YME1L1 (Human) Recombinant Protein (Q01)
- Known as:
- YME1L1 (Human) Recombinant Protein (Q01)
- Catalog number:
- H00010730-Q01-25
- Product Quantity:
- 25 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- YME1L1 (Human) Recombinant Protein (Q01)
Related genes to: YME1L1 (Human) Recombinant Protein (Q01)
- Gene:
- YME1L1 NIH gene
- Name:
- YME1 like 1 ATPase
- Previous symbol:
- -
- Synonyms:
- YME1L
- Chromosome:
- 10p12.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-04-15
- Date modifiied:
- 2019-04-15
Related products to: YME1L1 (Human) Recombinant Protein (Q01)
Related articles to: YME1L1 (Human) Recombinant Protein (Q01)
- Mitochondrial dysfunction and abnormal energy metabolism are important pathological features of Alzheimer's disease (AD). This study investigates how mitochondrial protease YME1L1 affects mitochondrial function and its upstream regulation in the pathogenesis of AD. The AD model was established by using APP/PS1 transgenic mice, primary neurons treated with Aβ1-42, and HT22 cells. The silencing of YME1L1 was achieved to evaluate its effects on mitochondrial function and OPA1 protein hydrolysis. RIP-qPCR and RNA pull-down test were used to evaluate the interaction between HNRNPC and YME1L1 mRNA. The protein succinylation level was detected by proteomic analysis of succinylation, and co-immunoprecipitation (Co-IP) was used to verify the succinylation of HNRNPC. Cognitive ability was tested by behavioral tests, including the Morris water maze, Y-maze, object recognition test, and olfactory test. Finally, the therapeutic potential of SIRT5 was studied by an overexpression experiment in an AD model. YME1L1 was significantly upregulated in the AD model, which promoted mitochondrial dysfunction and neuronal damage through OPA1 hydrolysis. HNRNPC enhances the stability of YME1L1 mRNA through an m6A-dependent mechanism, while its own K50 succinylation enhances the stability of HNRNPC by competitively inhibiting TRIM25-mediated ubiquitination, further amplifying the expression of YME1L1. SIRT5 downregulation in AD elevated HNRNPC succinylation levels. SIRT5 overexpression promoted HNRNPC desuccinylation, reduced YME1L1 expression, restored mitochondrial function, and ameliorated Aβ deposition and cognitive deficits in AD mice. The SIRT5-HNRNPC-YME1L1 axis contributes to AD pathogenesis by disrupting OPA1 proteolysis and mitochondrial dynamics. Targeting HNRNPC succinylation represents a promising therapeutic strategy for AD. - Source: PubMed
Li XueweiYang FanJiang YuyanZhao FeiLiu Fan - Bladder cancer is a common and aggressive disease with limited treatment options, highlighting the urgent need for new therapeutic strategies. Although mitochondrial proteins have been implicated in cancer progression, their role in bladder cancer remains unclear. This study aimed to investigate the function of the mitochondrial protease YME1L1 and its regulation by the E3 ubiquitin ligase TRIM21. By analyzing patient tissue samples, single-cell RNA data and performing experiments manipulating YME1L1 and TRIM21 levels in bladder cancer cells, we found that YME1L1 promotes cancer cell proliferation, invasion and mitochondrial energy production. Mechanistically, TRIM21 interacts with YME1L1 through its SPRY domain, facilitating K63-linked polyubiquitination of YME1L1 and accelerating its degradation. Furthermore, the K237 residue of YME1L1 is critical for TRIM21-mediated ubiquitination. These findings suggest that targeting the TRIM21-YME1L1 pathway could offer a novel strategy to inhibit bladder cancer progression. - Source: PubMed
Publication date: 2026/07/20
Sun LongYao YaoGong ShiweiChen ZhengliangXie WenjunWang LixiaLiu Xiaolong - Sepsis-induced acute kidney injury (AKI) is characterized by mitochondrial dysfunction and dysregulated inflammation, with a lack of effective therapies. Studies have found that down-regulation of Sirtuin 3 (Sirt3) expression in renal tubular epithelial cells is associated with mitochondrial imbalance, suggesting its potential as a therapeutic target. Based on this, the research team developed a targeted nanodelivery system: black phosphorus nanosheets loaded with a cortistatin agonist were encapsulated with macrophage membranes modified with (KKEEE)₃K peptides to specifically deliver Sirt3-activating components to the kidneys. This nanosystem demonstrated favorable stability and biocompatibility. Ex vivo experiments confirmed its ability to alleviate lipopolysaccharide-induced oxidative stress, apoptosis, and inflammation in HK-2 cells, while restoring mitochondrial function. Mechanistically, the nanomaterial regulates mitochondrial homeostasis by activating the Sirt3-YME1L1 deacetylation axis. This study provides a novel nano-therapeutic strategy for sepsis-induced AKI, combining targeting capability with metabolism regulation, and holds broad implications for the treatment of inflammatory organ damage. - Source: PubMed
