depletion was replicated with a range of mitotic inhibitors, suggesting that γ-actin loss reduces the ability of broad classes of anti-mitotic agents to induce mitotic arrest.
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In addition, partial depletion of γ-actin enhanced centrosome amplification in cancer cells and caused a significant delay in prometaphase/metaphase. This prolonged prometaphase/metaphase arrest was due to mitotic defects such as uncongressed and missegregated chromosomes, and correlated with an increased presence of mitotic spindle abnormalities in the γ-actin depleted cells. Collectively, these results demonstrate a previously unknown role for γ-actin in regulating centrosome function, chromosome alignment and maintenance of mitotic spindle integrity.
Links
Where it is published
- Repository landing page tandf.figshare.com/articles/dataset/Gamma_actin_is_involved_in_regulating_centros… ↗
landing page · from DataCite
- Repository landing page tandf.figshare.com/articles/Gamma_actin_is_involved_in_regulating_centrosome_func… ↗
landing page · from DataCite
- DOI doi.org/10.6084/m9.figshare.1627973 ↗
DOI / persistent id · from DataCite
- DOI doi.org/10.6084/m9.figshare.1627973.v1 ↗
DOI / persistent id · from DataCite
Documentation and papers
- Creative Commons Attribution 4.0 International creativecommons.org/licenses/by/4.0/legalcode ↗
license · from DataCite
- IsSupplementTo 10.1080/15384101.2015.1120920 doi.org/10.1080/15384101.2015.1120920 ↗
publication · from DataCite
Catalogue records · 4
- DataCite API api.datacite.org/dois/10.6084/m9.figshare.1627973.v1 ↗
metadata API · from DataCite
- DataCite API api.datacite.org/dois/10.6084/m9.figshare.1627973 ↗
metadata API · from DataCite
- DataCite Commons commons.datacite.org/doi.org/10.6084/m9.figshare.1627973.v1 ↗
catalogue entry · from DataCite
- DataCite Commons commons.datacite.org/doi.org/10.6084/m9.figshare.1627973 ↗
catalogue entry · from DataCite
Topics
- Stated by source
- Biological sciences · Biological sciences · Physical sciences · Physical sciences
Provenance · 2 source records, 14 field assertions
| Source | Key | Last seen | Raw |
|---|---|---|---|
| DataCite | 10.6084/m9.figshare.1627973 | 14 d ago | JSON v1 |
| DataCite | 10.6084/m9.figshare.1627973.v1 | 14 d ago | JSON v1 |
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|---|---|---|---|
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| byte_size | source · DataCite | connector:datacite@1.0.0 | |
| concepts[disease].local:disease:cancer | mapping · DataCite | vocabulary-mapper@1.0.0 | keywords['Cancer'] |
| concepts[disease].local:disease:cancer | mapping · DataCite | vocabulary-mapper@1.0.0 | keywords['Cancer'] |
| concepts[field].fos:biological-sciences | source · DataCite | connector:datacite@1.0.0 | |
| concepts[field].fos:biological-sciences | source · DataCite | connector:datacite@1.0.0 | |
| concepts[field].fos:physical-sciences | source · DataCite | connector:datacite@1.0.0 | |
| concepts[field].fos:physical-sciences | source · DataCite | connector:datacite@1.0.0 | |
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| description | source · DataCite | connector:datacite@1.0.0 | /data/attributes/descriptions |
| license | source · DataCite | connector:datacite@1.0.0 | /data/attributes/rightsList |
| publication_date | source · DataCite | connector:datacite@1.0.0 | /data/attributes/dates |
| title | source · DataCite | connector:datacite@1.0.0 | /data/attributes/titles/0/title |
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