Ask about this productRelated genes to: MRPL13 antibody
- Gene:
- MRPL13 NIH gene
- Name:
- mitochondrial ribosomal protein L13
- Previous symbol:
- -
- Synonyms:
- L13, RPL13, L13mt, RPML13, L13A
- Chromosome:
- 8q24.12
- Locus Type:
- gene with protein product
- Date approved:
- 2001-02-28
- Date modifiied:
- 2016-10-05
Related products to: MRPL13 antibody
Related articles to: MRPL13 antibody
- The liver is the largest metabolic organ in the human body, performing functions as metabolism, secretion, immunity, and detoxification. Due to the high energy demand, liver cells are rich in mitochondria. Mitochondrial homeostasis is crucial for liver development and function, yet the molecular pathways linking mitochondrial dysfunction to liver defects remain incompletely understood. In this study, using the zebrafish model, we show that loss of Mrpl13, a component of the mitochondrial ribosomal subunit, results in pronounced abnormalities in liver development. The deficiency of Mrpl13 disrupts mitochondrial homeostasis, as evidenced by fragmentated mitochondria, impaired energy metabolism, excessive reactive oxygen species, and lipid accumulation in liver cells. Notably, loss of Mrpl13 triggers mTORC1 signaling, and treatment with the mTORC1 inhibitor rapamycin significantly alleviates liver developmental defects, suggesting that mTORC1 signaling mediates the role of Mrpl13 in regulating mitochondrial homeostasis and liver development. Overall, our findings reveal a regulatory axis involving Mrpl13, mTORC1, and mitochondrial homeostasis during liver development, providing a theoretical basis for exploring therapeutic strategies for liver defects associated with mitochondrial dysfunction. - Source: PubMed
Publication date: 2026/04/30
Cheng XinkaiLi LeiFang ShiboYu LindongLiu ChenglinJiao YaqiFang YangLin LibaijiaZhao LongSu Ying - High-grade ovarian cancer (HGOC) remains a significant therapeutic challenge due to its aggressive nature and poor prognosis. The aim was to elucidate the molecular drivers of HGOC through an integrated bioinformatics analysis. - Source: PubMed
Timirci Kahraman Özlemİnal Gültekin GüldalBillur DeryanazBayralı Ülker Esinİşbilen MuratDurmuş SalihaÇakır TunahanYaylım İlhanİsbir Turgay - This study investigated the critical role of mitochondrial dysfunction in early-onset preeclampsia (EOPE), a major contributor to perinatal morbidity and mortality. We enrolled 12 patients diagnosed with EOPE and 8 healthy control women. Placental trophoblasts from these participants underwent comprehensive proteomic sequencing to identify differentially expressed proteins between the two groups. Key findings from proteomics were rigorously cross-verified using western blotting and immunofluorescence techniques. To further elucidate the functional consequences, we utilized the human placental trophoblast cell lines HTR8/SVneo and BeWo, employing small interfering RNA to reduce the expression of a target protein gene, and subsequently observing its effects on mitochondrial function and overall trophoblast cell behavior. Our results revealed 280 differentially expressed proteins, with a notable downregulation of mitochondrial ribosomal proteins. Specifically, the expression of mitochondrial ribosomal proteins L13 (MRPL13) and MRPL9 was significantly decreased in the EOPE group, alongside a significant reduction in the mitochondrial unfolded protein response (UPRmt)-related protein caseinolytic protease P (CLPP). In in vivo experiments, we found that the UPRmt became more severe in HTR8/SVneo and BeWo with reducing MRPL13, leading to a significant inhibition of cell migration and an enhancement of autophagy. Specifically, under tunicamycin-induced endoplasmic reticulum stress, MRPL13-knockdown also depleted Heat shock protein 60 (HSP60) and CLPP, aggravated UPRmt, and promoted mitochondrial dysfunction. In conclusion, our findings suggest that downregulation of MRPL13 may induce mitochondrial dysfunction via participating in the UPRmt, thereby negatively impacting the migration, proliferation, and invasion of trophoblast cells, and contributing to the pathogenesis of EOPE. - Source: PubMed
