General Information of the m6A Target Gene (ID: M6ATAR00630)
Target Name Extracellular sulfatase Sulf-2 (Sulf2)
Synonyms
hSulf-2
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Gene Name Sulf2
Chromosomal Location 20q13.12
Family Sulfatase family
Function
Exhibits arylsulfatase activity and highly specific endoglucosamine-6-sulfatase activity. It can remove sulfate from the C-6 position of glucosamine within specific subregions of intact heparin.
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Gene ID 55959
Uniprot ID
SULF2_HUMAN
HGNC ID
HGNC:20392
Ensembl Gene ID
ENSG00000196562
KEGG ID
hsa:55959
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
Sulf2 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 16 (METTL16) [WRITER]
In total 1 item(s) under this regulator
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene [1]
Response Summary METTL16 regulates Extracellular sulfatase Sulf-2 (Sulf2) expression via m6A modification and thereby contribute to PM2.5-induced pulmonary microvascular injury.
Target Regulation Down regulation
Responsed Disease Injury of pulmonary blood vessels ICD-11: NB30.4
In-vitro Model Rattus norvegicus (Rat pulmonary microvascular endothelial cells (PMVECs) were isolated from lung tissues)
In-vivo Model The rats were randomly divided into a fresh air group and a COPD group and each group contained 10 rats. The COPD group was placed into a breathable cage and exposed to PM2.5 (1.46 mg/m3) from the motor vehicle exhaust for two 2-h exposure periods (from 9:00 a.m. to 11:00 a.m. and from 15:00 p.m. to 17:00 p.m.), 5 days per week, for 7 months. After each period of exposure, the animals were exposed to fresh air for 30 min to take a rest. Gasoline-powered motorcycle used as of source of the Particulate matter (PM) pollution was located next door to the rat exposure room, and the PM was directed towards the exposure room through a metal tube. Fresh air was sent to through an air pump. After exposed for 7 months, rats were performed lung function test using a Forced Pulmonary Maneuver System (Buxco Research Systems, Wilmington, NC, USA).
Injury of blood vessels of thorax [ICD-11: NB30]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [1]
Response Summary METTL16 regulates Extracellular sulfatase Sulf-2 (Sulf2) expression via m6A modification and thereby contribute to PM2.5-induced pulmonary microvascular injury.
Responsed Disease Injury of pulmonary blood vessels [ICD-11: NB30.4]
Target Regulator Methyltransferase-like 16 (METTL16) WRITER
Target Regulation Down regulation
In-vitro Model Rattus norvegicus (Rat pulmonary microvascular endothelial cells (PMVECs) were isolated from lung tissues)
In-vivo Model The rats were randomly divided into a fresh air group and a COPD group and each group contained 10 rats. The COPD group was placed into a breathable cage and exposed to PM2.5 (1.46 mg/m3) from the motor vehicle exhaust for two 2-h exposure periods (from 9:00 a.m. to 11:00 a.m. and from 15:00 p.m. to 17:00 p.m.), 5 days per week, for 7 months. After each period of exposure, the animals were exposed to fresh air for 30 min to take a rest. Gasoline-powered motorcycle used as of source of the Particulate matter (PM) pollution was located next door to the rat exposure room, and the PM was directed towards the exposure room through a metal tube. Fresh air was sent to through an air pump. After exposed for 7 months, rats were performed lung function test using a Forced Pulmonary Maneuver System (Buxco Research Systems, Wilmington, NC, USA).
References
Ref 1 PM2.5 induces pulmonary microvascular injury in COPD via METTL16-mediated m6A modification. Environ Pollut. 2022 Jun 15;303:119115. doi: 10.1016/j.envpol.2022.119115. Epub 2022 Mar 5.