m6A Target Gene Information
General Information of the m6A Target Gene (ID: M6ATAR00372)
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
PPM1A
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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Methyltransferase-like 14 (METTL14) [WRITER]
Representative RNA-seq result indicating the expression of this target gene regulated by METTL14 | ||
Cell Line | Neural progenitor cell line | Mus musculus |
Treatment: METTL14 knockout NPCs
Control: Wild type NPCs
|
GSE158985 | |
Regulation |
|
logFC: 6.97E-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 | [1] | |||
Response Summary | m6A modification promoted translation of Protein phosphatase 1A (PPM1A) (protein phosphatase 1A, magnesium dependent, alpha isoform), a negative AMP-activated protein kinase (AMPK) regulator, but decreased expression of CAMKK2 (calcium/calmodulin-dependent protein kinase kinase 2, beta), a positive AMPK regulator, by reducing its RNA stability. Similar regulation of METTL14, ALKBH5, and m6A was also observed in LCs upon treatment with human chorionic gonadotropin (HsCG). Knock down of YTHDF1 failed to change the expression of CAMKK2 Providing insight into novel therapeutic strategies by exploiting m6A RNA methylation as targets for treating azoospermatism and oligospermatism patients with reduction in serum testosterone. | |||
Target Regulation | Up regulation | |||
Responsed Disease | Azoospermia | ICD-11: GB04.0 | ||
Pathway Response | Autophagy | hsa04140 | ||
Cell Process | RNA stability | |||
Cell autophagy | ||||
In-vitro Model | TM3 | Normal | Mus musculus | CVCL_4326 |
In-vivo Model | Male SPF BALB/c mice (qls02-0202) were purchased from Qinglongshan animal breeding farm. Mice were sacrificed by CO2 asphyxiation and testes were obtained for following histopathological analyses. | |||
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: -9.55E-01 p-value: 2.96E-02 |
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 | m6A modification promoted translation of Protein phosphatase 1A (PPM1A) (protein phosphatase 1A, magnesium dependent, alpha isoform), a negative AMP-activated protein kinase (AMPK) regulator, but decreased expression of CAMKK2 (calcium/calmodulin-dependent protein kinase kinase 2, beta), a positive AMPK regulator, by reducing its RNA stability. Similar regulation of METTL14, ALKBH5, and m6A was also observed in LCs upon treatment with human chorionic gonadotropin (HsCG). Knock down of YTHDF1 failed to change the expression of CAMKK2 Providing insight into novel therapeutic strategies by exploiting m6A RNA methylation as targets for treating azoospermatism and oligospermatism patients with reduction in serum testosterone. | |||
Target Regulation | Up regulation | |||
Responsed Disease | Azoospermia | ICD-11: GB04.0 | ||
Pathway Response | Autophagy | hsa04140 | ||
Cell Process | RNA stability | |||
Cell autophagy | ||||
In-vitro Model | TM3 | Normal | Mus musculus | CVCL_4326 |
In-vivo Model | Male SPF BALB/c mice (qls02-0202) were purchased from Qinglongshan animal breeding farm. Mice were sacrificed by CO2 asphyxiation and testes were obtained for following histopathological analyses. | |||
YTH domain-containing family protein 1 (YTHDF1) [READER]
Representative RIP-seq result supporting the interaction between PPM1A and the regulator | ||
Cell Line | Hela | Homo sapiens |
Regulation | logFC: 1.22E+00 | GSE63591 |
In total 2 item(s) under this regulator | ||||
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene | [1] | |||
