File:Inputs and outputs of KEAP1 NRF2 pathway.jpg
Size of this preview: 741 × 600 pixels. Other resolutions: 297 × 240 pixels | 593 × 480 pixels | 949 × 768 pixels | 1,265 × 1,024 pixels | 2,530 × 2,048 pixels | 2,627 × 2,127 pixels.
Original file (2,627 × 2,127 pixels, file size: 514 KB, MIME type: image/jpeg)
 | This is a file from the Wikimedia Commons. Information from its description page there is shown below. Commons is a freely licensed media file repository. You can help. |
 | This image was uploaded in the JPEG format even though it consists of non-photographic data. This information could be stored more efficiently or accurately in the PNG or SVG format. If possible, please upload a PNG or SVG version of this image without compression artifacts, derived from a non-JPEG source (or with existing artifacts removed). After doing so, please tag the JPEG version with {{Superseded|NewImage.ext}} and remove this tag. This tag should not be applied to photographs or scans. If this image is a diagram or other image suitable for vectorisation, please tag this image with {{Convert to SVG}} instead of {{BadJPEG}}. If not suitable for vectorisation, use {{Convert to PNG}}. For more information, see {{BadJPEG}}. |  |
Summary
| Description |
English: Figure 3 The major activating inputs and functional outputs of the NRF2 pathway. NRF2 is activated in response to oxidative stress, metabolic stress, and various oncogenic stress signals upstream. NRF2 is a pleiotropic transcription factor that induces the expression of a plethora of downstream target genes. Highlighted are some of the most well-studied functional outputs of the NRF2 pathway. Glutathione (GSR, GCLC, GCLM, GPX2, and SLC7A11), multidrug resistance–associated proteins (ABCC1 and ABCC2), and thioredoxin (TXN1, PRDX1, TXNRD1, and SRXN1) metabolism proteins mediate detoxification of ROS, drugs, and toxins (see Table 1). The glucose-dependent pentose phosphate pathway enzymes G6PD and PGD and the central carbon metabolism enzymes ME1 and IDH1 increase the reducing capacity of cells by regenerating NADPH. Heme degradation by HMOX1 and iron sequestration by FTL1 and FTH1 maintain heme and iron homeostasis, preventing iron accumulation and ferroptosis. |
| Date | |
| Source | https://www.annualreviews.org/doi/full/10.1146/annurev-cancerbio-030518-055627 |
| Author | Warren L. Wu and Thales Papagiannakopoulos |
Licensing
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 | 21:21, 12 September 2020 | | 2,627 × 2,127 (514 KB) | Elysia (AR) | Uploaded a work by Warren L. Wu and Thales Papagiannakopoulos from https://www.annualreviews.org/doi/full/10.1146/annurev-cancerbio-030518-055627 with UploadWizard |
File usage
The following pages on the English Wikipedia use this file (pages on other projects are not listed):
