m6A Target Gene Information

General Information of the m6A Target Gene (ID: M6ATAR00342)
Target Name Myeloid differentiation primary response protein MyD88 (MYD88)
Gene Name MYD88
Chromosomal Location 3p22.2
Function
Adapter protein involved in the Toll-like receptor and IL-1 receptor signaling pathway in the innate immune response. Acts via IRAK1, IRAK2, IRF7 and TRAF6, leading to NF-kappa-B activation, cytokine secretion and the inflammatory response. Increases IL-8 transcription. Involved in IL-18-mediated signaling pathway. Activates IRF1 resulting in its rapid migration into the nucleus to mediate an efficient induction of IFN-beta, NOS2/INOS, and IL12A genes. Upon TLR8 activation by GU-rich single-stranded RNA (GU-rich RNA) derived from viruses such as SARS-CoV-2, SARS-CoV and HIV-1, induces IL1B release through NLRP3 inflammasome activation. MyD88-mediated signaling in intestinal epithelial cells is crucial for maintenance of gut homeostasis and controls the expression of the antimicrobial lectin REG3G in the small intestine (By similarity).
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Gene ID 4615
Uniprot ID
MYD88_HUMAN
HGNC ID
HGNC:7562
Ensembl Gene ID
ENSG00000172936
KEGG ID
hsa:4615
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
MYD88 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]
 Regulator Info 
Representative RNA-seq result indicating the expression of this target gene regulated by METTL3
Cell Line MOLM-13 cell line Homo sapiens
Treatment: shMETTL3 MOLM13 cells
Control: MOLM13 cells
 GSE98623
Regulation
logFC: -1.07E+00
p-value: 1.83E-13
More Results Click to View More RNA-seq Results
Representative RIP-seq result supporting the interaction between MYD88 and the regulator
Cell Line MDA-MB-231 Homo sapiens
Regulation logFC: 1.16E+00 GSE60213
In total 2 item(s) under this regulator
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene [1]
Response Summary Knocked down METTL3 and demonstrated that METTL3 depletion decreased the expression of inflammatory cytokines and the phosphorylation of IKK-alpha/beta, p65 and IKappa-B-alpha in the NF-Kappa-B signalling pathway as well as p38, ERK and JNK in the MAPK signalling pathway in LPS-induced HDPCs. METTL3 inhibits the LPS-induced inflammatory response of HDPCs by regulating alternative splicing of Myeloid differentiation primary response protein MyD88 (MYD88).
Target Regulation Down regulation
Responsed Disease Pulpitis ICD-11: DA09
 Disease Info 
Pathway Response MAPK signaling pathway hsa04010
Cell Process Alternative splicing
Experiment 2 Reporting the m6A Methylation Regulator of This Target Gene [2]
Response Summary METTL3 positively regulates expression of Myeloid differentiation primary response protein MyD88 (MYD88), a critical upstream regulator of NF-Kappa-B signaling, by facilitating m6A methylation modification to MYD88-RNA, subsequently inducing the activation of NF-Kappa-B which is widely regarded as a repressor of osteogenesis and therefore suppressing osteogenic progression. The METTL3-mediated m6A methylation is found to be dynamically reversed by the demethylase ALKBH5.
Target Regulation Up regulation
Responsed Disease Skeletal anomaly ICD-11: LD24
 Disease Info 
Pathway Response Central carbon metabolism in cancer hsa05230
Cell Process Glucose metabolism
In-vitro Model Mesenchymal stem cell line (NP tissues were used to isolate NP cells)
RNA demethylase ALKBH5 (ALKBH5) [ERASER]
 Regulator Info 
Representative RNA-seq result indicating the expression of this target gene regulated by ALKBH5
Cell Line 143B cell line Homo sapiens
Treatment: siALKBH5 transfected 143B cells
Control: siControl 143B cells
 GSE154528
Regulation
logFC: 9.11E-01
p-value: 2.76E-05
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 [2]
Response Summary METTL3 positively regulates expression of Myeloid differentiation primary response protein MyD88 (MYD88), a critical upstream regulator of NF-Kappa-B signaling, by facilitating m6A methylation modification to MYD88-RNA, subsequently inducing the activation of NF-Kappa-B which is widely regarded as a repressor of osteogenesis and therefore suppressing osteogenic progression. The METTL3-mediated m6A methylation is found to be dynamically reversed by the demethylase ALKBH5.
Target Regulation Down regulation
Responsed Disease Skeletal anomaly ICD-11: LD24
 Disease Info 
Pathway Response Central carbon metabolism in cancer hsa05230
Cell Process Glucose metabolism
In-vitro Model Mesenchymal stem cell line (NP tissues were used to isolate NP cells)
RNA-binding motif protein 15 (RBM15) [WRITER]
 Regulator Info 
Representative RNA-seq result indicating the expression of this target gene regulated by RBM15
Cell Line Human BJ Fibroblast Homo sapiens
Treatment: siRBM15 BJ fibroblast
Control: siControl BJ fibroblast
 GSE154148
Regulation
logFC: -3.36E+00
p-value: 3.10E-04
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 [3]
Response Summary RBM15 silencing inhibited the CRC growth and metastasis in vitro and in vivo. RBM15 mediated m6A methylation modification of Myeloid differentiation primary response protein MyD88 (MYD88) mRNA in colorectal cancer cells.
