General Information of the m6A Target Gene (ID: M6ATAR00643)
Target Name Dexamethasone-induced Ras-related protein 1 (RASD1)
Synonyms
Activator of G-protein signaling 1
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Gene Name RASD1
Chromosomal Location 17p11.2
Family Small GTPase superfamily, RasD family
Function
Small GTPase. Negatively regulates the transcription regulation activity of the APBB1/FE65-APP complex via its interaction with APBB1/FE65 (By similarity).
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Gene ID 51655
Uniprot ID
RASD1_HUMAN
HGNC ID
HGNC:15828
Ensembl Gene ID
ENSG00000108551
KEGG ID
hsa:51655
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
RASD1 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 14 (METTL14) [WRITER]
Representative RNA-seq result indicating the expression of this target gene regulated by METTL14
Cell Line mouse embryonic stem cells Mus musculus
Treatment: METTL14-/- ESCs
Control: Wild type ESCs
GSE145309
Regulation
logFC: -1.81E+00
p-value: 2.87E-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 Mettl14-mediated m6A modification inhibited Dexamethasone-induced Ras-related protein 1 (RASD1) and induced the apoptosis of spinal cord neurons in SCI by promoting the transformation of pri-miR-375 to mature miR-375.
Target Regulation Down regulation
Responsed Disease Injuries of spine or trunk ICD-11: ND51
Pathway Response mTOR signaling pathway hsa04150
In-vitro Model C8-D1A Normal Mus musculus CVCL_6379
C8-B4 Normal Mus musculus CVCL_6378
In-vivo Model An incision was made in the skin along the medial dorsal line to the aponeurotic and muscular planes, and the posterior vertebral arches were exposed from T8 to T12. Under the dissection stereomicroscope, 3-mm-long laminectomy was performed on the caudal end of T10 vertebra and the rostral end of T11 vertebra. The Infinite Horizons impactor (Infinite Horizons, L.L.C., Lexington, KY, USA) was adopted to produce the contusion SCI using a force of 60 kdyn/cm2. The SCI model rats were established and randomly assigned to SCI model group, ant-NC (negative control, SCI rats treated with lentiviral (lv)-shRNA NC of Mettl14) group and ant-Mettl14 group (SCI rats treated with lv-shRNA of Mettl14). Rats were subjected to laminectomy and then treated with lv-shRNA Mettl14/lv-shRNA-NC (50 ul/day, 100 nmoL/mL; RiboBio, Guangzhou, China) via an intrathecal injection through lumbar puncture for 3 days (0, 1, and 2 days) after 15 min of SCI modelling. In addition, the unmodeled rats were set as sham group.
Injuries of spine or trunk [ICD-11: ND51]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [1]
Response Summary Mettl14-mediated m6A modification inhibited Dexamethasone-induced Ras-related protein 1 (RASD1) and induced the apoptosis of spinal cord neurons in SCI by promoting the transformation of pri-miR-375 to mature miR-375.
Responsed Disease Injuries of spine or trunk [ICD-11: ND51]
Target Regulator Methyltransferase-like 14 (METTL14) WRITER
Target Regulation Down regulation
Pathway Response mTOR signaling pathway hsa04150
In-vitro Model C8-D1A Normal Mus musculus CVCL_6379
C8-B4 Normal Mus musculus CVCL_6378
In-vivo Model An incision was made in the skin along the medial dorsal line to the aponeurotic and muscular planes, and the posterior vertebral arches were exposed from T8 to T12. Under the dissection stereomicroscope, 3-mm-long laminectomy was performed on the caudal end of T10 vertebra and the rostral end of T11 vertebra. The Infinite Horizons impactor (Infinite Horizons, L.L.C., Lexington, KY, USA) was adopted to produce the contusion SCI using a force of 60 kdyn/cm2. The SCI model rats were established and randomly assigned to SCI model group, ant-NC (negative control, SCI rats treated with lentiviral (lv)-shRNA NC of Mettl14) group and ant-Mettl14 group (SCI rats treated with lv-shRNA of Mettl14). Rats were subjected to laminectomy and then treated with lv-shRNA Mettl14/lv-shRNA-NC (50 ul/day, 100 nmoL/mL; RiboBio, Guangzhou, China) via an intrathecal injection through lumbar puncture for 3 days (0, 1, and 2 days) after 15 min of SCI modelling. In addition, the unmodeled rats were set as sham group.
References
Ref 1 Mettl14-mediated m6A modification modulates neuron apoptosis during the repair of spinal cord injury by regulating the transformation from pri-mir-375 to miR-375. Cell Biosci. 2021 Mar 11;11(1):52. doi: 10.1186/s13578-020-00526-9.