General Information of the m6A Target Gene (ID: M6ATAR00159)
Target Name eIF4E-binding protein 1 (4EBP1/EIF4EBP1)
Synonyms
4E-BP1; eIF4E-binding protein 1; Phosphorylated heat- and acid-stable protein regulated by insulin 1; PHAS-I
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Gene Name EIF4EBP1
Chromosomal Location 8p11.23
Family eIF4E-binding protein family
Function
Repressor of translation initiation that regulates EIF4E activity by preventing its assembly into the eIF4F complex: hypophosphorylated form competes with EIF4G1/EIF4G3 and strongly binds to EIF4E, leading to repress translation. In contrast, hyperphosphorylated form dissociates from EIF4E, allowing interaction between EIF4G1/EIF4G3 and EIF4E, leading to initiation of translation. Mediates the regulation of protein translation by hormones, growth factors and other stimuli that signal through the MAP kinase and mTORC1 pathways.
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Gene ID 1978
Uniprot ID
4EBP1_HUMAN
HGNC ID
HGNC:3288
Ensembl Gene ID
ENSG00000187840
KEGG ID
hsa:1978
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
EIF4EBP1 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]
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: 8.71E-01
p-value: 3.32E-08
More Results Click to View More RNA-seq Results
Representative RIP-seq result supporting the interaction between EIF4EBP1 and the regulator
Cell Line MDA-MB-231 Homo sapiens
Regulation logFC: 9.71E+00 GSE60213
In total 1 item(s) under this regulator
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene [1]
Response Summary METTL3 promotes the progression of retinoblastoma through PI3K/AKT/mTOR pathways in vitro and in vivo. METTL3 has an impact on the PI3K-AKT-mTOR-P70S6K/eIF4E-binding protein 1 (4EBP1/EIF4EBP1) pathway. The cell proliferation results show that the stimulatory function of METTL3 is lost after rapamycin treatment.
Target Regulation Down regulation
Responsed Disease Retinoblastoma ICD-11: 2D02.2
Pathway Response PI3K-Akt signaling pathway hsa04151
mTOR signaling pathway hsa04150
Cell Process Cell proliferation
Cell migration
Cell invasion
Cell apoptosis
In-vitro Model WERI-Rb-1 Retinoblastoma Homo sapiens CVCL_1792
Y-79 Retinoblastoma Homo sapiens CVCL_1893
In-vivo Model To establish a subcutaneous tumour model in nude mice, 2 × 107 Y79 cells (METTL3 knockdown group: shNC, shRNA1 and shRNA2; METTL3 up-regulated group: NC and METLL3) were resuspended in 1 mL of pre-cooled PBS, and 200 uL of the cell suspension was injected subcutaneously into the left side of the armpit to investigate tumour growth (4 × 106 per mouse).
RNA demethylase ALKBH5 (ALKBH5) [ERASER]
Representative RNA-seq result indicating the expression of this target gene regulated by ALKBH5
Cell Line MOLM-13 cell line Homo sapiens
Treatment: shALKBH5 MOLM-13 cells
Control: shNS MOLM-13 cells
GSE144968
Regulation
logFC: -7.12E-01
p-value: 2.44E-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 [2]
Response Summary Bioactive peptides can inhibit acute myeloid leukemia cell proliferation by downregulating ALKBH5-mediated m6A demethylation of eIF4E-binding protein 1 (4EBP1/EIF4EBP1) and MLST8 mRNAs, which have potential to prevent and treat this disease.
