m6A Target Gene Information

General Information of the m6A Target Gene (ID: M6ATAR00438)
Target Name Ubiquitin carboxyl-terminal hydrolase 1 (USP1)
Synonyms
Deubiquitinating enzyme 1; hUBP; Ubiquitin thioesterase 1; Ubiquitin-specific-processing protease 1
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Gene Name USP1
Chromosomal Location 1p31.3
Family peptidase C19 family
Function
Negative regulator of DNA damage repair which specifically deubiquitinates monoubiquitinated FANCD2. Also involved in PCNA-mediated translesion synthesis (TLS) by deubiquitinating monoubiquitinated PCNA . Has almost no deubiquitinating activity by itself and requires the interaction with WDR48 to have a high activity.
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Gene ID 7398
Uniprot ID
UBP1_HUMAN
HGNC ID
HGNC:12607
Ensembl Gene ID
ENSG00000162607
KEGG ID
hsa:7398
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
USP1 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).
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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: -6.03E-01
p-value: 1.12E-02
More Results Click to View More RNA-seq Results
In total 2 item(s) under this regulator
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene [1]
Response Summary ALKBH5 and Ubiquitin carboxyl-terminal hydrolase 1 (USP1) were upregulated in T-cell acute lymphoblastic leukemia, and ALKBH5-mediated m6A modification increased USP1 and Aurora B expression. Silencing USP1 increased CEM-C1 cell sensitivity to dexamethasone, reduced cell invasion, promoted cell apoptosis, and ameliorated glucocorticoid receptor (GR) expression.
Target Regulation Up regulation
Responsed Disease Mature T-cell lymphoma ICD-11: 2A90
 Disease Info 
Responsed Drug dexamethasone Approved
 Drug Info 
Cell Process Cell apoptosis
In-vitro Model CEM/C1 T acute lymphoblastic leukemia Homo sapiens CVCL_3496
CCRF-CEM C7 T acute lymphoblastic leukemia Homo sapiens CVCL_6825
HEK293T Normal Homo sapiens CVCL_0063
In-vivo Model Adult male C57BL/6J mice (weighting 18-25 g) were obtained from Laboratory Animal Center, Zhengzhou University. Mice were subcutaneously injected with 1 × 107 CEM-C1 cells for tumorigenesis and randomly divided into four group: control group; control + Dex; sh-RNA + Dex; sh-USP1 + Dex. Mice treatment with Dex were intraperitoneally injected with 8 mg/kg Dex every day for 10 consecutive days after tumor growth and mice treatment with sh-RNA or sh-USP1 were injected intravenously with 2 mg/Kg sh-RNA or USP1 sh-RNA. The control group of mice were injected with the same volume of normal saline. After the treatment of each group, the mice were housed and fed in a room with an ambient temperature of 25℃, and the survival time, weight of the mice, and tumor weight were recorded. When rats were sacrificed, tissues were harvested for Western blot analysis.
Experiment 2 Reporting the m6A Methylation Regulator of This Target Gene [1]
Response Summary ALKBH5 and Ubiquitin carboxyl-terminal hydrolase 1 (USP1) were upregulated in T-cell acute lymphoblastic leukemia, and ALKBH5-mediated m6A modification increased USP1 and Aurora B expression. Silencing USP1 increased CEM-C1 cell sensitivity to dexamethasone, reduced cell invasion, promoted cell apoptosis, and ameliorated glucocorticoid receptor (GR) expression.
Target Regulation Up regulation
Responsed Disease Mature T-cell lymphoma ICD-11: 2A90
 Disease Info 
Responsed Drug Glucocorticoid Investigative
 Drug Info 
Cell Process Cell apoptosis
In-vitro Model CEM/C1 T acute lymphoblastic leukemia Homo sapiens CVCL_3496
CCRF-CEM C7 T acute lymphoblastic leukemia Homo sapiens CVCL_6825
HEK293T Normal Homo sapiens CVCL_0063
In-vivo Model Adult male C57BL/6J mice (weighting 18-25 g) were obtained from Laboratory Animal Center, Zhengzhou University. Mice were subcutaneously injected with 1 × 107 CEM-C1 cells for tumorigenesis and randomly divided into four group: control group; control + Dex; sh-RNA + Dex; sh-USP1 + Dex. Mice treatment with Dex were intraperitoneally injected with 8 mg/kg Dex every day for 10 consecutive days after tumor growth and mice treatment with sh-RNA or sh-USP1 were injected intravenously with 2 mg/Kg sh-RNA or USP1 sh-RNA. The control group of mice were injected with the same volume of normal saline. After the treatment of each group, the mice were housed and fed in a room with an ambient temperature of 25℃, and the survival time, weight of the mice, and tumor weight were recorded. When rats were sacrificed, tissues were harvested for Western blot analysis.
