Literature summary for 3.4.22.B71 extracted from

Tan, M.; Zhang, D.; Zhang, E.; Xu, D.; Liu, Z.; Qiu, J.; Fan, Y.; Shen, B.
SENP2 suppresses epithelial-mesenchymal transition of bladder cancer cells through deSUMOylation of TGF-betaRI (2017), Mol. Carcinog., 56, 2332-2341 .

Search for more literature for 3.4.22.B71

Application

Application	Comment	Organism
medicine	SENP2 is frequently downregulated in bladder cancer, especially in metastatic bladder cancer. SENP2 downregulation is associated with more aggressive phenotypes and poor patient outcomes. SENP2 suppresses bladder cancer cell invasion in vitro and tumor metastasis in vivo, acts as a tumor suppressor gene in bladder cancer	Homo sapiens

Protein Variants

Protein Variants	Comment	Organism
R576L/K577M	catalytically inactive SENP2 mutant, unable to regulate TGF-beta signaling	Homo sapiens

Organism

Organism	UniProt	Comment	Textmining
Homo sapiens	Q9HC62	-	-

Substrates and Products (Substrate)

Substrates	Comment Substrates	Organism	Products	Comment (Products)	Rev.	Reac.
SUMOylated TGF-beta receptor + H2O	-	Homo sapiens	?	-	?

General Information

General Information	Comment	Organism
physiological function	SENP2 knockdown results in a decrease of E-cadherin and an increase of N-cadherin and fibronectin at both transcript and protein levels. SENP2 overexpression results in deSUMOylation of TGF-betaR I in bladder cancer cells and suppresses TGF-beta signaling and TGF-beta-induced epithelial-mesenchymal transition. SENP2 regulates TGF-beta signaling partly through deSUMOylation of TGFbeta receptor I	Homo sapiens

Use of this online version of BRENDA is free under the CC BY 4.0 license. See terms of use for full details.

Release 2023.1 (January 2023)