Target Regulation Up regulation
Responsed Disease Acute myeloid leukaemia ICD-11: 2A60
Cell Process Cell apoptosis
In-vitro Model MV4-11 Childhood acute monocytic leukemia Homo sapiens CVCL_0064
HL-60 Adult acute myeloid leukemia Homo sapiens CVCL_0002
HEK293T Normal Homo sapiens CVCL_0063
In-vivo Model HL-60 cells (1 × 107) suspended in 0.1 ml PBS containing 50% Matrigel were subcutaneously injected into the flanks of the mice. When tumor sizes reached 200 mm3, the mice were randomly distributed into four groups with the indicated dosages of saline, cytarabine and BP alone or in combination. For BP injections, the solution was delivered intraperitoneally at 106 ug/kg body weight for the first 8 consecutive days. For cytarabine injections, the solution was delivered intraperitoneally at 100 mg/kg body weight three times (once every three days). The combination group was administered intraperitoneally three times (once every three days) with the same dosages as described above. The control group was treated with an equivalent amount of saline.
Acute myeloid leukaemia [ICD-11: 2A60]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [2]
Response Summary Bioactive peptides can inhibit acute myeloid leukemia cell proliferation by downregulating ALKBH5-mediated m6A demethylation of eIF4E-binding protein 1 (4EBP1/EIF4EBP1) and MLST8 mRNAs, which have potential to prevent and treat this disease.
Responsed Disease Acute myeloid leukaemia [ICD-11: 2A60]
Target Regulator RNA demethylase ALKBH5 (ALKBH5) ERASER
Target Regulation Up regulation
Cell Process Cell apoptosis
In-vitro Model MV4-11 Childhood acute monocytic leukemia Homo sapiens CVCL_0064
HL-60 Adult acute myeloid leukemia Homo sapiens CVCL_0002
HEK293T Normal Homo sapiens CVCL_0063
In-vivo Model HL-60 cells (1 × 107) suspended in 0.1 ml PBS containing 50% Matrigel were subcutaneously injected into the flanks of the mice. When tumor sizes reached 200 mm3, the mice were randomly distributed into four groups with the indicated dosages of saline, cytarabine and BP alone or in combination. For BP injections, the solution was delivered intraperitoneally at 106 ug/kg body weight for the first 8 consecutive days. For cytarabine injections, the solution was delivered intraperitoneally at 100 mg/kg body weight three times (once every three days). The combination group was administered intraperitoneally three times (once every three days) with the same dosages as described above. The control group was treated with an equivalent amount of saline.
Retina cancer [ICD-11: 2D02]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [1]
Response Summary METTL3 promotes the progression of retinoblastoma through PI3K/AKT/mTOR pathways in vitro and in vivo. METTL3 has an impact on the PI3K-AKT-mTOR-P70S6K/eIF4E-binding protein 1 (4EBP1/EIF4EBP1) pathway. The cell proliferation results show that the stimulatory function of METTL3 is lost after rapamycin treatment.
Responsed Disease Retinoblastoma [ICD-11: 2D02.2]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
Target Regulation Down regulation
Pathway Response PI3K-Akt signaling pathway hsa04151
mTOR signaling pathway hsa04150
Cell Process Cell proliferation
Cell migration
Cell invasion
Cell apoptosis
In-vitro Model WERI-Rb-1 Retinoblastoma Homo sapiens CVCL_1792
Y-79 Retinoblastoma Homo sapiens CVCL_1893
In-vivo Model To establish a subcutaneous tumour model in nude mice, 2 × 107 Y79 cells (METTL3 knockdown group: shNC, shRNA1 and shRNA2; METTL3 up-regulated group: NC and METLL3) were resuspended in 1 mL of pre-cooled PBS, and 200 uL of the cell suspension was injected subcutaneously into the left side of the armpit to investigate tumour growth (4 × 106 per mouse).
References
Ref 1 m(6)A methyltransferase METTL3 promotes retinoblastoma progression via PI3K/AKT/mTOR pathway. J Cell Mol Med. 2020 Oct 8;24(21):12368-78. doi: 10.1111/jcmm.15736. Online ahead of print.
Ref 2 Bioactive peptide inhibits acute myeloid leukemia cell proliferation by downregulating ALKBH5-mediated m(6)A demethylation of EIF4EBP1 and MLST8 mRNA. Cell Oncol (Dordr). 2022 Jun;45(3):355-365. doi: 10.1007/s13402-022-00666-9. Epub 2022 May 17.