Evidence map›Paper›PMID 29118074›Full record

ArticleMolecular biology of the cell2018

Golgi stress-induced transcriptional changes mediated by MAPK signaling and three ETS transcription factors regulate MCL1 splicing.

Jan Baumann, Tatiana I Ignashkova, Sridhar R Chirasani, Silvia Ramírez-Peinado, Hamed Alborzinia, Mathieu Gendarme, Kyra Kuhnigk, Valentin Kramer, Ralph K Lindemann, Jan H Reiling

Abstract read
In one paragraph

Article in Molecular biology of the cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

23 citing papers in PubMed, 38 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

10 authors at 2 institutions in 1 country.

Jan BaumannBioMed X Innovation Center, 69120 Heidelberg, Germany.
Tatiana I IgnashkovaBioMed X Innovation Center, 69120 Heidelberg, Germany.
Sridhar R ChirasaniBioMed X Innovation Center, 69120 Heidelberg, Germany.
Silvia Ramírez-PeinadoBioMed X Innovation Center, 69120 Heidelberg, Germany.
Hamed AlborziniaBioMed X Innovation Center, 69120 Heidelberg, Germany.
Mathieu GendarmeBioMed X Innovation Center, 69120 Heidelberg, Germany.
Kyra KuhnigkBioMed X Innovation Center, 69120 Heidelberg, Germany.
Valentin KramerBioMed X Innovation Center, 69120 Heidelberg, Germany.
Ralph K LindemannTranslational Innovation Platform Oncology, Merck Biopharma, Merck KGaA, 64293 Darmstadt, Germany.
Jan H ReilingBioMed X Innovation Center, 69120 Heidelberg, Germany reiling@bio.mx.
BioMed X Institute · DEMerck (Germany) · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The secretory pathway is a major determinant of cellular homoeostasis. While research into secretory stress signaling has so far mostly focused on the endoplasmic reticulum (ER), emerging data suggest that the Golgi itself serves as an important signaling hub capable of initiating stress responses. To systematically identify novel Golgi stress mediators, we performed a transcriptomic analysis of cells exposed to three different pharmacological compounds known to elicit Golgi fragmentation: brefeldin A, golgicide A, and monensin. Subsequent gene-set enrichment analysis revealed a significant contribution of the ETS family transcription factors ELK1, GABPA/B, and ETS1 to the control of gene expression following compound treatment. Induction of Golgi stress leads to a late activation of the ETS upstream kinases MEK1/2 and ERK1/2, resulting in enhanced ETS factor activity and the transcription of ETS family target genes related to spliceosome function and cell death induction via alternate MCL1 splicing. Further genetic analyses using loss-of-function and gain-of-function experiments suggest that these transcription factors operate in parallel.

Indexed as

MAP Kinase Signaling SystemStress, PhysiologicalTranscription, GeneticA549 CellsAlternative SplicingApoptosisBrefeldin ACytoprotectionGene Expression ProfilingGene Knockdown TechniquesGolgi ApparatusHEK293 CellsHeLa CellsHumansMitogen-Activated Protein KinasesMonensinBrefeldin Agolgicide AMitogen-Activated Protein KinasesMonensinMyeloid Cell Leukemia Sequence 1 ProteinProto-Oncogene Proteins c-etsPyridinesQuinolinesSmall Molecule Libraries

Identifiers

PMID29118074
PMCPMC5746065
OpenAlexW2767756546

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.