Ask about this productRelated genes to: LCMT2 Blocking Peptide
- Gene:
- LCMT2 NIH gene
- Name:
- leucine carboxyl methyltransferase 2
- Previous symbol:
- -
- Synonyms:
- KIAA0547, MGC9534, TYW4, PPM2
- Chromosome:
- 15q15.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-01-29
- Date modifiied:
- 2014-11-19
Related products to: LCMT2 Blocking Peptide
Related articles to: LCMT2 Blocking Peptide
- Clear cell renal cell carcinoma (ccRCC) is the most prevalent type of kidney cancer. Defects in transfer RNA (tRNA) modification can lead to significantly impaired protein synthesis and misfolding, contributing to various pathologies, including malignancies. The present study aimed to develop a method predict survival outcomes and guide both immunotherapy and chemotherapy in patients with ccRCC. Patient data was collected from The Cancer Genome Atlas and tRNA modification-related genes from the Molecular Signature Database were identified. External validation of the prognostic model was conducted using the GSE29609 dataset from the Gene Expression Omnibus database. Molecular subtypes were determined through univariate Cox analysis of tRNA modification-related genes and the 'ConsensusClusterPlus' package. Multivariate Cox regression and the least absolute shrinkage and selection operator analyses were employed to establish a prognostic profile consisting of six independent prognostic genes: FTSJ1, LCMT2, METTL6, PUS1, TRMO and TRMT5. Higher risk scores and Cluster 2 classification were associated with poorer overall survival and increased expression of human leukocyte antigens and immune checkpoints. The assessment of immune cell infiltration and the tumor microenvironment was conducted using the ESTIMATE, CIBERSORT and single sample Gene Set Enrichment Analysis algorithms, were compared with the molecular subtypes and risk profiles of tRNA modification regulators. Additional analyses included somatic mutation analysis, nomogram construction, chemotherapy response prediction and small molecule drug prediction. Finally, the expression levels of the six identified genes in ccRCC cell lines were validated using reverse transcription-quantitative PCR, which confirmed consistency with the predictions made. The present study introduced a six-gene prognostic signature that may improve prognosis and facilitate personalized treatment strategies for patients with ccRCC in the future, thereby potentially enhancing individualized patient management. - Source: PubMed
Publication date: 2025/05/22
Zhu XuShen ChengZhang WeiJi YuanfeiXu SiyangZheng BingChen Zhan - Therapeutic approaches for acute myeloid leukaemia (AML) and myelodysplastic syndromes (MDS) differ due to distinct diagnostic criteria and treatment strengths. However, reliable biomarkers to differentiate AML from MDS are needed. This study investigated transfer RNA (tRNA) modifications, particularly hydroxy-wybutosine (OHyW), in the transition from MDS to AML. We found a significant decrease in OHyW and its biosynthetic enzyme leucine carboxyl methyltransferase 2 (LCMT2, alias symbol is TYW4) levels in AML compared to MDS. Mass spectrometric analysis revealed distinct tRNA modification patterns, with AML showing decreased OHyW and increased precursor levels, indicating a disrupted biosynthetic pathway. Lower LCMT2 expression correlated with reduced drug sensitivity and limited differentiation potential in AML cell lines. The results highlight the pivotal role of tRNA modifications in the progression from MDS to AML and suggest that targeting LCMT2 may enhance therapeutic outcomes in AML. By understanding these molecular mechanisms, we can develop new diagnostic markers and therapeutic strategies, potentially transforming the clinical management of AML and improving patient outcomes. - Source: PubMed
Publication date: 2024/11/10
Chen XuGong Rui-ZeMo Liu-YingCheng Ya-TingMa YuQi Yi-TaoYan Tong-MengJiang Zhi-Hong - Despite strong evidence of heritability, few studies have attempted to unveil the genetic underpinnings of testosterone levels. - Source: PubMed
Publication date: 2021/05/25
Fantus Richard JNa RongWei JunShi ZhuqingResurreccion W KyleHalpern Joshua AFranco OmarHayward Simon WIsaacs William BZheng S LillyXu JianfengHelfand Brian T - l-arginine:glycine amidinotransferase (AGAT) and its metabolites homoarginine (hArg) and creatine have been linked to stroke pathology in both human and mouse studies. However, a comprehensive understanding of the underlying molecular mechanism is lacking. To investigate transcriptional changes in cerebral AGAT metabolism, we applied a transcriptome analysis in brains of wild-type (WT) mice compared to untreated AGAT-deficient (AGAT) mice and AGAT mice with creatine or hArg supplementation. We identified significantly regulated genes between AGAT and WT mice in two independent cohorts of mice which can be linked to amino acid metabolism (, ), creatine metabolism (), cerebral myelination () and neuronal excitability (). While and showed regulation by hArg supplementation, and were creatine dependent. Additional regulated genes such as and need further evaluation of their influence on cerebral function. Experimental stroke models showed a significant regulation of and . Together, these results reveal that AGAT deficiency, hArg and creatine regulate gene expression in the brain, which may be critical in stroke pathology. - Source: PubMed
Publication date: 2020/03/09
Jensen MäritMüller ChristianSchwedhelm EdzardArunachalam PriyadharshiniGelderblom MathiasMagnus TimGerloff ChristianZeller TanjaChoe Chi-Un - Nicotine, a major addictive component in tobacco, plays an important role in the changes of body weight upon smoking and its cessation. Here we showed that nicotine-treated mice exhibited weight loss and nicotine withdrawal led to weight gain. Using TMT-based proteomic analysis, we obtained the different hypothalamic protein profiles in response to nicotine and its withdrawal. A total of ~5000 proteins were identified from the hypothalamus with 50 altered proteins upon 28-day nicotine treatment and 28 altered proteins upon 15-day nicotine withdrawal. Of the altered proteins, CASP3, LCMT2, GRIN2D, CCNT2, FADS3 and MRPS18B were inversely changed in response to nicotine and withdrawal, coincidence with the change of body weight. Of them, CASP3, LCMT2, GRIN2D and CCNT2 were found to be associated with several GO terms and KEGG pathways linking with cell apoptosis, neurotransmission and metabolism. Further Western blot and RT-qPCR analyses confirmed that the levels of the 4 proteins CASP3, LCMT2, GRIN2D and CCNT2, instead of their mRNA transcripts, altered in response to nicotine and withdrawal. Thus this study provides nicotine- and withdrawal-induced hypothalamic protein profiles and suggests potential roles of these altered proteins in the change of body weight. SIGNIFICANCE: Cigarette smoking is one of important factors harming human health. Most smokers tend to have lower body weights and smoking cessation often lead to overweight or obesity, which is an important reason for smokers to insist on smoking. It is known that nicotine, a critical component in tobacco, is associated with the alteration in body weight by affecting hypothalamic function. Through TMT-based proteomic analysis, this study identified differential hypothalamic protein profiles in response to nicotine treatment and its withdrawal, and 4 nicotine- and withdrawal-induced contrary proteins CASP3, LCMT2, GRIN2D and CCNT2 are involved in several enriched GO terms and KEGG pathways, which are associated with cell apoptosis, neurotransmission and metabolism. Our study may provide novel targets for further investigation of the molecular mechanisms of nicotine- and withdrawal-induced alteration in body weight. - Source: PubMed
Publication date: 2020/01/03
Gao Mei-MeiHu FeiZeng Xiang-DaTang Hui-LingZhang HuanJiang WeiYan Hua-JuanShi HangShu YoushengLong Yue-Sheng