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Last update 08 May 2025

UBL5

Last update 08 May 2025

Basic Info

Synonyms

ubiquitin like 5, Ubiquitin-like protein 5, UBL5

Introduction

Ubiquitin-like protein that plays a role in cell proliferation and sister chromatid cohesion by associating with spliceosomal proteins (PubMed:25092792). Participates thereby in pre-mRNA splicing by maintaining spliceosome integrity. Promotes the functional integrity of the Fanconi anemia DNA repair pathway by interacting with FANCI component and subsequently mediating the formation of FANCI homodimers (PubMed:25862789). Plays also a protective role against ER stress-induced apoptosis (PubMed:37315790).

Drugs associated with UBL5

TD02-OVL5

Target

UBL5

Mechanism

UBL5 modulators

Active Org.

Novo Nordisk A/S [+1]

Originator Org.

Tissue Dynamics Ltd.

Active Indication

Obesity

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with UBL5

100 Translational Medicine associated with UBL5

0 Patents (Medical) associated with UBL5

Literatures (Medical) associated with UBL5

01 Dec 2024·Science of The Total Environment

6-PPD quinone at environmentally relevant concentrations induced damage on longevity in C. elegans: Mechanistic insight from inhibition in mitochondrial UPR response

Article

Author: Wang, Dayong ; Hua, Xin

6-PPD quinone (6-PPDQ) exists widely in water environment media, causing acute lethality to some aquatic species. Long-term exposure to 6-PPDQ reduced the lifespan of Caenorhabditis elegans. However, the molecular basis for mitochondrial control of 6-PPDQ toxicity remains largely unclear. Using HSP-6 as marker of mitochondrial unfolded protein response (mt UPR), we observed activation of mt UPR by 0.1 and 1 μg/L 6-PPDQ and inhibition in mt UPR by 10 μg/L 6-PPDQ. Additionally, increased atfs-1, ubl-5, and dve-1 expressions were caused by 0.1 and 1 μg/L 6-PPDQ and decreased expressions of these genes were induced by 10 μg/L 6-PPDQ. Neuronal and intestinal RNA interference (RNAi) of hsp-6 caused susceptibility to 6-PPDQ toxicity on longevity, and atfs-1, ubl-5, and dve-1 acted in neurons and intestine to modulate mt UPR and 6-PPDQ toxicity on longevity. Meanwhile, 6-PPDQ (1 and 10 μg/L) increased expressions of histone methyltransferase genes met-2 and set-6, and decreased expressions of histone demethylase genes jmjd-1.2 and jmjd-3.1. Neuronal RNAi of set-6 and intestinal RNAi of met-2 accelerated hsp-6, atfs-1, ubl-5, and dve-1 expressions and extended lifespan of 6-PPDQ exposed nematodes. In contrast, neuronal RNAi of jmjd-1.2 and jmjd-3.1 and intestinal RNAi of jmjd-1.2 suppressed these 4 gene expressions and reduced lifespan of 6-PPDQ exposed nematodes o. In nematodes, RNAi of hsp-6 could also enhance mitochondrial dysfunction and mitochondrial reactive oxygen species (ROS) induced by 6-PPDQ. Therefore, 6-PPDQ caused damage on longevity was associated with suppression in mt UPR, which was under regulation of certain histone methylation related signals.

01 Sep 2024·Science of The Total Environment

Mitochondria UPR stimulation by pelargonidin-3-glucoside contributes to ameliorating lipid accumulation under copper exposure

Article

Author: Han, Xiao ; Bian, Cheng ; Chen, Wei ; Gao, Yufang ; Chen, Xinyi ; Yan, Fujie

Intensification of copper pollution in the environment has led to its excessive accumulation in humans, causing oxidative stress and lipid metabolism disorders. It is necessary to look for effective targets and safe methods to alleviate copper toxicity. Pelargonidin-3-glucoside (Pg3G) is a natural anthocyanin with metal ion chelating ability and multiple physiological activities. In this study, lipid accumulation was investigated under copper exposure in Caenorhabditis elegans which can be improved by Pg3G. Transcriptome analysis revealed that differentially expressed genes are enriched in lipid metabolism and protein folding/degradation. Pg3G activated mitochondrial unfold protein response (UPR^mt) to mitigate mitochondrial damage caused by copper and regulated the expression of genes involved in lipid absorption, transport, and synthesis, thereby reducing lipid levels in C. elegans. This improvement disappeared in the ubl-5 knockout strain, indicating that ubl-5 is one target of Pg3G. Meanwhile, in HepG2 cells, Pg3G enhanced the cellular antioxidant capacity by activating UPR^mt for maintaining mitochondrial homeostasis, followed by inhibition of excessive lipid accumulation. Overall, these results suggested that UPR^mt activation can be a strategy for mitigating lipid disorders induced by copper and Pg3G with excellent ability to resist oxidative stress specially targeted for ubl-5 has a promising application in controlling copper contamination.

01 Nov 2023·European journal of clinical investigation

Heart failure in patients is associated with downregulation of mitochondrial quality control genes.

Article

Author: Rudez, I ; Sepac, A ; Sikiric, S ; Seiwerth, S ; Biocina, B ; Milavic, M ; Ivankovic, S ; Svagusa, T ; Paic, F ; Varvodic, J ; Kulic, A ; Bakovic, P ; Udovicic, M ; Gasparovic, H ; Plestina, S ; Milicic, D ; Sedlic, F ; Sutlic, Z ; Manola, S ; Urlic, M

BACKGROUNDMitochondrial dysfunction is one of key factors causing heart failure. We performed a comprehensive analysis of expression of mitochondrial quality control (MQC) genes in heart failure.METHODSMyocardial samples were obtained from patients with ischemic and dilated cardiomyopathy in a terminal stage of heart failure and donors without heart disease. Using quantitative real-time PCR, we analysed a total of 45 MQC genes belonging to mitochondrial biogenesis, fusion-fission balance, mitochondrial unfolded protein response (UPRmt), translocase of the inner membrane (TIM) and mitophagy. Protein expression was analysed by ELISA and immunohistochemistry.RESULTSThe following genes were downregulated in ischemic and dilated cardiomyopathy: COX1, NRF1, TFAM, SIRT1, MTOR, MFF, DNM1L, DDIT3, UBL5, HSPA9, HSPE1, YME1L, LONP1, SPG7, HTRA2, OMA1, TIMM23, TIMM17A, TIMM17B, TIMM44, PAM16, TIMM22, TIMM9, TIMM10, PINK1, PARK2, ROTH1, PARL, FUNDC1, BNIP3, BNIP3L, TPCN2, LAMP2, MAP1LC3A and BECN1. Moreover, MT-ATP8, MFN2, EIF2AK4 and ULK1 were downregulated in heart failure from dilated, but not ischemic cardiomyopathy. VDAC1 and JUN were only genes that exhibited significantly different expression between ischemic and dilated cardiomyopathy. Expression of PPARGC1, OPA1, JUN, CEBPB, EIF2A, HSPD1, TIMM50 and TPCN1 was not significantly different between control and any form of heart failure. TOMM20 and COX proteins were downregulated in ICM and DCM.CONCLUSIONSHeart failure in patients with ischemic and dilated cardiomyopathy is associated with downregulation of large number of UPRmt, mitophagy, TIM and fusion-fission balance genes. This indicates multiple defects in MQC and represents one of potential mechanisms underlying mitochondrial dysfunction in patients with heart failure.

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UBL5

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