General Information of the m6A Target Gene (ID: M6ATAR00171)
Target Name Meltrin-beta (ADAM19)
Synonyms
ADAM 19; Disintegrin and metalloproteinase domain-containing protein 19; Metalloprotease and disintegrin dendritic antigen marker; MADDAM; MLTNB; FKSG34
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Gene Name ADAM19
Chromosomal Location 5q33.3
Function
Participates in the proteolytic processing of beta-type neuregulin isoforms which are involved in neurogenesis and synaptogenesis, suggesting a regulatory role in glial cell. Also cleaves alpha-2 macroglobulin. May be involved in osteoblast differentiation and/or osteoblast activity in bone (By similarity).
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Gene ID 8728
Uniprot ID
ADA19_HUMAN
HGNC ID
HGNC:197
Ensembl Gene ID
ENSG00000135074
KEGG ID
hsa:8728
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
ADAM19 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 14 (METTL14) [WRITER]
Representative RNA-seq result indicating the expression of this target gene regulated by METTL14
Cell Line MDA-MB-231 Homo sapiens
Treatment: siMETTL14 MDA-MB-231 cells
Control: MDA-MB-231 cells
GSE81164
Regulation
logFC: -1.69E+00
p-value: 2.38E-31
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 Knockdown of METTL3 or METTL14 induced changes in mRNA m6A enrichment and altered mRNA expression of genes (e.g., Meltrin-beta (ADAM19)) with critical biological functions in GSCs. Treatment with MA2, a chemical inhibitor of FTO, dramatically suppressed GSC-induced tumorigenesis and prolonged lifespan in GSC-grafted animals.
Target Regulation Down regulation
Responsed Disease Glioblastoma ICD-11: 2A00.00
Cell Process Cells growth
Cells self-renewal
Tumorigenesis
MicroRNAs in cancer (hsa05206)
In-vitro Model GSC Glioma Epinephelus akaara CVCL_M752
In-vivo Model 2 × 105 dissociated cells in 2 uL PBS were injected into the following site (anteroposterior [AP] +0.6 mm, mediolateral [ML] +1.6 mm, and dorsoventricular [DV] 2.6 mm) with a rate of 1 uL/min.
Methyltransferase-like 3 (METTL3) [WRITER]
Representative RNA-seq result indicating the expression of this target gene regulated by METTL3
Cell Line HUVEC cell line Homo sapiens
Treatment: shMETTL3 HUVEC cells
Control: shScramble HUVEC cells
GSE157544
Regulation
logFC: -7.06E-01
p-value: 4.35E-03
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 Knockdown of METTL3 or METTL14 induced changes in mRNA m6A enrichment and altered mRNA expression of genes (e.g., Meltrin-beta (ADAM19)) with critical biological functions in GSCs. Treatment with MA2, a chemical inhibitor of FTO, dramatically suppressed GSC-induced tumorigenesis and prolonged lifespan in GSC-grafted animals.
Target Regulation Down regulation
Responsed Disease Glioblastoma ICD-11: 2A00.00
Cell Process Cells growth
Cells self-renewal
Tumorigenesis
MicroRNAs in cancer (hsa05206)
In-vitro Model GSC Glioma Epinephelus akaara CVCL_M752
In-vivo Model 2 × 105 dissociated cells in 2 uL PBS were injected into the following site (anteroposterior [AP] +0.6 mm, mediolateral [ML] +1.6 mm, and dorsoventricular [DV] 2.6 mm) with a rate of 1 uL/min.
Brain cancer [ICD-11: 2A00]
In total 2 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [1]
Response Summary Knockdown of METTL3 or METTL14 induced changes in mRNA m6A enrichment and altered mRNA expression of genes (e.g., Meltrin-beta (ADAM19)) with critical biological functions in GSCs. Treatment with MA2, a chemical inhibitor of FTO, dramatically suppressed GSC-induced tumorigenesis and prolonged lifespan in GSC-grafted animals.
Responsed Disease Glioblastoma [ICD-11: 2A00.00]
Target Regulator Methyltransferase-like 14 (METTL14) WRITER
Target Regulation Down regulation
Cell Process Cells growth
Cells self-renewal
Tumorigenesis
MicroRNAs in cancer (hsa05206)
In-vitro Model GSC Glioma Epinephelus akaara CVCL_M752
In-vivo Model 2 × 105 dissociated cells in 2 uL PBS were injected into the following site (anteroposterior [AP] +0.6 mm, mediolateral [ML] +1.6 mm, and dorsoventricular [DV] 2.6 mm) with a rate of 1 uL/min.
Experiment 2 Reporting the m6A-centered Disease Response [1]
Response Summary Knockdown of METTL3 or METTL14 induced changes in mRNA m6A enrichment and altered mRNA expression of genes (e.g., Meltrin-beta (ADAM19)) with critical biological functions in GSCs. Treatment with MA2, a chemical inhibitor of FTO, dramatically suppressed GSC-induced tumorigenesis and prolonged lifespan in GSC-grafted animals.
Responsed Disease Glioblastoma [ICD-11: 2A00.00]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
Target Regulation Down regulation
Cell Process Cells growth
Cells self-renewal
Tumorigenesis
MicroRNAs in cancer (hsa05206)
In-vitro Model GSC Glioma Epinephelus akaara CVCL_M752
In-vivo Model 2 × 105 dissociated cells in 2 uL PBS were injected into the following site (anteroposterior [AP] +0.6 mm, mediolateral [ML] +1.6 mm, and dorsoventricular [DV] 2.6 mm) with a rate of 1 uL/min.
Solid tumour/cancer [ICD-11: 2A00-2F9Z]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response []
Response Summary In this review, we discuss the specific roles of m6A "writers", "erasers", and "readers" in normal physiology and how their altered expression promotes tumorigenesis. We also describe the potential of exploiting the aberrant expression of these enzymes for cancer diagnosis, prognosis, and the development of novel therapies. The abnormal expression of m6A regulatory enzymes affects m6A abundance and consequently dysregulates the expression of tumor suppressor genes and oncogenes, including MYC, SOCS2, Meltrin-beta (ADAM19), and PTEN.
Responsed Disease Solid tumour/cancer [ICD-11: 2A00-2F9Z]
References
Ref 1 m(6)A RNA Methylation Regulates the Self-Renewal and Tumorigenesis of Glioblastoma Stem Cells. Cell Rep. 2017 Mar 14;18(11):2622-2634. doi: 10.1016/j.celrep.2017.02.059.