Evidence map›Paper›PMID 27721410›Full record

ArticleOncogene2017

Deficiency of RITA results in multiple mitotic defects by affecting microtubule dynamics.

K Steinhäuser, P Klöble, N-N Kreis, A Ritter, A Friemel, S Roth, J M Reichel, J Michaelis, M A Rieger, F Louwen and 2 more

Abstract read
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In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 11% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 3 institutions in 1 country.

K SteinhäuserDepartment of Gynecology and Obstetrics, School of Medicine, J.W. Goethe University, Frankfurt, Germany.
P KlöbleDepartment of Internal Medicine I, Center for Internal Medicine, University Medical Center Ulm, Ulm, Germany.
N-N KreisDepartment of Gynecology and Obstetrics, School of Medicine, J.W. Goethe University, Frankfurt, Germany.
A RitterDepartment of Gynecology and Obstetrics, School of Medicine, J.W. Goethe University, Frankfurt, Germany.
A FriemelDepartment of Gynecology and Obstetrics, School of Medicine, J.W. Goethe University, Frankfurt, Germany.
S RothDepartment of Gynecology and Obstetrics, School of Medicine, J.W. Goethe University, Frankfurt, Germany.
J M ReichelBiophysics Institute, Ulm University, Ulm, Germany.
J MichaelisBiophysics Institute, Ulm University, Ulm, Germany.
M A RiegerDepartment of Hematology/Oncology, J.W. Goethe University, Frankfurt, Germany.
F LouwenDepartment of Gynecology and Obstetrics, School of Medicine, J.W. Goethe University, Frankfurt, Germany.
F OswaldDepartment of Internal Medicine I, Center for Internal Medicine, University Medical Center Ulm, Ulm, Germany.
J YuanDepartment of Gynecology and Obstetrics, School of Medicine, J.W. Goethe University, Frankfurt, Germany.
Goethe University Frankfurt · DEUniversität Ulm · DEDeutschen Konsortium für Translationale Krebsforschung · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Deregulation of mitotic microtubule (MT) dynamics results in defective spindle assembly and chromosome missegregation, leading further to chromosome instability, a hallmark of tumor cells. RBP-J interacting and tubulin-associated protein (RITA) has been identified as a negative regulator of the Notch signaling pathway. Intriguingly, deregulated RITA is involved in primary hepatocellular carcinoma and other malignant entities. We were interested in the potential molecular mechanisms behind its involvement. We show here that RITA binds to tubulin and localizes to various mitotic MT structures. RITA coats MTs and affects their structures in vitro as well as in vivo. Tumor cell lines deficient of RITA display increased acetylated α-tubulin, enhanced MT stability and reduced MT dynamics, accompanied by multiple mitotic defects, including chromosome misalignment and segregation errors. Re-expression of wild-type RITA, but not RITA Δtub ineffectively binding to tubulin, restores the phenotypes, suggesting that the role of RITA in MT modulation is mediated via its interaction with tubulin. Mechanistically, RITA interacts with tubulin/histone deacetylase 6 (HDAC6) and its suppression decreases the binding of the deacetylase HDAC6 to tubulin/MTs. Furthermore, the mitotic defects and increased MT stability are also observed in RITA

Indexed as

AcetylationAnimalsDNA-Binding ProteinsHCT116 CellsHeLa CellsHistone Deacetylase 6Histone DeacetylasesHumansMCF-7 CellsMiceMice, KnockoutMicrotubulesMitosisNeoplasm ProteinsSpindle ApparatusTubulinDNA-Binding ProteinsHDAC6 protein, humanHdac6 protein, mouseHistone Deacetylase 6Histone DeacetylasesNeoplasm ProteinsTubulinZNF331 protein, human

Identifiers

PMID27721410
OpenAlexW2531123396

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.