Evidence map›Paper›PMID 25348718›Full record

ArticleMolecular and cellular biology2015

A novel role for protein kinase Kin2 in regulating HAC1 mRNA translocation, splicing, and translation.

Ashish Anshu, M Amin-Ul Mannan, Abhijit Chakraborty, Saikat Chakrabarti, Madhusudan Dey

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

15 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Detection of HAC1 mRNA Splicing by RT-PCR in Saccharomyces cerevisiae.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
  6. Vps34 and TOR Kinases CoordinateMolecular and cellular biology · 2021
    Article
  7. Article
  8. Article
  9. Translation Control ofInternational journal of molecular sciences · 2019
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. 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

5 authors at 2 institutions in 2 countries.

Ashish AnshuDepartment of Biological Sciences, University of Wisconsin-Milwaukee, Milwaukee, Wisconsin, USA.
M Amin-Ul MannanDepartment of Biological Sciences, University of Wisconsin-Milwaukee, Milwaukee, Wisconsin, USA.
Abhijit ChakrabortyCSIR-Indian Institute of Chemical Biology, Kolkata, India.
Saikat ChakrabartiCSIR-Indian Institute of Chemical Biology, Kolkata, India.
Madhusudan DeyDepartment of Biological Sciences, University of Wisconsin-Milwaukee, Milwaukee, Wisconsin, USA deym@uwm.edu.
University of Wisconsin–Milwaukee · USIndian Institute of Chemical Biology · IN

Funding

Regulating the Unfolded Protein Response in YeastR01GM124183 · NIGMS · UNIVERSITY OF WISCONSIN MILWAUKEE · PI DEY, MADHUSUDAN · 2017 to 2020
$1.3M
NIGMS NIH HHS R01 GM124183
6 · The paper itself

Abstract

A signaling network called the unfolded protein response (UPR) resolves the protein-folding defects in the endoplasmic reticulum (ER) from yeasts to humans. In the yeast Saccharomyces cerevisiae, the UPR activation involves (i) aggregation of the ER-resident kinase/RNase Ire1 to form an Ire1 focus, (ii) targeting HAC1 pre-mRNA toward the Ire1 focus that cleaves out an inhibitory intron from the mRNA, and (iii) translation of Hac1 protein from the spliced mRNA. Targeting HAC1 mRNA to the Ire1 focus requires a cis-acting bipartite element (3'BE) located at the 3' untranslated leader. Here, we report that the 3'BE plays an additional role in promoting translation from the spliced mRNA. We also report that a high dose of either of two paralogue kinases, Kin1 and Kin2, overcomes the defective UPR caused by a mutation in the 3'BE. These results define a novel role for Kin kinases in the UPR beyond their role in cell polarity and exocytosis. Consistently, targeting, splicing, and translation of HAC1 mRNA are substantially reduced in the kin1Δ kin2Δ strain. Furthermore, we show that Kin2 kinase domain itself is sufficient to activate the UPR, suggesting that Kin2 initiates a signaling cascade to ensure an optimum UPR.

Indexed as

Gene Expression Regulation, FungalRNA Splicing3' Untranslated RegionsBasic-Leucine Zipper Transcription FactorsCytoplasmExocytosisGreen Fluorescent ProteinsMembrane GlycoproteinsMembrane ProteinsMicroscopy, ConfocalOpen Reading FramesProtein BiosynthesisProtein Serine-Threonine KinasesProtein Structure, TertiaryProtein TransportRepressor Proteins3' Untranslated RegionsBasic-Leucine Zipper Transcription FactorsGreen Fluorescent ProteinsHAC1 protein, S cerevisiaeIRE1 protein, S cerevisiaeKIN1 protein, S cerevisiaeKIN2 protein, S cerevisiaeMembrane GlycoproteinsMembrane ProteinsProtein Serine-Threonine KinasesRepressor ProteinsRNA, MessengerSaccharomyces cerevisiae Proteins

Identifiers

PMID25348718
PMCPMC4295377
OpenAlexW2137553372

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.