Ask about this productRelated genes to: LSM4 antibody
- Gene:
- LSM4 NIH gene
- Name:
- LSM4 homolog, U6 small nuclear RNA and mRNA degradation associated
- Previous symbol:
- -
- Synonyms:
- YER112W
- Chromosome:
- 19p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-02-17
- Date modifiied:
- 2015-08-25
Related products to: LSM4 antibody
Related articles to: LSM4 antibody
- To integrate multiscale embedded gene co-expression network analysis (MEGENA) and Mendelian randomisation (MR) to identify new pathogenic factors associated with breast cancer (BC). - Source: PubMed
Wang YangXie RuiZhang HuimingGe Zhicheng - Uterine diseases in dairy cattle are associated with reduced fertility, but the specific mechanisms of disease-mediated subfertility are not known. We hypothesized that intrauterine infusion of Escherichia coli and Trueperella pyogenes would alter the endometrial transcriptome and compromise oocyte developmental competence after disease resolution. Non-lactating Holstein cows received an intrauterine infusion of either sterile phosphate-buffered saline (n = 29) or pathogenic E. coli and T. pyogenes (n = 32) on day 3 of the estrous cycle to induce acute endometrial inflammation. Oocytes of antral follicles were collected by ovum pick-up following estrous synchronization 23 days after intrauterine infusion and underwent in vitro embryo production. Endometrial samples were collected on day 16 of the estrous cycle via cytobrush 41 days after infusion and analyzed by RNA sequencing. Bacterial infusion had no effect on oocyte development to the blastocyst stage, but increased blastocyst expression of CDK7, CHSY1, and LSM4 and tended to reduce the molecular signature of embryo competence for survival. Bacterial infusion altered the expression of 203 genes in the endometrium 41 days after infusion, increasing expression of GSTA3, PVALB, JAKMIP2, FOLH1B, and TCF23, and decreasing expression of MYMK, LOC104974498, CDRT1, KIAA0408, and SLC45A2. Differentially expressed genes were annotated to 54 canonical pathways, with glutathione-mediated detoxification being the top predicted pathway activated following bacterial infusion. Collectively, this work demonstrates that bacterial infections can have lasting effects on the uterus and potentially reduce the molecular competence of oocytes, providing a link to the long-term subfertility of cows after uterine disease. - Source: PubMed
Seekford Zachary KTariq ArslanHaimon McKenzie L JHoorn Quinn AMacay Gabriela AZhai YutingBlock JeremyRabaglino Maria BelenJeong Kwangcheol CHansen Peter JBromfield John J - The budding yeast has long served as a valuable model for investigating the molecular mechanisms underlying aging. Calorie restriction (CR) is a well-established intervention that extends lifespan across species, yet the underlying molecular mechanisms remain incompletely understood. In this study, we examined the effects of CR on the chronological lifespan, oxidative stress response, and autophagic activity of the mutant , which exhibits premature aging and elevated reactive oxygen species (ROS) levels due to defects in mRNA decapping and processing-bodies (PB) dynamics. We found that both moderate (0.1% glucose) and extreme (water incubation) CR significantly extended the lifespan of mutants and markedly reduced intracellular ROS accumulation without activating autophagy. These findings indicate that the beneficial effects of CR stem from improved redox homeostasis and metabolic adaptation, rather than from canonical autophagic pathways. Similar protective effects were observed in a chromosomal mutant generated via CRISPR-Cas9, confirming that CR rescues aging-related phenotypes in different genetic backgrounds. These insights reinforce the roles of nutrient signaling, RNA metabolism, and redox balance in lifespan regulation, offering new perspectives on the conserved anti-aging effects of calorie restriction. - Source: PubMed
Publication date: 2026/01/01
Caraba BenedettaStirpe MariaritaPalermo VanessaAyala Alban AlessiaMontanari AriannaBianchi Michele MariaFalcone ClaudioMazzoni Cristina - Pulmonary hypertension (PH) is a severe vascular disease characterized by pulmonary vascular remodeling (PVR), in which the abnormal proliferation of pulmonary artery endothelial cells (PAECs) plays a crucial role. A large body of research has demonstrated that non-coding RNAs exert significant effects on the occurrence and progression of PH. As a novel type of non-coding small RNAs, tRNA-derived small RNAs (tsRNAs) are involved in the key regulation of various diseases processes. However, their specific roles and mechanisms in PH have not been fully explored. This study aims to clarify the involvement and molecular mechanisms of tsRNAs in PH-related PAEC proliferation. The research revealed that under hypoxic conditions, the expression of tRF-31-PS5P4PW3FJHP (tRF-31) is downregulated in lung tissues and PAECs, which is associated with downregulation of the endonuclease Dicer. Overexpression of tRF-31 can inhibit hypoxia-induced proliferation of PAECs. Mechanistically, the reduction of tRF-31 under hypoxia leads to weakened binding between tRF-31 and LSM4, thereby decreasing the ubiquitination level of LSM4 and enhancing its protein stability. This increases the pool of free LSM4 that translocates into the nucleus and promotes the splicing of endothelin-1 (EDN1) precursor messenger RNA (pre-mRNA). Additionally, tRF-31 directly interacts with the 3' untranslated region (3' UTR) of EDN1 mRNA to reduce its degradation. These results suggest that tRF-31 may serve as a potential therapeutic target for PH. - Source: PubMed
Publication date: 2025/12/05
Wang ShanshanSong ShashaFeng HaoxueSun HanliangLiao XueyinGuan XiaoyuYuan HaoGao YupeiFu QiangQin WenGao DanniZhang LixinYu HangZhu Daling - LSM4 belongs to the LSM (Like-Sm) gene family; however, its role in triple-negative breast cancer (TNBC) progression remains mostly unclear. Consequently, this study aimed to explore the mechanistic importance of LSM4 as a regulatory element in the progression of TNBC. - Source: PubMed
Publication date: 2025/10/29
Ren ZhenLi YifanYang XiaobingZhang NannanWang FeiranHe Zhixian