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The Cell Surface Protein Ecm33 Is Involved in Negative Feedback Regulation of MAP Kinase Signalling and Development of the In Vivo Real-time Monitoring of MAP Kinase Signalling

Overview of attention for article published in Yakugaku Zasshi = Journal of Pharmaceutical Society of Japan, August 2011
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Title
The Cell Surface Protein Ecm33 Is Involved in Negative Feedback Regulation of MAP Kinase Signalling and Development of the In Vivo Real-time Monitoring of MAP Kinase Signalling
Published in
Yakugaku Zasshi = Journal of Pharmaceutical Society of Japan, August 2011
DOI 10.1248/yakushi.131.1195
Pubmed ID
Authors

Hirofumi Takada

Abstract

The mitogen-activated protein kinase (MAPK) pathways are signal transduction mechanisms that regulate many cellular processes in eukaryotic organisms, from yeasts to mammals. Multiple MAPKs regulate eukaryotic gene expression in response to various extracellular stimuli through phosphorylation of transcription factors. We have been studying the Pmk1 MAPK, a homologue of the mammalian ERK/MAPK in fission yeast. The Pmk1 MAPK regulates cell integrity and cell morphology. We have previously demonstrated that Atf1, a transcription factor downstream of the stress-activated MAPK pathway, serves also as a target of the Pmk1 MAPK signaling in fission yeast. Here, we identified ecm33⁺ gene, encoding a glycosyl-phosphatidylinositol (GPI)-anchored cell surface protein as a transcriptional target of Pmk1 and Atf1. The gene expression of ecm33⁺ is regulated by two transcription factors Atf1 and Mbx1. We also developed an in vivo real-time monitoring system of Atf1 or Mbx1 transcriptional activity, which enables to monitor the activation of the Pmk1 MAPK pathway by various stimuli. Finally, we demonstrated that Ecm33 is involved in the negative regulation of the Pmk1 MAPK signaling through the control of Ca²⁺ homeostasis. The ecm33 deleted cells displayed Ca²⁺ sensitivity and increased phosphorylation levels of Pmk1 MAPK. In addition, the Ecm33 overproducing cells displayed phenotypes closely similar to those of the pmk1 knockout cell. Collectively, Ecm33 plays a role in the negative feedback regulation of Pmk1 cell integrity signaling.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 7 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 7 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 4 57%
Unknown 3 43%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 1 14%
Agricultural and Biological Sciences 1 14%
Immunology and Microbiology 1 14%
Unknown 4 57%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 2. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 14 April 2014.
All research outputs
#16,375,964
of 25,850,671 outputs
Outputs from Yakugaku Zasshi = Journal of Pharmaceutical Society of Japan
#1,363
of 1,969 outputs
Outputs of similar age
#90,040
of 131,406 outputs
Outputs of similar age from Yakugaku Zasshi = Journal of Pharmaceutical Society of Japan
#8
of 16 outputs
Altmetric has tracked 25,850,671 research outputs across all sources so far. This one is in the 34th percentile – i.e., 34% of other outputs scored the same or lower than it.
So far Altmetric has tracked 1,969 research outputs from this source. They receive a mean Attention Score of 3.4. This one is in the 29th percentile – i.e., 29% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 131,406 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 29th percentile – i.e., 29% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 16 others from the same source and published within six weeks on either side of this one. This one has gotten more attention than average, scoring higher than 50% of its contemporaries.