m6A Target Gene Information

General Information of the m6A Target Gene (ID: M6ATAR00785)
Target Name microRNA 150 (MIR150)
Synonyms
hsa-mir-150; MIRN150
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Gene Name MIR150
Chromosomal Location 19q13.33
Family MicroRNA MIRLET7 family
Gene ID 406942
HGNC ID
HGNC:31537
miRBase ID
MI0000479
Ensembl Gene ID
ENSG00000207782
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
MIR150 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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Browse Disease
Methyltransferase-like 3 (METTL3) [WRITER]
 Regulator Info 
In total 1 item(s) under this regulator
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene [1]
Response Summary Enhanced METTL3 promoted the m6A methylation in total RNAs and inhibited neuropathic pain (NP) progression. Mechanistically, METTL3 accelerated microRNA 150 (MIR150) maturation via mediating m6A methylation of primiR-150 at locus 498, cooperating with the "m6A reader" YTHDF2. Therefore, the METTL3/miR-150/BDNF pathway is a promising therapeutic target for NP patients.
Target Regulation Up regulation
Responsed Disease Neuropathic Pain ICD-11: 8E43.0
 Disease Info 
In-vitro Model RN-sc (The rat neuron cell line RN-sc was purchased from ScienCell (ScienCell Research Laboratories Inc. catlog. #R1590, Carlsbad, CA).)
In-vivo Model Based on our study design, the enrolled animals were blindingly grouped and received the following treatments: (1)Sham-NC vectors, (2)Sham-sh-METTL3, (3)Sham-sh-METTL3 + miR-150, (4)Sham-sh-METTL3 + Lv-YTHDF2, (5)Sham-sh-METTL3 + sh-BDNF, (6)Sham-anti-miR150, (7)Sham-anti-miR150+sh-BDNF, (8)SNI-Lv-METTL3, (9)SNI-Lv-METTL3 + anti-miR-150, (10)SNI-Lv-METTL3 + sh-YTHDF2, (11)SNI-Lv-METTL3 + Lv-BDNF, (12)SNI-miR150, (13)SNI-miR150+Lv-BDNF. The pain behaviors were detected in the respective time points and the expressions of METTL3 and miR-150 were determined at day 14 after the rats were sacrificed.
Pain disorders [ICD-11: 8E43]
 Disease Info 
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [1]
Response Summary Enhanced METTL3 promoted the m6A methylation in total RNAs and inhibited neuropathic pain (NP) progression. Mechanistically, METTL3 accelerated microRNA 150 (MIR150) maturation via mediating m6A methylation of primiR-150 at locus 498, cooperating with the "m6A reader" YTHDF2. Therefore, the METTL3/miR-150/BDNF pathway is a promising therapeutic target for NP patients.
Responsed Disease Neuropathic Pain [ICD-11: 8E43.0]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
 Regulator Info 
Target Regulation Up regulation
In-vitro Model RN-sc (The rat neuron cell line RN-sc was purchased from ScienCell (ScienCell Research Laboratories Inc. catlog. #R1590, Carlsbad, CA).)
In-vivo Model Based on our study design, the enrolled animals were blindingly grouped and received the following treatments: (1)Sham-NC vectors, (2)Sham-sh-METTL3, (3)Sham-sh-METTL3 + miR-150, (4)Sham-sh-METTL3 + Lv-YTHDF2, (5)Sham-sh-METTL3 + sh-BDNF, (6)Sham-anti-miR150, (7)Sham-anti-miR150+sh-BDNF, (8)SNI-Lv-METTL3, (9)SNI-Lv-METTL3 + anti-miR-150, (10)SNI-Lv-METTL3 + sh-YTHDF2, (11)SNI-Lv-METTL3 + Lv-BDNF, (12)SNI-miR150, (13)SNI-miR150+Lv-BDNF. The pain behaviors were detected in the respective time points and the expressions of METTL3 and miR-150 were determined at day 14 after the rats were sacrificed.
References
Ref 1 METTL3 suppresses neuropathic pain via modulating N6-methyladenosine-dependent primary miR-150 processing. Cell Death Discov. 2022 Feb 24;8(1):80. doi: 10.1038/s41420-022-00880-2.