m6A Target Gene Information

General Information of the m6A Target Gene (ID: M6ATAR00162)
Target Name Neutral amino acid transporter B(0) (SLC1A5)
Synonyms
ATB(0); Baboon M7 virus receptor; RD114/simian type D retrovirus receptor; Sodium-dependent neutral amino acid transporter type 2; Solute carrier family 1 member 5; ASCT2; M7V1; RDR; RDRC
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Gene Name SLC1A5
Chromosomal Location 19q13.32
Family dicarboxylate/amino acid:cation symporter (DAACS) (TC 2;A;23) family; SLC1A5 subfamily
Function
Sodium-dependent amino acids transporter that has a broad substrate specificity, with a preference for zwitterionic amino acids. It accepts as substrates all neutral amino acids, including glutamine, asparagine, and branched-chain and aromatic amino acids, and excludes methylated, anionic, and cationic amino acids. Through binding of the fusogenic protein syncytin-1/ERVW-1 may mediate trophoblasts syncytialization, the spontaneous fusion of their plasma membranes, an essential process in placental development. (Microbial infection) Acts as a cell surface receptor for Feline endogenous virus RD114. (Microbial infection) Acts as a cell surface receptor for Baboon M7 endogenous virus. (Microbial infection) Acts as a cell surface receptor for type D simian retroviruses.
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Gene ID 6510
Uniprot ID
AAAT_HUMAN
HGNC ID
HGNC:10943
Ensembl Gene ID
ENSG00000105281
KEGG ID
hsa:6510
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
SLC1A5 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
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Fat mass and obesity-associated protein (FTO) [ERASER]
 Regulator Info 
Representative RNA-seq result indicating the expression of this target gene regulated by FTO
Cell Line 253J cell line Homo sapiens
Treatment: siFTO 253J cells
Control: 253J cells
 GSE150239
Regulation
logFC: -1.02E+00
p-value: 5.80E-30
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 Genetic inactivation of FTO using multiple orthogonal approaches revealed that FTO inhibition selectively reduces the growth and survival of VHL-deficient cells in vitro and in vivo. Integrated analysis of transcriptome-wide m6A-seq and mRNA-seq analysis identified the glutamine transporter Neutral amino acid transporter B(0) (SLC1A5) as an FTO target that promotes metabolic reprogramming and survival of VHL-deficient ccRCC cells. GLS1 inhibitors that target mitochondrial glutaminase and the conversion of glutamine to glutamate are currently being evaluated in early-phase clinical trials in ccRCC. These findings identify FTO as a potential HIF-independent therapeutic target for the treatment of VHL-deficient renal cell carcinoma.
Target Regulation Up regulation
Responsed Disease Renal cell carcinoma ICD-11: 2C90
 Disease Info 
Responsed Drug GLS-IN-968 Investigative
 Drug Info 
Pathway Response Central carbon metabolism in cancer hsa05230
HIF-1 signaling pathway hsa04066
Central carbon metabolism in cancer hsa05230
Metabolic pathways hsa01100
VEGF signaling pathway hsa04370
In-vitro Model UMRC2-vec (CCRCC isogenic cell lines that are VHL-deficient)
Renal cell carcinoma [ICD-11: 2C90]
 Disease Info 
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [1]
Response Summary Genetic inactivation of FTO using multiple orthogonal approaches revealed that FTO inhibition selectively reduces the growth and survival of VHL-deficient cells in vitro and in vivo. Integrated analysis of transcriptome-wide m6A-seq and mRNA-seq analysis identified the glutamine transporter Neutral amino acid transporter B(0) (SLC1A5) as an FTO target that promotes metabolic reprogramming and survival of VHL-deficient ccRCC cells. GLS1 inhibitors that target mitochondrial glutaminase and the conversion of glutamine to glutamate are currently being evaluated in early-phase clinical trials in ccRCC. These findings identify FTO as a potential HIF-independent therapeutic target for the treatment of VHL-deficient renal cell carcinoma.
Responsed Disease Renal cell carcinoma [ICD-11: 2C90]
Target Regulator Fat mass and obesity-associated protein (FTO) ERASER
 Regulator Info 
Target Regulation Up regulation
Responsed Drug GLS-IN-968 Investigative
 Drug Info 
Pathway Response Central carbon metabolism in cancer hsa05230
HIF-1 signaling pathway hsa04066
Central carbon metabolism in cancer hsa05230
Metabolic pathways hsa01100
VEGF signaling pathway hsa04370
In-vitro Model UMRC2-vec (CCRCC isogenic cell lines that are VHL-deficient)
GLS-IN-968 [Investigative]
 Drug Info 
In total 1 item(s) under this drug
Experiment 1 Reporting the m6A-centered Drug Response [1]
Response Summary Genetic inactivation of FTO using multiple orthogonal approaches revealed that FTO inhibition selectively reduces the growth and survival of VHL-deficient cells in vitro and in vivo. Integrated analysis of transcriptome-wide m6A-seq and mRNA-seq analysis identified the glutamine transporter Neutral amino acid transporter B(0) (SLC1A5) as an FTO target that promotes metabolic reprogramming and survival of VHL-deficient ccRCC cells. GLS1 inhibitors that target mitochondrial glutaminase and the conversion of glutamine to glutamate are currently being evaluated in early-phase clinical trials in ccRCC. These findings identify FTO as a potential HIF-independent therapeutic target for the treatment of VHL-deficient renal cell carcinoma.
Target Regulator Fat mass and obesity-associated protein (FTO) ERASER
 Regulator Info 
Target Regulation Up regulation
Responsed Disease Renal cell carcinoma ICD-11: 2C90
 Disease Info 
Pathway Response Central carbon metabolism in cancer hsa05230
HIF-1 signaling pathway hsa04066
Central carbon metabolism in cancer hsa05230
Metabolic pathways hsa01100
VEGF signaling pathway hsa04370
In-vitro Model UMRC2-vec (CCRCC isogenic cell lines that are VHL-deficient)
References
Ref 1 The m(6)A RNA demethylase FTO is a HIF-independent synthetic lethal partner with the VHL tumor suppressor. Proc Natl Acad Sci U S A. 2020 Sep 1;117(35):21441-21449. doi: 10.1073/pnas.2000516117. Epub 2020 Aug 19.