General Information of the m6A Target Gene (ID: M6ATAR00619)
Target Name Protocadherin Fat 4 (FAT4)
Synonyms
hFat4; Cadherin family member 14; FAT tumor suppressor homolog 4; Fat-like cadherin protein FAT-J
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Gene Name FAT4
Chromosomal Location 4q28.1
Function
Cadherins are calcium-dependent cell adhesion proteins. FAT4 plays a role in the maintenance of planar cell polarity as well as in inhibition of YAP1-mediated neuroprogenitor cell proliferation and differentiation (By similarity).
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Gene ID 79633
Uniprot ID
FAT4_HUMAN
HGNC ID
HGNC:23109
Ensembl Gene ID
ENSG00000196159
KEGG ID
hsa:79633
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
FAT4 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
Browse Disease
Methyltransferase-like 3 (METTL3) [WRITER]
Representative RNA-seq result indicating the expression of this target gene regulated by METTL3
Cell Line HUVEC cell line Homo sapiens
Treatment: shMETTL3 HUVEC cells
Control: shScramble HUVEC cells
GSE157544
Regulation
logFC: 9.37E-01
p-value: 7.13E-05
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 Specific depletion of METTL3 in pericytes suppressed diabetes-induced pericyte dysfunction and Microvascular complication in vivo. METTL3 overexpression impaired pericyte function by repressing PKC-Eta, Protocadherin Fat 4 (FAT4), and PDGFRA expression, which was mediated by YTHDF2-dependent mRNA decay.
Target Regulation Down regulation
Responsed Disease Diseases of arteries or arterioles ICD-11: BD5Y
In-vitro Model ACBRI-183 (Human retinal pericytes (ACBRI-183) was obtained from Cell Systems Corp. (CSC, USA))
In-vivo Model Mettl3 floxed mice were purchased from GemPharmatech Co. Ltd (Nanjing, China). Pdgfr-Beta-Cre mice were purchased from Beijing Biocytogen Co. Ltd (Beijing, China) generated on C57BL/6J background. Mettl3 flox/flox mice were crossed with Pdgfr-Beta-Cre mice to generate pericyte-specific Mettl3 knockout mice. All mice were bred under the specific-pathogen free condition with free access to diet and water or their nursing mothers with alternating 12/12 light-dark cycle (lights on at 08:00 and off at 20:00).
Diseases of arteries or arterioles [ICD-11: BD5Y]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [1]
Response Summary Specific depletion of METTL3 in pericytes suppressed diabetes-induced pericyte dysfunction and Microvascular complication in vivo. METTL3 overexpression impaired pericyte function by repressing PKC-Eta, Protocadherin Fat 4 (FAT4), and PDGFRA expression, which was mediated by YTHDF2-dependent mRNA decay.
Responsed Disease Diseases of arteries or arterioles [ICD-11: BD5Y]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
Target Regulation Down regulation
In-vitro Model ACBRI-183 (Human retinal pericytes (ACBRI-183) was obtained from Cell Systems Corp. (CSC, USA))
In-vivo Model Mettl3 floxed mice were purchased from GemPharmatech Co. Ltd (Nanjing, China). Pdgfr-Beta-Cre mice were purchased from Beijing Biocytogen Co. Ltd (Beijing, China) generated on C57BL/6J background. Mettl3 flox/flox mice were crossed with Pdgfr-Beta-Cre mice to generate pericyte-specific Mettl3 knockout mice. All mice were bred under the specific-pathogen free condition with free access to diet and water or their nursing mothers with alternating 12/12 light-dark cycle (lights on at 08:00 and off at 20:00).
References
Ref 1 METTL3-mediated N (6)-methyladenosine modification governs pericyte dysfunction during diabetes-induced retinal vascular complication. Theranostics. 2022 Jan 1;12(1):277-289. doi: 10.7150/thno.63441. eCollection 2022.