General Information of the m6A Target Gene (ID: M6ATAR00050)
Target Name hsa-miR-143-3p
Synonyms
hsa_miR_143_3p
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Gene Name hsa-miR-143-3p
miRBase ID
MIMAT0000435
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
hsa-miR-143-3p 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
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Protein virilizer homolog (VIRMA) [WRITER]
In total 1 item(s) under this regulator
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene [1]
Response Summary KIAA1429 is downregulated while ALKBH5 is upregulated in aortic tissues from aortic dissection patients. KIAA1429/ALKBH5-mediated m6A modifications can regulate the processing of hsa-miR-143-3p through interacting with the microprocessor protein DGCR8. KIAA1429 and ALKBH5 can oppositely regulate HASMC proliferation, HAEC apoptosis, and AD progression in AngII-infused mice via the miR-143-3p/DDX6 pathway.
Target Regulation Down regulation
Responsed Disease Aortic aneurysm or dissection ICD-11: BD50
Pathway Response RNA degradation hsa03018
Cell Process Cell apoptosis
In-vitro Model IM-HAEC Normal Homo sapiens CVCL_B5WL
In-vivo Model Osmotic mini-pumps containing AngII (1 ug/kg/min, Enzo Bioche) were implanted in 7-week-old male mice. To interfere with the expression of KIAA1429, ALKBH5, or DDX6 in vivo, adeno-associated virus 9 (AAV9) vectors carrying a variety of overexpression plasmids or interfering RNA were randomly injected through the tail vein to C57BL/6N mice.
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 KIAA1429 is downregulated while ALKBH5 is upregulated in aortic tissues from aortic dissection patients. KIAA1429/ALKBH5-mediated m6A modifications can regulate the processing of hsa-miR-143-3p through interacting with the microprocessor protein DGCR8. KIAA1429 and ALKBH5 can oppositely regulate HASMC proliferation, HAEC apoptosis, and AD progression in AngII-infused mice via the miR-143-3p/DDX6 pathway.
Target Regulation Down regulation
Responsed Disease Aortic aneurysm or dissection ICD-11: BD50
Pathway Response RNA degradation hsa03018
Cell Process Cell apoptosis
In-vitro Model IM-HAEC Normal Homo sapiens CVCL_B5WL
In-vivo Model Osmotic mini-pumps containing AngII (1 ug/kg/min, Enzo Bioche) were implanted in 7-week-old male mice. To interfere with the expression of KIAA1429, ALKBH5, or DDX6 in vivo, adeno-associated virus 9 (AAV9) vectors carrying a variety of overexpression plasmids or interfering RNA were randomly injected through the tail vein to C57BL/6N mice.
Aortic aneurysm or dissection [ICD-11: BD50]
In total 2 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [1]
Response Summary KIAA1429 is downregulated while ALKBH5 is upregulated in aortic tissues from aortic dissection patients. KIAA1429/ALKBH5-mediated m6A modifications can regulate the processing of hsa-miR-143-3p through interacting with the microprocessor protein DGCR8. KIAA1429 and ALKBH5 can oppositely regulate HASMC proliferation, HAEC apoptosis, and AD progression in AngII-infused mice via the miR-143-3p/DDX6 pathway.
Responsed Disease Aortic aneurysm or dissection [ICD-11: BD50]
Target Regulator Protein virilizer homolog (VIRMA) WRITER
Target Regulation Down regulation
Pathway Response RNA degradation hsa03018
Cell Process Cell apoptosis
In-vitro Model IM-HAEC Normal Homo sapiens CVCL_B5WL
In-vivo Model Osmotic mini-pumps containing AngII (1 ug/kg/min, Enzo Bioche) were implanted in 7-week-old male mice. To interfere with the expression of KIAA1429, ALKBH5, or DDX6 in vivo, adeno-associated virus 9 (AAV9) vectors carrying a variety of overexpression plasmids or interfering RNA were randomly injected through the tail vein to C57BL/6N mice.
Experiment 2 Reporting the m6A-centered Disease Response [1]
Response Summary KIAA1429 is downregulated while ALKBH5 is upregulated in aortic tissues from aortic dissection patients. KIAA1429/ALKBH5-mediated m6A modifications can regulate the processing of hsa-miR-143-3p through interacting with the microprocessor protein DGCR8. KIAA1429 and ALKBH5 can oppositely regulate HASMC proliferation, HAEC apoptosis, and AD progression in AngII-infused mice via the miR-143-3p/DDX6 pathway.
Responsed Disease Aortic aneurysm or dissection [ICD-11: BD50]
Target Regulator RNA demethylase ALKBH5 (ALKBH5) ERASER
Target Regulation Down regulation
Pathway Response RNA degradation hsa03018
Cell Process Cell apoptosis
In-vitro Model IM-HAEC Normal Homo sapiens CVCL_B5WL
In-vivo Model Osmotic mini-pumps containing AngII (1 ug/kg/min, Enzo Bioche) were implanted in 7-week-old male mice. To interfere with the expression of KIAA1429, ALKBH5, or DDX6 in vivo, adeno-associated virus 9 (AAV9) vectors carrying a variety of overexpression plasmids or interfering RNA were randomly injected through the tail vein to C57BL/6N mice.
References
Ref 1 KIAA1429 and ALKBH5 Oppositely Influence Aortic Dissection Progression via Regulating the Maturation of Pri-miR-143-3p in an m6A-Dependent Manner. Front Cell Dev Biol. 2021 Aug 19;9:668377. doi: 10.3389/fcell.2021.668377. eCollection 2021.