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Pin1 promotes neuronal death in stroke by stabilizing Notch intracellular domain

Overview of attention for article published in Annals of Neurology, February 2015
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  • Above-average Attention Score compared to outputs of the same age (63rd percentile)
  • Average Attention Score compared to outputs of the same age and source

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2 Facebook pages

Citations

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30 Dimensions

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32 Mendeley
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Title
Pin1 promotes neuronal death in stroke by stabilizing Notch intracellular domain
Published in
Annals of Neurology, February 2015
DOI 10.1002/ana.24347
Pubmed ID
Authors

Sang-Ha Baik, Mitchell Fane, Joon Hyung Park, Yi-Lin Cheng, David Yang-Wei Fann, Ui Jeong Yun, Yuri Choi, Jong-Sung Park, Bing Han Chai, Jin Su Park, Seung Hyun Back, Jae In Jeong, Ye Jin Jang, Gahee Bahn, Joo-Yong Lee, Yu-I Li, Christopher G. Sobey, Takafumi Uchida, Jae Hyung Park, Hong Tae Kim, Sung-Chun Tang, Thiruma V. Arumugam, Dong-Gyu Jo

Abstract

Objective: Stroke is a leading cause of mortality and disability. The peptidyl-prolyl cis/trans isomerase Pin1 regulates factors involved in cell growth. Recent evidence has shown that Pin1 plays a major role in apoptosis. However the role of Pin1 in ischemic stroke remains to be investigated. Methods: We used Pin1 overexpression and knockdown to manipulate Pin1 expression and explore the effects of Pin1 in cell death on ischemic stress in vitro and in a mouse stroke model. We also used Pin 1 inhibitor, γ-secretase inhibitor, NICD1 domain-deleted mutant cells and Pin1 mutant cells to investigate the underlying mechanisms of Pin1-NICD1 mediated cell death. Results: Our findings indicate that Pin1 facilitates NICD1 stability and its pro-apoptotic function following ischemic stroke. Thus, overexpression of Pin1 increased NICD1 levels and enhanced its potentiation of neuronal death in simulated ischemia. By contrast, depletion or knockout of Pin1 reduced the NICD1 level, which in turn desensitized neurons to ischemic conditions. Pin1 interacted with NICD1 and increased its stability by inhibiting FBW7-induced poly-ubiquitination. We also demonstrate that Pin1 and NICD1 levels increase following stroke. Pin1 heterozygote (+/-) and knockout (-/-) mice, and also wild-type mice treated with an inhibitor of Pin1, each showed reduced brain damage and improved functional outcomes in a model of focal ischemic stroke. Interpretation: These results suggest that Pin1 contributes to the pathogenesis of ischemic stroke by promoting Notch signaling, and that inhibition of Pin1 is a novel approach for treating ischemic stroke. This article is protected by copyright. All rights reserved.

Twitter Demographics

The data shown below were collected from the profiles of 4 tweeters who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 32 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Brazil 1 3%
Unknown 31 97%

Demographic breakdown

Readers by professional status Count As %
Unspecified 6 19%
Student > Ph. D. Student 6 19%
Student > Bachelor 5 16%
Researcher 3 9%
Student > Master 3 9%
Other 9 28%
Readers by discipline Count As %
Agricultural and Biological Sciences 11 34%
Unspecified 6 19%
Biochemistry, Genetics and Molecular Biology 6 19%
Neuroscience 3 9%
Medicine and Dentistry 2 6%
Other 4 13%

Attention Score in Context

This research output has an Altmetric Attention Score of 3. 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 07 January 2015.
All research outputs
#6,383,551
of 12,176,469 outputs
Outputs from Annals of Neurology
#2,985
of 3,792 outputs
Outputs of similar age
#99,603
of 275,139 outputs
Outputs of similar age from Annals of Neurology
#41
of 73 outputs
Altmetric has tracked 12,176,469 research outputs across all sources so far. This one is in the 47th percentile – i.e., 47% of other outputs scored the same or lower than it.
So far Altmetric has tracked 3,792 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 10.8. This one is in the 21st percentile – i.e., 21% 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 275,139 tracked outputs that were published within six weeks on either side of this one in any source. This one has gotten more attention than average, scoring higher than 63% of its contemporaries.
We're also able to compare this research output to 73 others from the same source and published within six weeks on either side of this one. This one is in the 42nd percentile – i.e., 42% of its contemporaries scored the same or lower than it.