Response Summary | m6A modification promoted translation of Protein phosphatase 1A (PPM1A) (protein phosphatase 1A, magnesium dependent, alpha isoform), a negative AMP-activated protein kinase (AMPK) regulator, but decreased expression of CAMKK2 (calcium/calmodulin-dependent protein kinase kinase 2, beta), a positive AMPK regulator, by reducing its RNA stability. Similar regulation of METTL14, ALKBH5, and m6A was also observed in LCs upon treatment with human chorionic gonadotropin (HsCG). Knock down of YTHDF1 failed to change the expression of CAMKK2 Providing insight into novel therapeutic strategies by exploiting m6A RNA methylation as targets for treating azoospermatism and oligospermatism patients with reduction in serum testosterone. Rapamycin could effectively inhibit phosphorylation of RPS6KB1. | |||
Target Regulation | Up regulation | |||
Responsed Disease | Azoospermia | ICD-11: GB04.0 | ||
Pathway Response | Autophagy | hsa04140 | ||
Cell Process | RNA stability | |||
Cell autophagy | ||||
In-vitro Model | TM3 | Normal | Mus musculus | CVCL_4326 |
In-vivo Model | Male SPF BALB/c mice (qls02-0202) were purchased from Qinglongshan animal breeding farm. Mice were sacrificed by CO2 asphyxiation and testes were obtained for following histopathological analyses. | |||
Experiment 2 Reporting the m6A Methylation Regulator of This Target Gene | [1] | |||
Response Summary | m6A modification promoted translation of Protein phosphatase 1A (PPM1A) (protein phosphatase 1A, magnesium dependent, alpha isoform), a negative AMP-activated protein kinase (AMPK) regulator, but decreased expression of CAMKK2 (calcium/calmodulin-dependent protein kinase kinase 2, beta), a positive AMPK regulator, by reducing its RNA stability. Similar regulation of METTL14, ALKBH5, and m6A was also observed in LCs upon treatment with human chorionic gonadotropin (HsCG). Knock down of YTHDF1 failed to change the expression of CAMKK2 Providing insight into novel therapeutic strategies by exploiting m6A RNA methylation as targets for treating azoospermatism and oligospermatism patients with reduction in serum testosterone. | |||
Target Regulation | Up regulation | |||
Responsed Disease | Male infertility | ICD-11: GB04 | ||
Pathway Response | Autophagy | hsa04140 | ||
Cell Process | RNA stability | |||
Cell autophagy | ||||
In-vitro Model | TM3 | Normal | Mus musculus | CVCL_4326 |
In-vivo Model | Male SPF BALB/c mice (qls02-0202) were purchased from Qinglongshan animal breeding farm. Mice were sacrificed by CO2 asphyxiation and testes were obtained for following histopathological analyses. | |||
Male infertility [ICD-11: GB04]
In total 4 item(s) under this disease | ||||
Experiment 1 Reporting the m6A-centered Disease Response | [1] | |||
Response Summary | m6A modification promoted translation of Protein phosphatase 1A (PPM1A) (protein phosphatase 1A, magnesium dependent, alpha isoform), a negative AMP-activated protein kinase (AMPK) regulator, but decreased expression of CAMKK2 (calcium/calmodulin-dependent protein kinase kinase 2, beta), a positive AMPK regulator, by reducing its RNA stability. Similar regulation of METTL14, ALKBH5, and m6A was also observed in LCs upon treatment with human chorionic gonadotropin (HsCG). Knock down of YTHDF1 failed to change the expression of CAMKK2 Providing insight into novel therapeutic strategies by exploiting m6A RNA methylation as targets for treating azoospermatism and oligospermatism patients with reduction in serum testosterone. | |||
Responsed Disease | Azoospermia [ICD-11: GB04.0] | |||
Target Regulator | Methyltransferase-like 14 (METTL14) | WRITER | ||
Target Regulation | Up regulation | |||
Pathway Response | Autophagy | hsa04140 | ||
Cell Process | RNA stability | |||
Cell autophagy | ||||
In-vitro Model | TM3 | Normal | Mus musculus | CVCL_4326 |
In-vivo Model | Male SPF BALB/c mice (qls02-0202) were purchased from Qinglongshan animal breeding farm. Mice were sacrificed by CO2 asphyxiation and testes were obtained for following histopathological analyses. | |||
Experiment 2 Reporting the m6A-centered Disease Response | [1] | |||
