m6A Target Gene Information
General Information of the m6A Target Gene (ID: M6ATAR00648)
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
TIMP2
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).
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Methyltransferase-like 3 (METTL3) [WRITER]
| Representative RNA-seq result indicating the expression of this target gene regulated by METTL3 | ||
| Cell Line | LX2 cell line | Homo sapiens |
|
Treatment: shMETTL3 LX2 cells
Control: shLuc LX2 cells
|
GSE207909 | |
| Regulation |
  |
logFC: 6.36E-01 p-value: 3.68E-18 |
| More Results | Click to View More RNA-seq Results | |
| Representative RIP-seq result supporting the interaction between TIMP2 and the regulator | ||
| Cell Line | MDA-MB-231 | Homo sapiens |
| Regulation | logFC: 1.22E+00 | GSE60213 |
| In total 2 item(s) under this regulator | ||||
| Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene | [1] | |||
| Response Summary | METTL3 is involved in OA probably by regulating the inflammatory response. METTL3 overexpression affects extracellular matrix degradation in OA by adjusting the balance between Metalloproteinase inhibitor 2 (TIMP2) and MMPs. | |||
| Target Regulation | Down regulation | |||
| Responsed Disease | Osteoarthritis | ICD-11: FA05 | ||
| Cell Process | Inflammatory response | |||
| In-vitro Model | SW1353 | Primary central chondrosarcoma | Homo sapiens | CVCL_0543 |
| Experiment 2 Reporting the m6A Methylation Regulator of This Target Gene | [2] | |||
| Response Summary | METTL3 modulated Notch signaling via the m6A modification of Metalloproteinase inhibitor 2 (TIMP2) in IGF2BP2-dependent manner and exerted pro-inflammatory and pro-apoptotic effects. This study suggested that METTL3-mediated m6A modification is an important mechanism of podocyte injury in DN. | |||
| Target Regulation | Up regulation | |||
| Responsed Disease | Chronic kidney disease | ICD-11: GB61.Z | ||
| Pathway Response | Notch signaling pathway | hsa04330 | ||
| In-vitro Model | MPC-5 | Normal | Mus musculus | CVCL_AS87 |
| In-vivo Model | After 7 days of acclimatization, STZ, dissolved in 0.1 M citrate buffer, was intraperitoneally administered daily to mice at a dose of 50 mg/kg after 12 h of food deprivation each day for 5 consecutive days. The type 1 mice diabetic mice were randomly separated into four groups (n = 5-8): AAV9-scramble-control group; AAV9-scramble-STZ; AAV9-shRNA-control; and AAV9-shRNA-STZ group (Hanbio Biotechnology, China). The 50 UL titer of 1 × 1012 virus was injected into the renal pelvis using an insulin needle and maintained there for 2 to 3 s. The type 2 diabetic mice were randomly separated into four groups (n = 5-8): AAV9-scramble-db/m group; AAV9-scramble-db/db group; AAV9-shRNA-db/m group; and AAV9-shRNA-db/db group (Hanbio Biotechnology, China). The 100 UL titer of 1 × 1012 virus was injected into the tail vein using an insulin needle and maintained there for 2 to 3 s. Blood glucose was monitored weekly in mice. At the end of 12 weeks, the 24-h urine samples were collected from the mice kept in metabolic cages. | |||
Osteoarthritis [ICD-11: FA05]
| In total 1 item(s) under this disease | ||||
| Experiment 1 Reporting the m6A-centered Disease Response | [1] | |||
| Response Summary | METTL3 is involved in OA probably by regulating the inflammatory response. METTL3 overexpression affects extracellular matrix degradation in OA by adjusting the balance between Metalloproteinase inhibitor 2 (TIMP2) and MMPs. | |||
| Responsed Disease | Osteoarthritis [ICD-11: FA05] | |||
| Target Regulator | Methyltransferase-like 3 (METTL3) | WRITER | ||
| Target Regulation | Down regulation | |||
| Cell Process | Inflammatory response | |||
| In-vitro Model | SW1353 | Primary central chondrosarcoma | Homo sapiens | CVCL_0543 |
Chronic kidney disease [ICD-11: GB61]
| In total 1 item(s) under this disease | ||||
| Experiment 1 Reporting the m6A-centered Disease Response | [2] | |||
| Response Summary | METTL3 modulated Notch signaling via the m6A modification of Metalloproteinase inhibitor 2 (TIMP2) in IGF2BP2-dependent manner and exerted pro-inflammatory and pro-apoptotic effects. This study suggested that METTL3-mediated m6A modification is an important mechanism of podocyte injury in DN. | |||
| Responsed Disease | Chronic kidney disease [ICD-11: GB61.Z] | |||
| Target Regulator | Methyltransferase-like 3 (METTL3) | WRITER | ||
| Target Regulation | Up regulation | |||
| Pathway Response | Notch signaling pathway | hsa04330 | ||
| In-vitro Model | MPC-5 | Normal | Mus musculus | CVCL_AS87 |
| In-vivo Model | After 7 days of acclimatization, STZ, dissolved in 0.1 M citrate buffer, was intraperitoneally administered daily to mice at a dose of 50 mg/kg after 12 h of food deprivation each day for 5 consecutive days. The type 1 mice diabetic mice were randomly separated into four groups (n = 5-8): AAV9-scramble-control group; AAV9-scramble-STZ; AAV9-shRNA-control; and AAV9-shRNA-STZ group (Hanbio Biotechnology, China). The 50 UL titer of 1 × 1012 virus was injected into the renal pelvis using an insulin needle and maintained there for 2 to 3 s. The type 2 diabetic mice were randomly separated into four groups (n = 5-8): AAV9-scramble-db/m group; AAV9-scramble-db/db group; AAV9-shRNA-db/m group; and AAV9-shRNA-db/db group (Hanbio Biotechnology, China). The 100 UL titer of 1 × 1012 virus was injected into the tail vein using an insulin needle and maintained there for 2 to 3 s. Blood glucose was monitored weekly in mice. At the end of 12 weeks, the 24-h urine samples were collected from the mice kept in metabolic cages. | |||
References