File:Histone acetylation in regulating glial response after CNS injury.jpg
Jump to navigation
Jump to search
Size of this preview: 787 × 600 pixels. Other resolutions: 315 × 240 pixels | 630 × 480 pixels | 1,008 × 768 pixels | 1,026 × 782 pixels.
Original file (1,026 × 782 pixels, file size: 580 KB, MIME type: image/jpeg)
Captions
Captions
Add a one-line explanation of what this file represents
Summary
[edit]
| Description | Figure 3 Histone acetylation in regulating glial response after CNS (Central nervous system) injury. Top, depiction of timelines of activation of different immune cells and astroglia at the injury site after CNS injury. Bottom, in microglia/macrophages, HDAC inhibition reduces inflammation by enhancing anti-inflammatory/pro-repair phenotype and by inducing apoptosis through p53 and caspase. Different micro-RNAs also regulate inflammatory phenotypes of microglia/macrophage. HDAC inhibition by CI-994 suppresses neutrophil accumulation and reduces inflammatory cytokine expression. BETs are epigenetic readers of acetylated histones and promote transcription of inflammatory genes. BET inhibitor JQ1 reduced inflammatory cytokine expression and leukocyte recruitment to the injury site. In astrocytes, transcriptional module consisting of STAT3, p300 and Smad1 induces GFAP expression. HDAC inhibition reduces secretion of inflammatory cytokines, and increases neurotrophic cytokines from reactive astrocytes. |
| Date | |
| Source | https://www.researchgate.net/publication/334326677_Epigenetic_Regulation_Of_Axon_Regeneration_and_Glial_Activation_in_Injury_Responses Epigenetic Regulation of Axon Regeneration and Glial Activation in Injury Responses. Front. Genet. 10:640 Volume 10 - 2019 https://doi.org/10.3389/fgene.2019.00640 |
| Author | Wahane S, Halawani D, Zhou X and Zou H |
|
This file, which was originally posted to an external website, has not yet been reviewed by an administrator or reviewer to confirm that the above license is valid. See Category:License review needed for further instructions.
|
Copyright © 2019 Wahane, Halawani, Zhou and Zou. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
Licensing
[edit]
This file is licensed under the Creative Commons Attribution 4.0 International license.
- You are free:
- to share – to copy, distribute and transmit the work
- to remix – to adapt the work
- Under the following conditions:
- attribution – You must give appropriate credit, provide a link to the license, and indicate if changes were made. You may do so in any reasonable manner, but not in any way that suggests the licensor endorses you or your use.
File history
Click on a date/time to view the file as it appeared at that time.
| Date/Time | Thumbnail | Dimensions | User | Comment | |
|---|---|---|---|---|---|
| current | 14:35, 22 May 2024 | | 1,026 × 782 (580 KB) | Rasbak (talk | contribs) | {{Information |description= Figure 3 Histone acetylation in regulating glial response after CNS (Central nervous system) injury. Top, depiction of timelines of activation of different immune cells and astroglia at the injury site after CNS injury. Bottom, in microglia/macrophages, HDAC inhibition reduces inflammation by enhancing anti-inflammatory/pro-repair phenotype and by inducing apoptosis through p53 and caspase. Different micro-RNAs also regulate inflammatory phenotypes of microglia/mac... |
You cannot overwrite this file.
File usage on Commons
There are no pages that use this file.
