General Information of the m6A Target Gene (ID: M6ATAR00746)
Target Name Pescadillo homolog (PES1)
Gene Name PES1
Chromosomal Location 22q12.2
Family Pescadillo family
Function
Component of the PeBoW complex, which is required for maturation of 28S and 5.8S ribosomal RNAs and formation of the 60S ribosome.
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Gene ID 23481
Uniprot ID
PESC_HUMAN
HGNC ID
HGNC:8848
Ensembl Gene ID
ENSG00000100029
KEGG ID
hsa:23481
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
PES1 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 HeLa cell line Homo sapiens
Treatment: METTL3 knockdown HeLa cells
Control: HeLa cells
GSE70061
Regulation
logFC: 7.23E-01
p-value: 7.36E-03
More Results Click to View More RNA-seq Results
Representative RIP-seq result supporting the interaction between PES1 and the regulator
Cell Line MDA-MB-231 Homo sapiens
Regulation logFC: 2.38E+00 GSE60213
In total 1 item(s) under this regulator
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene [1]
Response Summary m6A methyltransferase complex METTL3/METTL14 is upregulated in CML patients and that is required for proliferation of primary CML cells and CML cell lines sensitive and resistant to the TKI imatinib. METTL3 directly regulates the level of Pescadillo homolog (PES1) protein identified as an oncogene in several tumors. These results point to METTL3 as a novel relevant oncogene in CML and as a promising therapeutic target for TKI resistant CML.
Target Regulation Down regulation
Responsed Disease Chronic myeloid leukaemia ICD-11: 2B33.2
Pathway Response Cell cycle hsa04110
Cell Process Decrease of S phase
In-vitro Model U-937 Adult acute monocytic leukemia Homo sapiens CVCL_0007
NB4 Acute promyelocytic leukemia Homo sapiens CVCL_0005
LAMA-84 Chronic myelogenous leukemia Homo sapiens CVCL_0388
KCL-22 Chronic myelogenous leukemia Homo sapiens CVCL_2091
K-562 Chronic myelogenous leukemia Homo sapiens CVCL_0004
HL-60 Adult acute myeloid leukemia Homo sapiens CVCL_0002
HEL Erythroleukemia Homo sapiens CVCL_0001
Methyltransferase-like 14 (METTL14) [WRITER]
In total 1 item(s) under this regulator
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene [1]
Response Summary m6A methyltransferase complex METTL3/METTL14 is upregulated in CML patients and that is required for proliferation of primary CML cells and CML cell lines sensitive and resistant to the TKI imatinib. METTL3 directly regulates the level of Pescadillo homolog (PES1) protein identified as an oncogene in several tumors. These results point to METTL3 as a novel relevant oncogene in CML and as a promising therapeutic target for TKI resistant CML.
Target Regulation Down regulation
Responsed Disease Chronic myeloid leukaemia ICD-11: 2B33.2
Pathway Response Cell cycle hsa04110
Cell Process Decrease of S phase
In-vitro Model U-937 Adult acute monocytic leukemia Homo sapiens CVCL_0007
NB4 Acute promyelocytic leukemia Homo sapiens CVCL_0005
LAMA-84 Chronic myelogenous leukemia Homo sapiens CVCL_0388
KCL-22 Chronic myelogenous leukemia Homo sapiens CVCL_2091
K-562 Chronic myelogenous leukemia Homo sapiens CVCL_0004
HL-60 Adult acute myeloid leukemia Homo sapiens CVCL_0002
HEL Erythroleukemia Homo sapiens CVCL_0001
Malignant haematopoietic neoplasm [ICD-11: 2B33]
In total 2 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [1]
Response Summary m6A methyltransferase complex METTL3/METTL14 is upregulated in CML patients and that is required for proliferation of primary CML cells and CML cell lines sensitive and resistant to the TKI imatinib. METTL3 directly regulates the level of Pescadillo homolog (PES1) protein identified as an oncogene in several tumors. These results point to METTL3 as a novel relevant oncogene in CML and as a promising therapeutic target for TKI resistant CML.
Responsed Disease Chronic myeloid leukaemia [ICD-11: 2B33.2]
Target Regulator Methyltransferase-like 14 (METTL14) WRITER
Target Regulation Down regulation
Pathway Response Cell cycle hsa04110
Cell Process Decrease of S phase
In-vitro Model U-937 Adult acute monocytic leukemia Homo sapiens CVCL_0007
NB4 Acute promyelocytic leukemia Homo sapiens CVCL_0005
LAMA-84 Chronic myelogenous leukemia Homo sapiens CVCL_0388
KCL-22 Chronic myelogenous leukemia Homo sapiens CVCL_2091
K-562 Chronic myelogenous leukemia Homo sapiens CVCL_0004
HL-60 Adult acute myeloid leukemia Homo sapiens CVCL_0002
HEL Erythroleukemia Homo sapiens CVCL_0001
Experiment 2 Reporting the m6A-centered Disease Response [1]
Response Summary m6A methyltransferase complex METTL3/METTL14 is upregulated in CML patients and that is required for proliferation of primary CML cells and CML cell lines sensitive and resistant to the TKI imatinib. METTL3 directly regulates the level of Pescadillo homolog (PES1) protein identified as an oncogene in several tumors. These results point to METTL3 as a novel relevant oncogene in CML and as a promising therapeutic target for TKI resistant CML.
Responsed Disease Chronic myeloid leukaemia [ICD-11: 2B33.2]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
Target Regulation Down regulation
Pathway Response Cell cycle hsa04110
Cell Process Decrease of S phase
In-vitro Model U-937 Adult acute monocytic leukemia Homo sapiens CVCL_0007
NB4 Acute promyelocytic leukemia Homo sapiens CVCL_0005
LAMA-84 Chronic myelogenous leukemia Homo sapiens CVCL_0388
KCL-22 Chronic myelogenous leukemia Homo sapiens CVCL_2091
K-562 Chronic myelogenous leukemia Homo sapiens CVCL_0004
HL-60 Adult acute myeloid leukemia Homo sapiens CVCL_0002
HEL Erythroleukemia Homo sapiens CVCL_0001
References
Ref 1 New insight into the catalytic -dependent and -independent roles of METTL3 in sustaining aberrant translation in chronic myeloid leukemia. Cell Death Dis. 2021 Sep 24;12(10):870. doi: 10.1038/s41419-021-04169-7.