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UBE2N deficiency contributes to MASH development via p62-regulated mitophagy and PANoptosis

ABSTRACT: RNA-seq analysis of Liver tissue from Ubc13 flox/flox Alb negative and Ubc13 flox/flox Alb positive mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE286122 | GEO | 2026/07/07

REPOSITORIES: GEO

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UBE2N deficiency contributes to MASH development via p62-regulated mitophagy and PANoptosis

Project description:UBE2N deficiency contributes to MASH development via p62-regulated mitophagy and PANoptosis

| PRJNA1207969 | ENA

Quantitative proteomic analysis of the livers from 5-week-old HyD-LIRflox/flox and HyD-LIRflox/flox; Alb-Cre mice.

Project description:We have previously shown that the HyD-LIR-Venus probe can specifically inhibit selective autophagy by suppressing the interaction of LIR-containing selective autophagy substrates and receptors with ATG8-family proteins in vivo. We generated hepatocyte-specific HyD-LIR-Venus-expressing mice (HyD-LIRflox/flox; Alb-Cre) by crossing HyD-LIRflox/flox mice, in which HyD-LIR-Venus is expressed under CAG promoter in a Cre-recombinase-dependent manner, with Alb-Cre transgenic mice that express Cre under the control of the Albumin promoter. We performed quantitative proteomic analysis of the livers of 5-week-old HyD-LIRflox/flox and HyD-LIRflox/flox; Alb-Cre mice using the RTS-SPS-MS3 method on Tribrid mass spectrometry.

2023-04-24 | PXD037013 | JPOST Repository

Transcription profiling of mouse liver from conditional Keap1 knockout mice vs. genetic control mice

Project description:To compare hepatic gene expression in conditional Keap1 knockout (Alb-Cre:Keap1(flox/-)) and genetic control mice. Disruption of Keap1-mediated repression of Nrf2 signaling was expected to result in increased expression of Nrf2-regulated genes. Experiment Overall Design: Hepatic gene expression was compared in conditional Keap1 knockout and genetic control mice (Alb-Cre:Keap1(flox/+)) mice. Male 9 week old mice were used, n=3/group.

2008-06-11 | E-GEOD-11287 | biostudies-arrayexpress

Albiflorin Alleviates Osteoporosis through Suppression of Osteoclast Mitophagy via the Rap1a/ERK Signaling Pathway

Project description:Objectives：Dysregulated mitophagy coupled with osteoclast activation orchestrates the development and progression of osteoporosis.Although albiflorin (ALB) exhibits bone-protective effects through anti-inflammatory and antioxidant activities, its precise mechanism—particularly regarding mitochondrial regulation—remains unknown. This study therefore investigates ALB as a novel osteoclast inhibitor by examining its molecular mechanism in regulating mitophagy via the Rap1a/ERK signaling pathway. Materials and Methods: ALB was evaluated using murine models of postmenopausal osteoporosis. Key methodologies included RNA sequencing (RNA-seq) for gene expression pathway analysis, transmission electron microscopy (TEM) for visualization of mitochondrial and autophagic structures, MitoTracker/LysoTracker co-staining for assessment of mitophagy, and Western blotting for protein signaling validation. The effects of ALB on osteoclast differentiation and bone loss mitigation were assessed both in vitro and in vivo. Results:ALB significantly inhibited osteoclastogenesis and osteoclast differentiation, thereby effectively reducing osteoporosis in murine models. RNA-seq analysis revealed that ALB modulated mitophagy by regulating the expression of Rap1a and components of the ERK signaling pathway. Validation through TEM demonstrated suppressed mitochondrial autophagy, while MitoTracker/LysoTracker co-staining confirmed a reduction in mitophagy. Furthermore, Western blot analysis showed that ALB inhibited osteoclast activation via the Rap1a/ERK signaling axis. Conclusion:ALB mitigates postmenopausal osteoporosis by suppressing osteoclast activation through Rap1a/ERK-dependent inhibition of mitophagy. These findings identify ALB as a promising therapeutic strategy for osteoporosis, addressing the need for safer long-term treatment options.

2026-07-01 | GSE316205 | GEO

DEPDC5 deficiency contributes to resistance to leucine starvation via p62 accumulation in hepatocellular carcinoma.

Project description: Not available

| S-EPMC5758822 | biostudies-literature

JNK-mediated control of gene expression in liver

Project description:RNAseq analysis of gene expression in Liver of Control and JNK deficient mice fed a control or a High fat diet Contro(Albcre+)l and mice with liver-specific defiency of JNK (Alb Cre+ Jnk1flox/flox, Jnk2flox/flox or Jnk1flox/floxJnk2flox/flox) were fed a control or a high fat diet for 16 weeks. Gene expression analysis in liver was analyzed by RNAseq

2015-03-06 | E-GEOD-55190 | biostudies-arrayexpress

Tetrahydrobiopterin modulates ubiquitin conjugation to UBC13/UBE2N and proteasome activity by S-nitrosation

Project description:Nitric Oxide (NO) is an intracellular signalling mediator, which affects many biological processes via the posttranslational modification of proteins through S-nitrosation. The availability of NO and NOS-derived reactive oxygen species (ROS) from enzymatic uncoupling are determined by the NO synthase cofactor Tetrahydrobiopterin (BH4). Here, using a global proteomics “biotin-switch” approach, we identified components of the ubiquitin-proteasome system to be altered via BH4-dependent NO signalling by protein S-nitrosation. We show S-nitrosation of ubiquitin conjugating E2 enzymes, in particular the catalytic residue C87 of UBC13/UBE2N, leading to impaired polyubiquitylation by interfering with the formation of UBC13~Ub thioester intermediates. In addition, proteasome cleavage activity in cells also seems to be altered by S-nitrosation, correlating with the modification of cysteine residues within the 19S regulatory particle and catalytic subunits of the 20S complex. Our results highlight the widespread impact of BH4 on downstream cellular signalling as evidenced by the effect of a perturbed BH4-dependent NO-Redox balance on critical processes within the ubiquitin-proteasome system (UPS). These studies thereby uncover a novel aspect of NO associated modulation of cellular homeostasis.

2018-10-02 | PXD010430 | Pride

Effect of depletion of Rcrin on gene expression in mouse liver tissues

Project description:To investigate the function of Rcrin in liver, we established Rcrin flox mice and crossed with Alb-cre mice, then we generated Rcrin conditional knockout mice. Then we got liver tissues from Rcrin conditional knockout mice and Rcrin flox mice. We then performed gene expression profiling analysis using data obtained from RNA-seq of Rcrin conditional knockout mice (Rcrin knockout) and Rcrin flox mice (WT) at age of 8 weeks old.

2022-09-08 | GSE212739 | GEO

Mus musculus

Project description:IL-13 Overexpression in IL4Ra^Flox Alb^Cre mice

| PRJNA289397 | ENA

Keap1-dependent gene expression determined in the liver using conditional Keap1 knockout mice vs. genetic control mice

2008-05-01 | GSE11287 | GEO