Evidence map›Paper›PMID 35883622›Full record

ArticleCells2022

The N-Terminal Domain of Bfa1 Coordinates Mitotic Exit Independent of GAP Activity in

Yan Li, Kiwon Song

Open access · goldAbstract read
In one paragraph

Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 53% 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

3 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. A noncanonical GTPase signaling mechanism controls exit from mitosis in budding yeast.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  3. Article
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

2 authors at 1 institution in 1 country.

Yan LiDepartment of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul 03722, Korea.
Kiwon SongDepartment of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul 03722, Korea.
Yonsei University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The spindle position checkpoint (SPOC) of budding yeast delays mitotic exit in response to misaligned spindles to ensure cell survival and the maintenance of genomic stability. The GTPase-activating protein (GAP) complex Bfa1-Bub2, a key SPOC component, inhibits the GTPase Tem1 to induce mitotic arrest in response to DNA and spindle damage, as well as spindle misorientation. However, previous results strongly suggest that Bfa1 exerts a GAP-independent function in blocking mitotic exit in response to misaligned spindles. Thus, the molecular mechanism by which Bfa1 controls mitotic exit in response to misaligned spindles remains unclear. Here, we observed that overexpression of the N-terminal domain of Bfa1 (Bfa1-D16), which lacks GAP activity and cannot localize to the spindle pole body (SPB), induced cell cycle arrest along with hyper-elongation of astral microtubules (aMTs) as Bfa1 overexpression in Δ

Indexed as

Cell Cycle ProteinsCytoskeletal ProteinsSaccharomyces cerevisiae ProteinsGTPase-Activating ProteinsMitosisMonomeric GTP-Binding ProteinsSaccharomyces cerevisiaeSpindle ApparatusBFA1 protein, S cerevisiaeCell Cycle ProteinsCytoskeletal ProteinsGTPase-Activating ProteinsMonomeric GTP-Binding ProteinsSaccharomyces cerevisiae ProteinsTEM1 protein, S cerevisiaeBfa1budding yeastmicrotubule hyper-elongationmitotic exitspindle misorientationspindle pole bodySPOC

Identifiers

PMID35883622
PMCPMC9316867
OpenAlexW4285088775

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.