General Information of the Drug (ID: M6APDG04348)
Name
TNFQb therapeutic vaccines
Synonyms
TNFQb; CYT-020-TNFQb; TNF-targeted vaccine (inflammation, Immunodrug), Cytos Biotechnology; TNFQb therapeutic vaccines (rheumatoid arthritis/psoriasis/Crohn's disease); TNFQb therapeutic vaccines (rheumatoid arthritis/psoriasis/Crohn's disease), Cytos; Immunodrug vaccines (TNF) (rheumatoid arthritis/psoriasis/Crohn's disease), Cytos
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Status
Terminated
TTD Drug ID
D06MJP
Target Gene(s) and Their Upstream m6A Regulator, Together with the Effect of Target Gene(s) in Drug Response
The target genes involved in drug-target interaction (such as drug-metabolizing enzymes, drug transporters and therapeutic targets) and drug-mediated cell death signaling (including modulating DNA damage and repair capacity, escaping from drug-induced apoptosis, autophagy, cellular metabolic reprogramming, oncogenic bypass signaling, cell microenvironment, cell stemness, etc.) could be regulated by m6A regulator(s) and affected their corresponding drug response. You can browse detailed information on drug-related target gene(s) mediated by m6A regulators.
Tumor necrosis factor (TNF)
Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2)
In total 1 mechanisms lead to this potential drug response
Response Summary Tumor necrosis factor (TNF) is a therapeutic target for TNFQb therapeutic vaccines. The Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) has potential in affecting the response of TNFQb therapeutic vaccines through regulating the expression of Tumor necrosis factor (TNF). [1], [2]
Methyltransferase-like 14 (METTL14)
In total 1 mechanisms lead to this potential drug response
Response Summary Tumor necrosis factor (TNF) is a therapeutic target for TNFQb therapeutic vaccines. The Methyltransferase-like 14 (METTL14) has potential in affecting the response of TNFQb therapeutic vaccines through regulating the expression of Tumor necrosis factor (TNF). [2], [3]
Methyltransferase-like 3 (METTL3)
In total 1 mechanisms lead to this potential drug response
Response Summary Tumor necrosis factor (TNF) is a therapeutic target for TNFQb therapeutic vaccines. The Methyltransferase-like 3 (METTL3) has potential in affecting the response of TNFQb therapeutic vaccines through regulating the expression of Tumor necrosis factor (TNF). [2], [4]
YTH domain-containing family protein 1 (YTHDF1)
In total 1 mechanisms lead to this potential drug response
Response Summary Tumor necrosis factor (TNF) is a therapeutic target for TNFQb therapeutic vaccines. The YTH domain-containing family protein 1 (YTHDF1) has potential in affecting the response of TNFQb therapeutic vaccines through regulating the expression of Tumor necrosis factor (TNF). [2], [4]
YTH domain-containing family protein 3 (YTHDF3)
In total 1 mechanisms lead to this potential drug response
Response Summary Tumor necrosis factor (TNF) is a therapeutic target for TNFQb therapeutic vaccines. The YTH domain-containing family protein 3 (YTHDF3) has potential in affecting the response of TNFQb therapeutic vaccines through regulating the expression of Tumor necrosis factor (TNF). [1], [2]
References
Ref 1 N6-methyladenosine reader YTH N6-methyladenosine RNA binding protein 3 or insulin like growth factor 2 mRNA binding protein 2 knockdown protects human bronchial epithelial cells from hypoxia/reoxygenation injury by inactivating p38 MAPK, AKT, ERK1/2, and NF-KappaB pathways. Bioengineered. 2022 May;13(5):11973-11986. doi: 10.1080/21655979.2021.1999550.
Ref 2 Effect of the carbocyclic nucleoside analogue MDL 201,112 on inhibition of interferon-gamma-induced priming of Lewis (LEW/N) rat macrophages for enhanced respiratory burst and MHC class II Ia+ antigen expression. J Leukoc Biol. 1994 Aug;56(2):133-44. doi: 10.1002/jlb.56.2.133.
Ref 3 METTL14 promotes glomerular endothelial cell injury and diabetic nephropathy via m6A modification of Alpha-klotho. Mol Med. 2021 Sep 9;27(1):106. doi: 10.1186/s10020-021-00365-5.
Ref 4 Mettl3 inhibits the apoptosis and autophagy of chondrocytes in inflammation through mediating Bcl2 stability via Ythdf1-mediated m(6)A modification. Bone. 2022 Jan;154:116182. doi: 10.1016/j.bone.2021.116182. Epub 2021 Sep 13.