| Gene symbol |
Species |
Enzyme |
Editing site(s) |
Editing Type |
PMID |
RADAR |
REDIportal |
Description |
| AZIN1 |
Human |
ADAR1;ADAR2 |
2 |
A-to-I |
|
|
|
The edited AZIN1 promotes cell proliferation and possibly the Hepatocellular Carcinoma onset and progression. The wild-type AZIN1 could promote the tumorigenicity, the edited AZIN1 conferred gain-of-function phenotypes that were manifested by more aggressive behaviors during Esophageal Squamous Cell Carcinoma progression. |
| FLNB |
Human |
ADAR1;ADAR2 |
1 |
A-to-I |
|
|
|
In the Hepatocellular Carcinoma samples and Esophageal Squamous Cell Carcinoma samples, FLNB demonstrate a higher editing level compare to the normal sample. |
| COPA |
Human |
ADAR1;ADAR2 |
1 |
A-to-I |
|
|
|
The hyper-editing of COPA are closely associated with hepatocellular carcinoma pathogenesis. And in the hepatocellular carcinoma samples, COPA editing level is significantly lower than normal samples. The previous study has identified two RNA-editing sites at codon 164 (Ile-Val) of the COPA gene. |
| IGFBP7 |
Human |
ADAR1;ADAR2 |
3 |
A-to-I |
|
|
|
RNA editing in IGFBP7 promotes cell apoptosis in the tumor, but the inadequate A-to-I editing of IGFBP7 may be used by tumor cells to escape the cellular control of proliferation. |
| SLC22A3 |
Human |
ADAR2 |
1 |
A-to-I |
|
|
|
A-to-I RNA editing may decrease the stability of SLC22A3 in familial cases, deregulated SLC22A3 Is an Early Risk Factor for Progression of Familial ESCC. |
EDK
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