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Mutant huntingtin induces iron overload via up-regulating IRP1 in Huntington’s disease

Overview of attention for article published in Cell & Bioscience, July 2018
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Title
Mutant huntingtin induces iron overload via up-regulating IRP1 in Huntington’s disease
Published in
Cell & Bioscience, July 2018
DOI 10.1186/s13578-018-0239-x
Pubmed ID
Authors

Li Niu, Cuifang Ye, Yun Sun, Ting Peng, Shiming Yang, Weixi Wang, He Li

Abstract

Iron accumulation in basal ganglia accompanies neuronal loss in Huntington's disease (HD) patients and mouse disease models. Disruption of HD brain iron homeostasis occurs before the onset of clinical signs. Therefore, investigating the mechanism of iron accumulation is essential to understanding its role in disease pathogenesis. N171-82Q HD transgenic mice brain iron was detected by using Diaminobenzidine-enhanced Perls' stain. Iron homeostatic proteins including iron response protein 1 (IRP1), transferrin (Tf), ferritin and transferrin receptor (TfR) were determined by using western blotting and immunohistochemistry, and their relative expression levels of RNA were measured by RT-PCR in both N171-82Q HD transgenic mice and HEK293 cells expressing N-terminal of huntingtin. Iron was increased in striatum and cortex of N171-82Q HD transgenic mice. Analysis of iron homeostatic proteins revealed increased expression of IRP1, Tf, ferritin and TfR in N171-82Q mice striatum and cortex. The same results were obtained in HEK293 cells expressing N-terminal of mutant huntingtin containing 160 CAG repeats. We conclude that mutant huntingtin may cause abnormal iron homeostatic pathways by increasing IRP1 expression in Huntington's disease, suggesting potential therapeutic target.

Twitter Demographics

The data shown below were collected from the profile of 1 tweeter 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 26 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 26 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 7 27%
Student > Bachelor 4 15%
Student > Master 4 15%
Researcher 3 12%
Other 1 4%
Other 2 8%
Unknown 5 19%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 6 23%
Medicine and Dentistry 4 15%
Neuroscience 4 15%
Social Sciences 2 8%
Pharmacology, Toxicology and Pharmaceutical Science 2 8%
Other 2 8%
Unknown 6 23%

Attention Score in Context

This research output has an Altmetric Attention Score of 1. 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 05 July 2018.
All research outputs
#10,504,638
of 13,184,150 outputs
Outputs from Cell & Bioscience
#185
of 311 outputs
Outputs of similar age
#199,752
of 267,449 outputs
Outputs of similar age from Cell & Bioscience
#2
of 5 outputs
Altmetric has tracked 13,184,150 research outputs across all sources so far. This one is in the 11th percentile – i.e., 11% of other outputs scored the same or lower than it.
So far Altmetric has tracked 311 research outputs from this source. They receive a mean Attention Score of 2.1. This one is in the 11th percentile – i.e., 11% 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 267,449 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 13th percentile – i.e., 13% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 5 others from the same source and published within six weeks on either side of this one. This one has scored higher than 3 of them.