MRPL13 Over-expression Lysate Product
- Known as:
- MRPL13 Over-expression Lysate Product
- Catalog number:
- GWB-8C57F0
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- GenWay
- Gene target:
- MRPL13 Over-expression Lysate Product
Related genes to: MRPL13 Over-expression Lysate Product
- 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 Over-expression Lysate Product
(META) Human Metapneumovirus Type 16 (A1) Lysate(META) Human Metapneumovirus Type 18 (B2) Lysate(META) Human Metapneumovirus Type 20 (A2) Lysate(META) Human Metapneumovirus Type 27 (A2) Lysate(META) Human Metapneumovirus Type 3 (B1) Lysate(META) Human Metapneumovirus Type 4 (B2) Lysate(META) Human Metapneumovirus Type 5 (B1) Lysate(META) Human Metapneumovirus Type 8 (B2) Lysate(META) Human Metapneumovirus Type 9 (A1) Lysate0 day neonate eyeball cDNA. RIKEN full-length enriched library. clone E130107M17 product hypothetical protein. full insert seque - N_A Polyclonal0 day neonate head cDNA. RIKEN full-length enriched library. clone 4831434J02 product nuclear factor of activated T-cells. cytop - N_A Polyclonal0 day neonate head cDNA. RIKEN full-length enriched library. clone 4832421E02 product myocyte enhancer factor 2C. full insert se - N_A Polyclonal1,2,3,4-Tetrahydro-1,2-dimethyl-4,6-isoquinolinediol
(Major Product) CAS: 102830-16-0 Formula: C11H15NO21,2,3,4-tetrahydro-1,2-dimethyl-4,8-isoquinolinediol
(Minor Product) CAS: 102830-20-6 Formula: C11H15NO210 days embryo whole body cDNA. RIKEN full-length enriched library. clone 2610510L15 product poly(A)-specific ribonuclease (dead - N_A Polyclonal Related articles to: MRPL13 Over-expression Lysate Product
- Multiple myeloma (MM) is a clonal plasma cell malignancy with high heterogeneity and poor prognosis. Mitochondrial ribosomal protein L13 (MRPL13) has been linked to tumor progression, but its role in MM remains unclear. - Source: PubMed
Publication date: 2026/08/05
Liu WanyiYan ChangjianWu HuiqiangWu ChaolingCai ZhiyinWang ZechuanZhuang WeihuangLi MeilingGuo Jianxin - Mitochondrial ribosomal protein L13 (MRPL13) has been implicated in tumor progression, but its relevance to esophageal squamous cell carcinoma (ESCC) remains insufficiently defined. Because mitochondrial adaptation can influence tumor cell fitness under oncogenic and oxidative stress, we investigated whether MRPL13 is associated with aggressive ESCC biology and mitochondrial functional states. - Source: PubMed
Publication date: 2026/07/17
Luo ShujuanLiu TaoWang QiaojuanCai BangwuNurbahati AididarLiu QingLu XiaomeiZheng Shutao - 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