Target Regulation Down regulation
Responsed Disease Colorectal cancer ICD-11: 2B91
 Disease Info 
Cell Process Cell proliferative
Cell invasive
In-vitro Model HCT 116 Colon carcinoma Homo sapiens CVCL_0291
SW480 Colon adenocarcinoma Homo sapiens CVCL_0546
Colorectal cancer [ICD-11: 2B91]
 Disease Info 
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [3]
Response Summary RBM15 silencing inhibited the CRC growth and metastasis in vitro and in vivo. RBM15 mediated m6A methylation modification of Myeloid differentiation primary response protein MyD88 (MYD88) mRNA in colorectal cancer cells.
Responsed Disease Colorectal cancer [ICD-11: 2B91]
Target Regulator RNA-binding motif protein 15 (RBM15) WRITER
 Regulator Info 
Target Regulation Down regulation
Cell Process Cell proliferative
Cell invasive
In-vitro Model HCT 116 Colon carcinoma Homo sapiens CVCL_0291
SW480 Colon adenocarcinoma Homo sapiens CVCL_0546
Pulpitis [ICD-11: DA09]
 Disease Info 
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [1]
Response Summary Knocked down METTL3 and demonstrated that METTL3 depletion decreased the expression of inflammatory cytokines and the phosphorylation of IKK-alpha/beta, p65 and IKappa-B-alpha in the NF-Kappa-B signalling pathway as well as p38, ERK and JNK in the MAPK signalling pathway in LPS-induced HDPCs. METTL3 inhibits the LPS-induced inflammatory response of HDPCs by regulating alternative splicing of Myeloid differentiation primary response protein MyD88 (MYD88).
Responsed Disease Pulpitis [ICD-11: DA09]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
 Regulator Info 
Target Regulation Down regulation
Pathway Response MAPK signaling pathway hsa04010
Cell Process Alternative splicing
Skeletal anomaly [ICD-11: LD24]
 Disease Info 
In total 2 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [2]
Response Summary METTL3 positively regulates expression of Myeloid differentiation primary response protein MyD88 (MYD88), a critical upstream regulator of NF-Kappa-B signaling, by facilitating m6A methylation modification to MYD88-RNA, subsequently inducing the activation of NF-Kappa-B which is widely regarded as a repressor of osteogenesis and therefore suppressing osteogenic progression. The METTL3-mediated m6A methylation is found to be dynamically reversed by the demethylase ALKBH5.
Responsed Disease Skeletal anomaly [ICD-11: LD24]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
 Regulator Info 
Target Regulation Up regulation
Pathway Response Central carbon metabolism in cancer hsa05230
Cell Process Glucose metabolism
In-vitro Model Mesenchymal stem cell line (NP tissues were used to isolate NP cells)
Experiment 2 Reporting the m6A-centered Disease Response [2]
Response Summary METTL3 positively regulates expression of Myeloid differentiation primary response protein MyD88 (MYD88), a critical upstream regulator of NF-Kappa-B signaling, by facilitating m6A methylation modification to MYD88-RNA, subsequently inducing the activation of NF-Kappa-B which is widely regarded as a repressor of osteogenesis and therefore suppressing osteogenic progression. The METTL3-mediated m6A methylation is found to be dynamically reversed by the demethylase ALKBH5.
Responsed Disease Skeletal anomaly [ICD-11: LD24]
Target Regulator RNA demethylase ALKBH5 (ALKBH5) ERASER
 Regulator Info 
Target Regulation Down regulation
Pathway Response Central carbon metabolism in cancer hsa05230
Cell Process Glucose metabolism
In-vitro Model Mesenchymal stem cell line (NP tissues were used to isolate NP cells)
References
Ref 1 METTL3 regulates alternative splicing of MyD88 upon the lipopolysaccharide-induced inflammatory response in human dental pulp cells. J Cell Mol Med. 2018 May;22(5):2558-2568. doi: 10.1111/jcmm.13491. Epub 2018 Mar 4.
Ref 2 The m6A methyltransferase METTL3 cooperates with demethylase ALKBH5 to regulate osteogenic differentiation through NF-KappaB signaling. Mol Cell Biochem. 2020 Jan;463(1-2):203-210. doi: 10.1007/s11010-019-03641-5. Epub 2019 Oct 23.
Ref 3 Knockdown RBM15 Inhibits Colorectal Cancer Cell Proliferation and Metastasis Via N6-Methyladenosine (m6A) Modification of MyD88 mRNA. Cancer Biother Radiopharm. 2021 Nov 25. doi: 10.1089/cbr.2021.0226. Online ahead of print.