Ask about this productRelated genes to: PTPMT1 antibody
- Gene:
- PTPMT1 NIH gene
- Name:
- protein tyrosine phosphatase mitochondrial 1
- Previous symbol:
- -
- Synonyms:
- PLIP, DUSP23, MOSP
- Chromosome:
- 11p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-03-15
- Date modifiied:
- 2019-02-14
Related products to: PTPMT1 antibody
Related articles to: PTPMT1 antibody
- 1. Indigenous poultry breeds, like Kadaknath and Aseel, represent invaluable genetic resources, combining unique nutritional and cultural traits. The Kadaknath breed is famed for its black, lean, iron-rich meat with high protein and antioxidant content, while Aseel is a muscular breed prized for endurance, stress tolerance and fighting abilities. Despite their economic and nutritional value, the genetic and metabolic underpinnings of their distinct traits remain underexplored.2. This study conducted a comparative transcriptomic analysis of liver tissue from Kadaknath and Aseel chickens using RNA sequencing (RNA-seq) to uncover the molecular mechanisms driving their phenotypic diversity. The results identified 435 differentially expressed genes (DEG) linked to key processes such as lipid metabolism, oxidative phosphorylation and stress response.3. In Kadaknath chickens, up-regulated genes, including , and , were associated with efficient triglyceride breakdown, strong antioxidant defence and optimised energy metabolism. This likely contributes to the characteristic lean, nutrient-rich meat with high protein and low fat content.4. In contrast, Aseel birds showed elevated expression of stress response genes ( and ) and mitochondrial genes ( and ), supporting its high energy requirements and resilience to stress, crucial for its endurance as a fighter breed. Gene co-expression network analysis highlighted critical hub genes driving these breed-specific adaptations. - Source: PubMed
Publication date: 2025/10/22
Bagiyal MAhlawat SChhabra PSharma UArora RSharma RKhatak SParsad RGera R - Loss of host-microbiota balance promotes gut inflammation, colitis and inflammatory bowel disease. Yet, whether host or microbial factors are the critical driver of the pathology remains unclear. Here, we investigate how cardiolipin maintains metabolic fitness of regulatory T (T) cells to preserve gut-immune homeostasis. We discover that deleting the cardiolipin-synthesizing enzyme protein tyrosine phosphatase mitochondrial 1 (PTPMT1) in T cells predisposes mice to colitis due to impaired T cell function in the absence of dysbiosis. Subsequent pathobiont infections accelerate the progression and severity of gut inflammation. Mechanistically, the absence of cardiolipin impairs T cell metabolic fitness and triggers a maladaptive integrated stress response, which can be reversed pharmacologically or genetically, restoring gut homeostasis and extending lifespan in PTPMT1 ΔT mice. Barth syndrome, a genetic disorder marked by severe cardiolipin deficiency, also exhibits gastrointestinal symptoms and inflammation associated with helper T cell imbalance and an active integrated stress response signature. Overall, these results suggest that a cardiolipin-mediated mitonuclear axis in T cells preserves gut-immune homeostasis and dictates outcome in pathobiont infections. - Source: PubMed
Publication date: 2026/05/18
Regina AnnamariaSolagna FrancescaEstrada Malkon SanchezJacobs Maaike M EMartinez-Martinez DanielGeorgomanolis TheodorosAlibashikj IrmaGjurgji SaraPearson ClaireChang DehuiMoschandrea ChrysanthiAparisi Ana SagreraCrespo ElenaBuechel JessicaSchneider FarinaTrojahn LeaPfelzer PaulinaPopovic MilicaPotenza ElenaKabat Agnieszka MNiessen CarienAmulic BorkoSafinia NiloufarCogliati SaraSanin David EVilla MatteoPearce Edward JFrezza ChristianPearce Erika LCabreiro FilipePowrie FionaCorrado Mauro - Anxiety disorders are highly heritable, but their underlying genetic mechanisms remain poorly understood. This study aimed to identify and functionally characterize genes whose expression is causally linked to anxiety disorder risk by integrating the parallel single-tissue genetic data. - Source: PubMed
Publication date: 2026/04/21
Wang LeshengXu ZhipengLuo GaomengWei WeiGuo MeimeiYuan YunheShi BeiGuan HaowenLiu ShaLi Xiang - Targeting metabolic vulnerabilities, particularly mitochondrial dysfunction, has emerged as a promising therapeutic strategy for glioma. However, the precise induction of specific cell death pathways non-genetic nanotherapeutics remains a significant challenge. Here, we report a triple-targeted DNA nanozyme designed to eliminate aggressive glioma by precisely inducing disulfidptosis. - Source: PubMed
Publication date: 2026/03/30
Wu TiantianLi LeZhang ShunZhang GuannanLi ChenMei JiamingChen XiaoyuanCheng Junjie - To investigate the causal relationship between mitochondrial genes and the pathogenesis of carotid plaque (CP), a multiomics-integrated Mendelian randomization (MR) analysis was performed in this study. - Source: PubMed
Publication date: 2025/11/01
Yu ZhuyuanMeng XiangyuanZong ZiyuSong QiHuo YingchaoChen Hao