Mature T-cell lymphoma [ICD-11: 2A90]
 Disease Info 
In total 2 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [1]
Response Summary ALKBH5 and Ubiquitin carboxyl-terminal hydrolase 1 (USP1) were upregulated in T-cell acute lymphoblastic leukemia, and ALKBH5-mediated m6A modification increased USP1 and Aurora B expression. Silencing USP1 increased CEM-C1 cell sensitivity to dexamethasone, reduced cell invasion, promoted cell apoptosis, and ameliorated glucocorticoid receptor (GR) expression.
Responsed Disease Mature T-cell lymphoma [ICD-11: 2A90]
Target Regulator RNA demethylase ALKBH5 (ALKBH5) ERASER
 Regulator Info 
Target Regulation Up regulation
Responsed Drug dexamethasone Approved
 Drug Info 
Cell Process Cell apoptosis
In-vitro Model CEM/C1 T acute lymphoblastic leukemia Homo sapiens CVCL_3496
CCRF-CEM C7 T acute lymphoblastic leukemia Homo sapiens CVCL_6825
HEK293T Normal Homo sapiens CVCL_0063
In-vivo Model Adult male C57BL/6J mice (weighting 18-25 g) were obtained from Laboratory Animal Center, Zhengzhou University. Mice were subcutaneously injected with 1 × 107 CEM-C1 cells for tumorigenesis and randomly divided into four group: control group; control + Dex; sh-RNA + Dex; sh-USP1 + Dex. Mice treatment with Dex were intraperitoneally injected with 8 mg/kg Dex every day for 10 consecutive days after tumor growth and mice treatment with sh-RNA or sh-USP1 were injected intravenously with 2 mg/Kg sh-RNA or USP1 sh-RNA. The control group of mice were injected with the same volume of normal saline. After the treatment of each group, the mice were housed and fed in a room with an ambient temperature of 25℃, and the survival time, weight of the mice, and tumor weight were recorded. When rats were sacrificed, tissues were harvested for Western blot analysis.
Experiment 2 Reporting the m6A-centered Disease Response [1]
Response Summary ALKBH5 and Ubiquitin carboxyl-terminal hydrolase 1 (USP1) were upregulated in T-cell acute lymphoblastic leukemia, and ALKBH5-mediated m6A modification increased USP1 and Aurora B expression. Silencing USP1 increased CEM-C1 cell sensitivity to dexamethasone, reduced cell invasion, promoted cell apoptosis, and ameliorated glucocorticoid receptor (GR) expression.
Responsed Disease Mature T-cell lymphoma [ICD-11: 2A90]
Target Regulator RNA demethylase ALKBH5 (ALKBH5) ERASER
 Regulator Info 
Target Regulation Up regulation
Responsed Drug Glucocorticoid Investigative
 Drug Info 
Cell Process Cell apoptosis
In-vitro Model CEM/C1 T acute lymphoblastic leukemia Homo sapiens CVCL_3496
CCRF-CEM C7 T acute lymphoblastic leukemia Homo sapiens CVCL_6825
HEK293T Normal Homo sapiens CVCL_0063
In-vivo Model Adult male C57BL/6J mice (weighting 18-25 g) were obtained from Laboratory Animal Center, Zhengzhou University. Mice were subcutaneously injected with 1 × 107 CEM-C1 cells for tumorigenesis and randomly divided into four group: control group; control + Dex; sh-RNA + Dex; sh-USP1 + Dex. Mice treatment with Dex were intraperitoneally injected with 8 mg/kg Dex every day for 10 consecutive days after tumor growth and mice treatment with sh-RNA or sh-USP1 were injected intravenously with 2 mg/Kg sh-RNA or USP1 sh-RNA. The control group of mice were injected with the same volume of normal saline. After the treatment of each group, the mice were housed and fed in a room with an ambient temperature of 25℃, and the survival time, weight of the mice, and tumor weight were recorded. When rats were sacrificed, tissues were harvested for Western blot analysis.
dexamethasone [Approved]
 Drug Info 
In total 1 item(s) under this drug
Experiment 1 Reporting the m6A-centered Drug Response [1]
Response Summary ALKBH5 and Ubiquitin carboxyl-terminal hydrolase 1 (USP1) were upregulated in T-cell acute lymphoblastic leukemia, and ALKBH5-mediated m6A modification increased USP1 and Aurora B expression. Silencing USP1 increased CEM-C1 cell sensitivity to dexamethasone, reduced cell invasion, promoted cell apoptosis, and ameliorated glucocorticoid receptor (GR) expression.
