Evidence map›Paper›PMID 16240118›Full record

ArticleCurrent genetics2005

A role for KEM1 at the START of the cell cycle in Saccharomyces cerevisiae.

Ritu Pathak, Lydia M Bogomolnaya, Jinbai Guo, Michael Polymenis

Abstract read
PubMed Publisher
In one paragraph

Article in Current genetics, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.3field-weighted citation impact, top 45% 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

1 citing paper in PubMed, 4 citations in OpenAlex.

  1. 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

4 authors at 1 institution in 1 country.

Ritu PathakDepartment of Biochemistry and Biophysics, Texas A&M University, 2128 TAMU, College Station, TX 77843, USA.
Lydia M Bogomolnaya
Jinbai Guo
Michael Polymenis
Texas A&M University · US

Funding

Coordination of Cell Growth with Cell DivisionR01GM062377 · NIGMS · TEXAS A&M UNIVERSITY SYSTEM · PI POLYMENIS, MICHAEL S · 2001 to 2005
$1.1M
NIGMS NIH HHS R01 GM062377NIGMS NIH HHS R01-GM062377
6 · The paper itself

Abstract

KEM1 is a Saccharomyces cerevisiae gene, conserved in all eukaryotes, whose deletion leads to pleiotropic phenotypes. For the most part, these phenotypes are thought to arise from Kem1p's role in RNA turnover, because Kem1p is a major 5'-3' cytoplasmic exonuclease. For example, the exonuclease-dependent role of Kem1p is involved in the exit from mitosis, by degrading the mRNA of the mitotic cyclin CLB2. Here, we describe the identification of a KEM1 truncation, KEM1(1-975), that accelerated the G1 to S transition and initiation of DNA replication when over-expressed. Interestingly, although this truncated Kem1p lacked exonuclease activity, it could efficiently complement another function affected by the loss of KEM1, microtubule-dependent nuclear migration. Taken together, the results we report here suggest that Kem1p might have a previously unrecognized role at the G1 to S transition, but not through its exonuclease activity. Our findings also support the notion that Kem1p is a multifunctional protein with distinct and separable roles.

Indexed as

Cell Cycle ProteinsCell Nucleus DivisionCyclin BExoribonucleasesG1 PhaseMutant ProteinsProtein Structure, TertiaryRNA, MessengerRNA StabilitySaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsS PhaseCell Cycle ProteinsCLB2 protein, S cerevisiaeCyclin BExoribonucleasesMutant ProteinsRNA, MessengerSaccharomyces cerevisiae ProteinsXRN1 protein, S cerevisiae

Identifiers

PMID16240118
OpenAlexW2046837452

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.