Response Summary | m6A modification promoted translation of Protein phosphatase 1A (PPM1A) (protein phosphatase 1A, magnesium dependent, alpha isoform), a negative AMP-activated protein kinase (AMPK) regulator, but decreased expression of CAMKK2 (calcium/calmodulin-dependent protein kinase kinase 2, beta), a positive AMPK regulator, by reducing its RNA stability. Similar regulation of METTL14, ALKBH5, and m6A was also observed in LCs upon treatment with human chorionic gonadotropin (HsCG). Knock down of YTHDF1 failed to change the expression of CAMKK2 Providing insight into novel therapeutic strategies by exploiting m6A RNA methylation as targets for treating azoospermatism and oligospermatism patients with reduction in serum testosterone. | |||
Responsed Disease | Azoospermia [ICD-11: GB04.0] | |||
Target Regulator | RNA demethylase ALKBH5 (ALKBH5) | ERASER | ||
Target Regulation | Up regulation | |||
Pathway Response | Autophagy | hsa04140 | ||
Cell Process | RNA stability | |||
Cell autophagy | ||||
In-vitro Model | TM3 | Normal | Mus musculus | CVCL_4326 |
In-vivo Model | Male SPF BALB/c mice (qls02-0202) were purchased from Qinglongshan animal breeding farm. Mice were sacrificed by CO2 asphyxiation and testes were obtained for following histopathological analyses. | |||
Experiment 3 Reporting the m6A-centered Disease Response | [1] | |||
Response Summary | m6A modification promoted translation of Protein phosphatase 1A (PPM1A) (protein phosphatase 1A, magnesium dependent, alpha isoform), a negative AMP-activated protein kinase (AMPK) regulator, but decreased expression of CAMKK2 (calcium/calmodulin-dependent protein kinase kinase 2, beta), a positive AMPK regulator, by reducing its RNA stability. Similar regulation of METTL14, ALKBH5, and m6A was also observed in LCs upon treatment with human chorionic gonadotropin (HsCG). Knock down of YTHDF1 failed to change the expression of CAMKK2 Providing insight into novel therapeutic strategies by exploiting m6A RNA methylation as targets for treating azoospermatism and oligospermatism patients with reduction in serum testosterone. Rapamycin could effectively inhibit phosphorylation of RPS6KB1. | |||
Responsed Disease | Azoospermia [ICD-11: GB04.0] | |||
Target Regulator | YTH domain-containing family protein 1 (YTHDF1) | READER | ||
Target Regulation | Up regulation | |||
Pathway Response | Autophagy | hsa04140 | ||
Cell Process | RNA stability | |||
Cell autophagy | ||||
In-vitro Model | TM3 | Normal | Mus musculus | CVCL_4326 |
In-vivo Model | Male SPF BALB/c mice (qls02-0202) were purchased from Qinglongshan animal breeding farm. Mice were sacrificed by CO2 asphyxiation and testes were obtained for following histopathological analyses. | |||
Experiment 4 Reporting the m6A-centered Disease Response | [1] | |||
Response Summary | m6A modification promoted translation of Protein phosphatase 1A (PPM1A) (protein phosphatase 1A, magnesium dependent, alpha isoform), a negative AMP-activated protein kinase (AMPK) regulator, but decreased expression of CAMKK2 (calcium/calmodulin-dependent protein kinase kinase 2, beta), a positive AMPK regulator, by reducing its RNA stability. Similar regulation of METTL14, ALKBH5, and m6A was also observed in LCs upon treatment with human chorionic gonadotropin (HsCG). Knock down of YTHDF1 failed to change the expression of CAMKK2 Providing insight into novel therapeutic strategies by exploiting m6A RNA methylation as targets for treating azoospermatism and oligospermatism patients with reduction in serum testosterone. | |||
Responsed Disease | Male infertility [ICD-11: GB04] | |||
Target Regulator | YTH domain-containing family protein 1 (YTHDF1) | READER | ||
Target Regulation | Up regulation | |||
Pathway Response | Autophagy | hsa04140 | ||
Cell Process | RNA stability | |||
Cell autophagy | ||||
In-vitro Model | TM3 | Normal | Mus musculus | CVCL_4326 |
In-vivo Model | Male SPF BALB/c mice (qls02-0202) were purchased from Qinglongshan animal breeding farm. Mice were sacrificed by CO2 asphyxiation and testes were obtained for following histopathological analyses. | |||