General Information of the m6A Target Gene (ID: M6ATAR00232)
Target Name Dual specificity protein phosphatase 2 (DUSP2)
Synonyms
Dual specificity protein phosphatase PAC-1; PAC1
    Click to Show/Hide
Gene Name DUSP2
Chromosomal Location 2q11.2
Family protein-tyrosine phosphatase family; Non-receptor class dual specificity subfamily
Function
Regulates mitogenic signal transduction by dephosphorylating both Thr and Tyr residues on MAP kinases ERK1 and ERK2.
    Click to Show/Hide
Gene ID 1844
Uniprot ID
DUS2_HUMAN
HGNC ID
HGNC:3068
Ensembl Gene ID
ENSG00000158050
KEGG ID
hsa:1844
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
DUSP2 can be regulated by the following regulator(s), and cause disease/drug response(s). You can browse detail information of regulator(s) or disease/drug response(s).
Browse Regulator
Browse Disease
Methyltransferase-like 3 (METTL3) [WRITER]
Representative RNA-seq result indicating the expression of this target gene regulated by METTL3
Cell Line Caco-2 cell line Homo sapiens
Treatment: shMETTL3 Caco-2 cells
Control: shNTC Caco-2 cells
GSE167075
Regulation
logFC: 7.70E-01
p-value: 1.05E-14
More Results Click to View More RNA-seq Results
In total 1 item(s) under this regulator
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene [1]
Response Summary METTL3-mediated formation of EV miR-93, facilitated by m6A, is implicated in the aberrant cross-talk of epithelium-macrophages, indicating that this process is involved in the smoking-related emphysema. EV miR-93 was used as a novel risk biomarker for CS-induced emphysema. MiR-93 activated the JNK pathway by targeting Dual specificity protein phosphatase 2 (DUSP2), which elevated the levels of matrix metalloproteinase 9 (MMP9) and matrix metalloproteinase 12 (MMP12) and induced elastin degradation, leading to emphysema.
Target Regulation Down regulation
Responsed Disease Emphysema ICD-11: CA21
Pathway Response MAPK signaling pathway hsa04010
Emphysema [ICD-11: CA21]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [1]
Response Summary METTL3-mediated formation of EV miR-93, facilitated by m6A, is implicated in the aberrant cross-talk of epithelium-macrophages, indicating that this process is involved in the smoking-related emphysema. EV miR-93 was used as a novel risk biomarker for CS-induced emphysema. MiR-93 activated the JNK pathway by targeting Dual specificity protein phosphatase 2 (DUSP2), which elevated the levels of matrix metalloproteinase 9 (MMP9) and matrix metalloproteinase 12 (MMP12) and induced elastin degradation, leading to emphysema.
Responsed Disease Emphysema [ICD-11: CA21]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
Target Regulation Down regulation
Pathway Response MAPK signaling pathway hsa04010
References
Ref 1 The aberrant cross-talk of epithelium-macrophages via METTL3-regulated extracellular vesicle miR-93 in smoking-induced emphysema. Cell Biol Toxicol. 2022 Feb;38(1):167-183. doi: 10.1007/s10565-021-09585-1. Epub 2021 Mar 4.