m6A Target Gene Information
General Information of the m6A Target Gene (ID: M6ATAR00030)
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
hsa-mir-181b-1
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]
In total 1 item(s) under this regulator | ||||
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene | [1] | |||
Response Summary | ALKBH5 is an anti-tumor factor or a pro-apoptotic factor, acting at least partially by suppressing YAP expression through dual mechanisms with direct m6A methylation of YAP and indirect downregulation of YAP level due to methylation of hsa-mir-181b-1. Further results revealed that m6A methylated pre-miR-181b-1 was subsequently recognized by m6A-binding protein YTHDF2 to mediate RNA degradation. However, methylated YAP transcripts were recognized by YTHDF1 to promote its translation. ALKBH5 overexpression was considered a new approach of replacement therapy for osteosarcoma treatment. | |||
Target Regulation | Down regulation | |||
Responsed Disease | Osteosarcoma | ICD-11: 2B51 | ||
Cell Process | Cell growth | |||
Cell migration | ||||
Cell invasion | ||||
Cell apoptosis | ||||
In-vitro Model | U2OS | Osteosarcoma | Homo sapiens | CVCL_0042 |
In-vivo Model | Three-week-old BABL/c female nude mice were randomized into three groups. 5 × 106 143B cells were subcutaneously injected in mice, and the tumor volume was assessed every 2 weeks. Eight weeks after injection, the animals were killed. The xenograft tumors were harvested and the tumor volumes were calculated by the standard formula: length × width2/2. | |||
YTH domain-containing family protein 2 (YTHDF2) [READER]
In total 1 item(s) under this regulator | ||||
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene | [1] | |||
Response Summary | ALKBH5 is an anti-tumor factor or a pro-apoptotic factor, acting at least partially by suppressing YAP expression through dual mechanisms with direct m6A methylation of YAP and indirect downregulation of YAP level due to methylation of hsa-mir-181b-1. Further results revealed that m6A methylated pre-miR-181b-1 was subsequently recognized by m6A-binding protein YTHDF2 to mediate RNA degradation. However, methylated YAP transcripts were recognized by YTHDF1 to promote its translation. ALKBH5 overexpression was considered a new approach of replacement therapy for osteosarcoma treatment. | |||
Target Regulation | Down regulation | |||
Responsed Disease | Osteosarcoma | ICD-11: 2B51 | ||
Cell Process | Cell growth | |||
Cell migration | ||||
Cell invasion | ||||
Cell apoptosis | ||||
In-vitro Model | U2OS | Osteosarcoma | Homo sapiens | CVCL_0042 |
In-vivo Model | Three-week-old BABL/c female nude mice were randomized into three groups. 5 × 106 143B cells were subcutaneously injected in mice, and the tumor volume was assessed every 2 weeks. Eight weeks after injection, the animals were killed. The xenograft tumors were harvested and the tumor volumes were calculated by the standard formula: length × width2/2. | |||
Osteosarcoma [ICD-11: 2B51]
In total 2 item(s) under this disease | ||||
Experiment 1 Reporting the m6A-centered Disease Response | [1] | |||
Response Summary | ALKBH5 is an anti-tumor factor or a pro-apoptotic factor, acting at least partially by suppressing YAP expression through dual mechanisms with direct m6A methylation of YAP and indirect downregulation of YAP level due to methylation of hsa-mir-181b-1. Further results revealed that m6A methylated pre-miR-181b-1 was subsequently recognized by m6A-binding protein YTHDF2 to mediate RNA degradation. However, methylated YAP transcripts were recognized by YTHDF1 to promote its translation. ALKBH5 overexpression was considered a new approach of replacement therapy for osteosarcoma treatment. | |||
Responsed Disease | Osteosarcoma [ICD-11: 2B51] | |||
Target Regulator | RNA demethylase ALKBH5 (ALKBH5) | ERASER | ||
Target Regulation | Down regulation | |||
Cell Process | Cell growth | |||
Cell migration | ||||
Cell invasion | ||||
Cell apoptosis | ||||
In-vitro Model | U2OS | Osteosarcoma | Homo sapiens | CVCL_0042 |
In-vivo Model | Three-week-old BABL/c female nude mice were randomized into three groups. 5 × 106 143B cells were subcutaneously injected in mice, and the tumor volume was assessed every 2 weeks. Eight weeks after injection, the animals were killed. The xenograft tumors were harvested and the tumor volumes were calculated by the standard formula: length × width2/2. | |||
Experiment 2 Reporting the m6A-centered Disease Response | [1] | |||
Response Summary | ALKBH5 is an anti-tumor factor or a pro-apoptotic factor, acting at least partially by suppressing YAP expression through dual mechanisms with direct m6A methylation of YAP and indirect downregulation of YAP level due to methylation of hsa-mir-181b-1. Further results revealed that m6A methylated pre-miR-181b-1 was subsequently recognized by m6A-binding protein YTHDF2 to mediate RNA degradation. However, methylated YAP transcripts were recognized by YTHDF1 to promote its translation. ALKBH5 overexpression was considered a new approach of replacement therapy for osteosarcoma treatment. | |||
Responsed Disease | Osteosarcoma [ICD-11: 2B51] | |||
Target Regulator | YTH domain-containing family protein 2 (YTHDF2) | READER | ||
Target Regulation | Down regulation | |||
Cell Process | Cell growth | |||
Cell migration | ||||
Cell invasion | ||||
Cell apoptosis | ||||
In-vitro Model | U2OS | Osteosarcoma | Homo sapiens | CVCL_0042 |
In-vivo Model | Three-week-old BABL/c female nude mice were randomized into three groups. 5 × 106 143B cells were subcutaneously injected in mice, and the tumor volume was assessed every 2 weeks. Eight weeks after injection, the animals were killed. The xenograft tumors were harvested and the tumor volumes were calculated by the standard formula: length × width2/2. | |||