Target Regulator RNA demethylase ALKBH5 (ALKBH5) ERASER
 Regulator Info 
Target Regulation Up regulation
Responsed Disease Mature T-cell lymphoma ICD-11: 2A90
 Disease Info 
Cell Process Cell apoptosis
In-vitro Model CEM/C1 T acute lymphoblastic leukemia Homo sapiens CVCL_3496
CCRF-CEM C7 T acute lymphoblastic leukemia Homo sapiens CVCL_6825
HEK293T Normal Homo sapiens CVCL_0063
In-vivo Model Adult male C57BL/6J mice (weighting 18-25 g) were obtained from Laboratory Animal Center, Zhengzhou University. Mice were subcutaneously injected with 1 × 107 CEM-C1 cells for tumorigenesis and randomly divided into four group: control group; control + Dex; sh-RNA + Dex; sh-USP1 + Dex. Mice treatment with Dex were intraperitoneally injected with 8 mg/kg Dex every day for 10 consecutive days after tumor growth and mice treatment with sh-RNA or sh-USP1 were injected intravenously with 2 mg/Kg sh-RNA or USP1 sh-RNA. The control group of mice were injected with the same volume of normal saline. After the treatment of each group, the mice were housed and fed in a room with an ambient temperature of 25℃, and the survival time, weight of the mice, and tumor weight were recorded. When rats were sacrificed, tissues were harvested for Western blot analysis.
Glucocorticoid [Investigative]
 Drug Info 
In total 1 item(s) under this drug
Experiment 1 Reporting the m6A-centered Drug Response [1]
Response Summary ALKBH5 and Ubiquitin carboxyl-terminal hydrolase 1 (USP1) were upregulated in T-cell acute lymphoblastic leukemia, and ALKBH5-mediated m6A modification increased USP1 and Aurora B expression. Silencing USP1 increased CEM-C1 cell sensitivity to dexamethasone, reduced cell invasion, promoted cell apoptosis, and ameliorated glucocorticoid receptor (GR) expression.
Target Regulator RNA demethylase ALKBH5 (ALKBH5) ERASER
 Regulator Info 
Target Regulation Up regulation
Responsed Disease Mature T-cell lymphoma ICD-11: 2A90
 Disease Info 
Cell Process Cell apoptosis
In-vitro Model CEM/C1 T acute lymphoblastic leukemia Homo sapiens CVCL_3496
CCRF-CEM C7 T acute lymphoblastic leukemia Homo sapiens CVCL_6825
HEK293T Normal Homo sapiens CVCL_0063
In-vivo Model Adult male C57BL/6J mice (weighting 18-25 g) were obtained from Laboratory Animal Center, Zhengzhou University. Mice were subcutaneously injected with 1 × 107 CEM-C1 cells for tumorigenesis and randomly divided into four group: control group; control + Dex; sh-RNA + Dex; sh-USP1 + Dex. Mice treatment with Dex were intraperitoneally injected with 8 mg/kg Dex every day for 10 consecutive days after tumor growth and mice treatment with sh-RNA or sh-USP1 were injected intravenously with 2 mg/Kg sh-RNA or USP1 sh-RNA. The control group of mice were injected with the same volume of normal saline. After the treatment of each group, the mice were housed and fed in a room with an ambient temperature of 25℃, and the survival time, weight of the mice, and tumor weight were recorded. When rats were sacrificed, tissues were harvested for Western blot analysis.
References
Ref 1 ALKBH5-mediated m6A-demethylation of USP1 regulated T-cell acute lymphoblastic leukemia cell glucocorticoid resistance by Aurora B. Mol Carcinog. 2021 Sep;60(9):644-657. doi: 10.1002/mc.23330. Epub 2021 Jun 25.