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Looking downstream: the role of cyclic AMP-regulated genes in axonal regeneration

Overview of attention for article published in Frontiers in Molecular Neuroscience, June 2015
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Title
Looking downstream: the role of cyclic AMP-regulated genes in axonal regeneration
Published in
Frontiers in Molecular Neuroscience, June 2015
DOI 10.3389/fnmol.2015.00026
Pubmed ID
Authors

Mustafa M. Siddiq, Sari S. Hannila

Abstract

Elevation of intracellular cyclic AMP (cAMP) levels has proven to be one of the most effective means of overcoming inhibition of axonal regeneration by myelin-associated inhibitors such as myelin-associated glycoprotein (MAG), Nogo, and oligodendrocyte myelin glycoprotein. Pharmacological manipulation of cAMP through the administration of dibutyryl cAMP or rolipram leads to enhanced axonal growth both in vivo and in vitro, and importantly, upregulation of cAMP within dorsal root ganglion neurons is responsible for the conditioning lesion effect, which indicates that cAMP plays a significant role in the endogenous mechanisms that promote axonal regeneration. The effects of cAMP are transcription-dependent and are mediated through the activation of protein kinase A (PKA) and the transcription factor cyclic AMP response element binding protein (CREB). This leads to the induction of a variety of genes, several of which have been shown to overcome myelin-mediated inhibition in their own right. In this review, we will highlight the pro-regenerative effects of arginase I (ArgI), interleukin (IL)-6, secretory leukocyte protease inhibitor (SLPI), and metallothionein (MT)-I/II, and discuss their potential for therapeutic use in spinal cord injury.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 51 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 51 100%

Demographic breakdown

Readers by professional status Count As %
Student > Master 10 20%
Student > Ph. D. Student 9 18%
Researcher 8 16%
Student > Bachelor 3 6%
Professor > Associate Professor 3 6%
Other 6 12%
Unknown 12 24%
Readers by discipline Count As %
Agricultural and Biological Sciences 12 24%
Neuroscience 8 16%
Biochemistry, Genetics and Molecular Biology 6 12%
Medicine and Dentistry 4 8%
Nursing and Health Professions 2 4%
Other 4 8%
Unknown 15 29%
Attention Score in Context

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 03 June 2015.
All research outputs
#19,944,091
of 25,373,627 outputs
Outputs from Frontiers in Molecular Neuroscience
#2,384
of 3,335 outputs
Outputs of similar age
#189,861
of 278,171 outputs
Outputs of similar age from Frontiers in Molecular Neuroscience
#18
of 26 outputs
Altmetric has tracked 25,373,627 research outputs across all sources so far. This one is in the 18th percentile – i.e., 18% of other outputs scored the same or lower than it.
So far Altmetric has tracked 3,335 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 6.2. 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 278,171 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 26th percentile – i.e., 26% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 26 others from the same source and published within six weeks on either side of this one. This one is in the 23rd percentile – i.e., 23% of its contemporaries scored the same or lower than it.