Evidence map›Paper›PMID 18022394›Full record

ArticleFEBS letters2007

SIT4 regulation of Mig1p-mediated catabolite repression in Saccharomyces cerevisiae.

Can Jin, Antoni Barrientos, Charles B Epstein, Ronald A Butow, Alexander Tzagoloff

Open access · greenAbstract read
In one paragraph

Article in FEBS letters, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.4field-weighted citation impact, top 37% 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

10 citing papers in PubMed, 18 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

5 authors at 2 institutions in 1 country.

Can JinDepartment of Biological Sciences, Columbia University, New York, NY 10027, USA.
Antoni Barrientos
Charles B Epstein
Ronald A Butow
Alexander Tzagoloff
Columbia University · USThe University of Texas Southwestern Medical Center · US

Funding

ASSEMBLY OF MEMBRANES IN HEART AND YEAST MITOCHONDRIAR01HL022174 · NHLBI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI TZAGOLOFF, ALEXANDER A · 1985 to 2014
$3.3M
MAPPING NETWORKS OF GENE INTERACTIONS IN YEASTR01CA077811 · NCI · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI BUTOW, RONALD A · 1997 to 1999
–
NCI NIH HHS CA77811NHLBI NIH HHS HL2274NHLBI NIH HHS R01 HL022174
6 · The paper itself

Abstract

E153 is a respiratory deficient mutant of Saccharomyces cerevisiae with a mutation in the active site of the Sit4p protein phosphatase. Measurements of mitochondrial respiration and cytochromes indicate that the mutation suppresses glucose repression. The escape from catabolite repression is accompanied by a marked reduction of the transcriptional repressor Mig1p. The presence of normal levels of MIG1 mRNA in the mutant and its association with the polysome fraction suggests that depletion of Mig1p is the result of protein degradation. This study shows that in addition to phosphorylation by Snf1p, the transcriptional repressor activity of Mig1p is also regulated by a post-transcriptional Sit4p-dependent pathway. Our evidence suggests that this pathway involves turnover of Mig1p.

Indexed as

Gene Expression Regulation, FungalAllelesDNA-Binding ProteinsModels, BiologicalMutationPhenotypePhosphorylationProtein Phosphatase 2Protein Serine-Threonine KinasesRepressor ProteinsSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSignal TransductionDNA-Binding ProteinsISF1 protein, S cerevisiaeMIG1 protein, S cerevisiaeProtein Phosphatase 2Protein Serine-Threonine KinasesRepressor ProteinsSaccharomyces cerevisiae ProteinsSIT4 protein, S cerevisiaeSNF1-related protein kinases

Identifiers

PMID18022394
PMCPMC2247712
OpenAlexW2069430473

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.