Chen XiaoxuZhu QinyingWang LiyingChen ZiyiZhao QingyangShi XiaohuaHu HuiyingTang PingpingZhong YifengLiu JuntaoGao Jinsong - While spermatogenesis has been extensively characterized in mammals, its molecular underpinnings in avian species remain largely unexplored. To address this knowledge gap, we performed single-cell transcriptomic profiling of duck testes across developmental stages (10-week immature vs. 23-week mature). Our analysis generated a comprehensive cellular atlas comprising 54,702 cells, resolving eight germ cell clusters (three spermatogonia [SPG], three spermatocytes [SPC], two spermatozoa [SPT]) and nine somatic populations, including peritubular myoid cells, immune subsets (T cells, macrophages, granulocytes), endothelial cells, Leydig cells, and three Sertoli cell subtypes, each defined by unique marker gene signatures. Furthermore, novel marker genes were identified, including EXFABP for granulocyte, ARHGAP15 for T cell regulation, FDX1 specific to Leydig cells (LC), and TSSK3/TSSK2 linked to elongated spermatid formation (SPT). Notably, we identified some novel molecular markers distinguishing these populations. Pseudotemporal trajectory reconstruction of germline development revealed stage-specific enrichment of ribosome, endoplasmic reticulum protein processing, and autophagy pathways. Core regulators MRPL13, MRPL2, MRPL22, MRPS14, MRPS7 (ribosome), HSPA5 (ER stress response), and PIK3C3 (autophagy) emerged as molecular hubs showing progressive downregulation during differentiation. Comparative transcriptomic analysis of germ cells and Sertoli cells between immature (IMT) and mature (MT) testes revealed significant enrichment of the spliceosome pathway in both germ and Sertoli cells. Critical spliceosome components SNRPG, SF3B3, and SNRPF exhibited coordinated downregulation during testicular maturation, suggesting their role as negative regulators of spermatogenic progression. This study establishes the first high-resolution cellular blueprint of avian spermatogenesis, delineating regulatory networks of duck testis cell development. Our findings provide valuable datasets and mechanistic insights into the evolutionary specialization of reproductive strategies in poultry. - Source: PubMed
Publication date: 2025/08/22
Tao ZhiyunXu WenjuanSong WeitaoLu LizhiZhang ShuangjieLiu HongxiangWang ZhichengGu HaotianZhu ChunhongLi Huifang - Tumor cells typically exhibit dysregulation of mitochondrial energy metabolism and cell death. The role of mitochondrial function in ovarian cancer (OC) progression has garnered substantial attention, yet its precise molecular mechanisms remain elusive. Mitochondrial ribosomal protein L13 (MRPL13), involved in the translation of oxidative phosphorylation (OXPHOS) complex subunits, plays a critical role in regulating mitochondrial function. Our study demonstrated that MRPL13 is highly expressed in OC tissues and correlated with poor prognosis. Both in vitro and in vivo experiments confirmed that MRPL13 overexpression significantly promotes the malignant biological behavior of OC, while MRPL13 knockdown induces the opposite phenotype. Moreover, MRPL13 knockdown impairs mitochondrial function in OC cells, leading to decreased OXPHOS and ATP levels, increased reactive oxygen species (ROS) generation, mitochondrial depolarization, aberrant opening of the mitochondrial permeability transition pore (mPTP), and mitochondrial structural damage. Mechanistically, MRPL13 specifically interacts with SLC25A6 and facilitates its degradation via lysine (K)48-linked ubiquitination. MRPL13 inhibits mPTP opening by accelerating the degradation of SLC25A6, thereby preventing cytochrome c release into the cytoplasm, inhibiting cell death, and enhancing mitochondrial function. In conclusion, our study elucidates the mechanism by which the MRPL13-SLC25A6 axis enhances mitochondrial function and promotes tumor progression in OC by inhibiting mPTP opening, suggesting that MRPL13 holds significant potential for prognostic evaluation and targeted therapy in OC. - Source: PubMed
Publication date: 2025/08/21
Liu OuxuanHu YuexinWang ShuangNie XinWang YuxuanFan XiangchengZeng KaiLi XiaoLiu BingyingLin Bei