DESI2

Last update 08 May 2025

Basic Info

Synonyms

C1orf121, CGI-146, DESI-2

+ [9]

Introduction

Has deubiquitinating activity towards 'Lys-48'- and 'Lys-63'-linked polyubiquitin chains. Deubiquitinates 'Lys-48'-linked polyubiquitination of RPS7 leading to its stabilization (PubMed:28483520). Exhibits palmitoyl protein thioesterase (S-depalmitoylation) activity towards synthetic substrates 4-methylumbelliferyl-6-S-palmitoyl-beta-D-glucopyranoside and S-depalmitoylation probe 5 (DPP-5) (PubMed:35427157).

100 Clinical Results associated with DESI2

100 Translational Medicine associated with DESI2

0 Patents (Medical) associated with DESI2

Literatures (Medical) associated with DESI2

01 Jul 2023·The Plant journal : for cell and molecular biology

A Phytophthora infestans RXLR effector AVR8 suppresses plant immunity by targeting a desumoylating isopeptidase DeSI2.

Article

Author: Mu, Yang ; Wu, Jiahui ; Song, Jingyi ; Song, Botao ; Jiang, Rui ; Liu, Huiming ; Vleeshouwers, Vivianne G A A ; Tian, Zhendong ; Yu, Jian ; Xie, Conghua ; Du, Juan ; He, Qin ; Liu, Zeng ; Hu, Kefan

The potato's most devastating disease is late blight, which is caused by Phytophthora infestans.Whereas various resistance (R) genes are known, most are typically defeated by this fast-evolving oomycete pathogen.However, the broad-spectrum and durable R8 is a vital gene resource for potato resistance breeding.To support an educated deployment of R8, we embarked on a study on the corresponding avirulence gene Avr8.We overexpressed Avr8 by transient and stable transformation, and found that Avr8 promotes colonization of P. infestans in Nicotiana benthamiana and potato, resp.A yeast-two-hybrid (Y2H) screen showed that AVR8 interacts with a desumoylating isopeptidase (StDeSI2) of potato.We overexpressed DeSI2 and found that DeSI2 pos. regulates resistance to P. infestans, while silencing StDeSI2 downregulated the expression of a set of defense-related genes.By using a specific proteasome inhibitor, we found that AVR8 destabilized StDeSI2 through the 26S proteasome and attenuated early PTI responses.Altogether, these results indicate that AVR8 manipulates desumoylation, which is a new strategy that adds to the plethora of mechanisms that Phytophthora exploits to modulate host immunity, and StDeSI2 provides a new target for durable resistance breeding against P. infestans in potato.

15 Apr 2022·Science Advances

Cln5 represents a new type of cysteine-based S -depalmitoylase linked to neurodegeneration

Article

Author: Hofmann, Kay ; Bellotti, Cristina ; Luebben, Anna V. ; Steinfeld, Robert ; Qiu, Tian ; Krätzner, Ralph ; Erven, Ilka ; Klemp, Henry ; Stäuble, Andreas ; Sheldrick, George M. ; Gärtner, Jutta ; Becker, Stefan ; Dickinson, Bryan C. ; Crowther, Lisa M. ; Kathayat, Rahul S. ; Bender, Daniel ; Söding, Johannes

Genetic CLN5 variants are associated with childhood neurodegeneration and Alzheimer’s disease; however, the molecular function of ceroid lipofuscinosis neuronal protein 5 (Cln5) is unknown. We solved the Cln5 crystal structure and identified a region homologous to the catalytic domain of members of the N1pC/P60 superfamily of papain-like enzymes. However, we observed no protease activity for Cln5; and instead, we discovered that Cln5 and structurally related PPPDE1 and PPPDE2 have efficient cysteine palmitoyl thioesterase ( S -depalmitoylation) activity using fluorescent substrates. Mutational analysis revealed that the predicted catalytic residues histidine-166 and cysteine-280 are critical for Cln5 thioesterase activity, uncovering a new cysteine-based catalytic mechanism for S -depalmitoylation enzymes. Last, we found that Cln5-deficient neuronal progenitor cells showed reduced thioesterase activity, confirming live cell function of Cln5 in setting S -depalmitoylation levels. Our results provide new insight into the function of Cln5, emphasize the importance of S -depalmitoylation in neuronal homeostasis, and disclose a new, unexpected enzymatic function for the N1pC/P60 superfamily of proteins.

01 May 2021·Journal of Human Genetics

Molecular pathogenesis of breast cancer: impact of miR-99a-5p and miR-99a-3p regulation on oncogenic genes

Article

Author: Toda, Hiroko ; Okada, Reona ; Hirashima, Tadahiro ; Tanaka, Takako ; Hozaka, Yuto ; Shinden, Yoshiaki ; Nohata, Nijiro ; Kijima, Yuko ; Asai, Shunichi ; Seki, Naohiko ; Ohtsuka, Takao

Our recent research has revealed that passenger strands of certain microRNAs (miRNAs) function as tumor-suppressive miRNAs in cancer cells, e.g., miR-101-5p, miR-143-5p, miR-144-5p, miR-145-3p, and miR-150-3p. Thus, they are important in cancer pathogenesis. Analysis of the miRNA expression signature of breast cancer (BrCa) showed that the expression levels of two miRNAs derived from pre-miR-99a (miR-99a-5p and miR-99a-3p) were suppressed in cancerous tissues. The aim of this study was to identify oncogenic genes controlled by pre-miR-99a that are closely involved in the molecular pathogenesis of BrCa. A total of 113 genes were identified as targets of pre-miR-99a regulation (19 genes modulated by miR-99a-5p, and 95 genes regulated by miR-99a-3p) in BrCa cells. Notably, FAM64A was targeted by both of the miRNAs. Among these targets, high expression of 16 genes (C5orf22, YOD1, SLBP, F11R, C12orf49, SRPK1, ZNF250, ZNF695, CDK1, DNMT3B, TRIM25, MCM4, CDKN3, PRPS, FAM64A, and DESI2) significantly predicted reduced survival of BrCa patients based upon The Cancer Genome Atlas (TCGA) database. In this study, we focused on FAM64A and investigated the relationship between FAM64A expression and molecular pathogenesis of BrCa subtypes. The upregulation of FAM64A was confirmed in BrCa clinical specimens. Importantly, the expression of FAM64A significantly differed between patients with Luminal-A and Luminal-B subtypes. Our data strongly suggest that the aberrant expression of FAM64A is involved in the malignant transformation of BrCa. Our miRNA-based approaches (identification of tumor-suppressive miRNAs and their controlled targets) will provide novel information regarding the molecular pathogenesis of BrCa.

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DESI2

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