Publication date: 2026/06/29
Yang YiqiongZuo RuiWang YiLiu RumengZhou YiWang Jun - How mitochondrial respiration is tightly regulated by energy demand remains incompletely defined. When mammalian cells switch from glucose to galactose as a carbon source, we observed the enhanced assembly of respiratory chain complexes accompanied by a marked reduction in TMEM141, a mitochondrial inner membrane protein. Loss of TMEM141 increased mitochondrial respiration and promoted complex I assembly, whereas galactose-induced complex I assembly was markedly blunted in TMEM141-deficient cells. TMEM141 interacts with the complex I assembly factor TIMMDC1, limiting its association with complex I subunits. TMEM141 is degraded by the mitochondrial proteases AFG3L2 and YME1L1, and galactose treatment strengthens their interactions. TMEM141 deficiency increases oxidative damage and mtDNA release, leading to activation of the cGAS-STING pathway. In Drosophila, dTMEM141 localizes to mitochondria, modulates mitochondrial activity, and is required for glial cell integrity in the eye. Together, our findings reveal TMEM141 as a negative regulator of complex I assembly that adapts to oxidative phosphorylation (OXPHOS) demands. - Source: PubMed
Publication date: 2026/06/26
Li ZhirongChen NuoZhou CaixiaXu LingnaWang XiyuanXu HongShang WeinaLiu Jun-PingWang LiquanTong Chao - Esophageal squamous cell carcinoma (ESCC) continues to pose significant therapeutic challenges due to its aggressive behavior and suboptimal outcomes. The mitochondrial unfolded protein response (MUPR) pathway has emerged as a potential contributor to tumor progression, yet its role in ESCC prognosis and therapy remains insufficiently characterized. This study therefore seeks to systematically identify MUPR-associated prognostic genes in ESCC and to evaluate their potential as targets for therapeutic intervention. This study analyzed public databases to correlate MUPR pathway genes with ESCC prognosis, identifying YME1L1 and ACP2. These genes were used to construct a prognostic risk model, and single-cell RNA sequencing (scRNA-seq) was employed to determine their cellular expression patterns. Furthermore, the expression levels of the identified genes were experimentally validated in human ESCC cell lines using Reverse Transcription-quantitative PCR (RT-qPCR). Subsequently, the potential of these genes as drug targets was assessed. Following computational screening, lycorine emerged as a promising candidate. Rather than relying solely on molecular docking, this study performed molecular dynamics (MD) simulations to assess the stability of the binding interactions over time. The prognostic model was able to stratify patients into high- and low-risk groups that showed significantly different survival outcomes. At the cellular level, YME1L1 and ACP2 exhibited pronounced activity in B cells and neutrophils. RT-qPCR analysis demonstrated a significant downregulation of YME1L1 and ACP2 in ESCC cell lines compared to normal esophageal epithelial cells (P < 0.05), demonstrating high concordance between our bioinformatics predictions and experimental evidence. The drug screening identified lycorine as a promising candidate, with a predicted binding energy of − 9.0 kcal/mol to ACP2. MD simulations demonstrated the stability of these interactions: both the ACP2-lycorine and YME1L1-lycorine complexes remained stable throughout the simulation period, maintaining their structural integrity and key hydrogen bonds. This study identified ACP2 and YME1L1 as a novel prognostic signature in ESCC, supported by preliminary transcriptional validation, and proposed the natural compound lycorine as a computational candidate for inhibiting this axis. Our work established a conceptual link between prognostic biomarkers and a candidate therapeutic, providing a computationally derived rationale for future experimental and translational studies in ESCC. Further investigations are warranted to validate lycorine’s efficacy in vivo and to explore its potential synergy with existing therapies, with the ultimate goal of improving clinical outcomes. - Source: PubMed
Publication date: 2026/04/06
Chen FangZhang JunpengXu YingWang YalinCheng Jian