Ask about this productRelated genes to: LANCL1 antibody
- Gene:
- LANCL1 NIH gene
- Name:
- LanC like 1
- Previous symbol:
- GPR69A
- Synonyms:
- p40
- Chromosome:
- 2q34
- Locus Type:
- gene with protein product
- Date approved:
- 1999-06-02
- Date modifiied:
- 2016-01-06
Related products to: LANCL1 antibody
Related articles to: LANCL1 antibody
- Lanthionine synthetase C-like protein (Lancl) gene family members 1-3 play roles in responses to oxidative stress and cellular metabolic processes. Lancl1 in particular functions as a neuroprotective factor in the central nervous system (CNS), but it is unknown whether experimentally upregulating Lancl1 in neurons could also repair injured circuits by regenerating damaged axons. We recently identified Lancl1 as a gene upregulated in response to an axon-regenerating treatment, which prompted us to ask here if Lancl1 could directly repair injured axons. First, we characterized expression of Lancl1-3 family genes in single-cell RNA-seq (scRNA-seq)-profiled retinal ganglion cell (RGC) CNS projection neurons, then we investigated through gain-of-function experiments whether Lancl1 promotes axon regeneration after CNS injury in vivo, and finally we tested if Lancl1 transgene activates the mTOR pathway's pS6 marker, which is associated with Pten knockout-promoted axon regeneration. We show that within the retina, Lancl1 and Lancl2 are enriched in the RGCs, whereas Lancl3 is not considerably expressed in retinal cell types. Within the RGCs, there is moderate subtype-to-subtype variability in Lancl1 and Lancl2 expression, whereas Lancl3 is enriched in αRGCs but expressed at modest levels. We then found that after optic nerve injury, Lancl1 transgene targeted to RGCs through intravitreal AAV2 promotes neuroprotection and axon regeneration, with axons extending through the full-length of the optic nerve when co-treated with a fibronectin-based recombinant small protein. However, we did not find that Lancl1 transgene activates the mTOR pathway's pS6 marker in injured RGCs. Thus, Lancl1 is a novel axon regeneration-promoting factor with a therapeutic potential for treating CNS injury and disease, and future studies need to investigate downstream mechanisms of its neurotherapeutic efficacy. - Source: PubMed
Publication date: 2026/04/17
Lukomska AgnieszkaFrost Matthew PBrady JacobKearney AnjaBalaji Arnav JD'Souza ClydeTrakhtenberg Ephraim F - Obstructive jaundice (OJ) is a major cause of hepatic injury, yet its underlying molecular mechanisms remain incompletely understood. Through proteomic analysis of serum from OJ children, we identified a significant downregulation of Lanthionine synthetase C-like protein 1 (LANCL1). To investigate its functional role, we employed an in vivo model of bile duct ligation (BDL) and an in vitro model using BDL serum-treated BRL-3A hepatocytes. Western blotting confirmed the suppression of LANCL1 in both models. Overexpression of LANCL1 was performed to assess its protective effects. Liver injury was evaluated via H&E staining, serum biomarkers (ALT, AST, TBIL), and hepatocyte apoptosis rates. Oxidative stress was measured in vitro (MitoSOX, MDA, SOD) and in vivo (ATP, MDA, SOD, mtDNA). The downstream LANCL1-SIRT3-SOD2 pathway was analyzed by assessing SIRT3 expression and SOD2 deacetylation. Our results demonstrate that OJ-induced downregulation of LanCL1 inhibits the SIRT3-mediated deacetylation of SOD2, thereby impairing antioxidant capacity. This leads to increased oxidative stress and hepatocyte apoptosis, culminating in liver injury. Importantly, LANCL1 overexpression mitigated these pathological changes, attenuating oxidative stress, apoptosis, and histological damage. In conclusion, the LANCL1-SIRT3-SOD2 axis plays a crucial role in OJ-induced hepatotoxicity, and these findings identify LANCL1 as a novel key regulator of OJ-induced liver injury, providing a foundational basis for the development of targeted therapeutic interventions. - Source: PubMed
Publication date: 2026/04/17
Yang XilanLiu XiaoyuWang WeiyuanGuo AlinChen YoushuaiYang YangyangTong PingfanZhang MinTian ManDing Ling - Prominent features of diabetic corneal disease are oxidative stress, neuropathy and epitheliopathy including delayed wound healing and dysfunction of limbal epithelial stem cells. We hypothesised that regulatory miRNAs altered in the diabetic cornea, such as miR-10b-5p, may be responsible for these abnormalities. We aimed to understand the molecular impact of miR-10b-5p increase in human diabetic vs non-diabetic limbal epithelial cells (LECs) enriched in limbal epithelial stem cells by identifying its target genes and proteins and testing it as a potential therapy for inhibiting oxidative stress in diabetic corneas. - Source: PubMed
Publication date: 2025/10/20
Zha DaxianGamez JoshuaEbrahimi Shaghaiegh MWang YizhouVerma NagendraPoe Adam JWhite SeokShah RuchiKramerov Andrei ASawant Onkar BSantiskulvong ChintdaStotland Aleksandr BWang Zhiping PVan Eyk Jennifer ELjubimov Alexander VSaghizadeh Mehrnoosh - Gliomas are highly aggressive and heterogeneous brain tumors with poor clinical outcomes, necessitating an urgent need for novel prognostic biomarkers and therapeutic targets. Redox regulation, which balances reactive oxygen species (ROS) generation with antioxidant defense mechanisms, has emerged as a crucial adaptive mechanism supporting glioma progression. However, the precise roles and clinical implications of redox-associated genes in glioma remain poorly defined. Here, we employed integrative analyses to explore the functional impact of redox-related genes in glioma and identified LanCL1 as a key regulator in glioma malignancy. Consensus clustering of 97 redox-related genes stratified gliomas into prognostic subtypes, with high LanCL1 expression correlating with low tumor grade, favorable molecular features (e.g., IDH1 mutation, 1p/19q co-deletion), and superior patient survival. Functional assays further revealed that LanCL1 inhibited glioma cell growth and migration by coordinately activating mitochondrial metabolism at the transcriptional level and inducing cell cycle arrest via modulation of CDK1/p27 axis. These findings highlight the critical role of redox regulation in glioma pathogenesis and establish LanCL1 as both a prognostic biomarker and potential therapeutic target for exploiting redox vulnerabilities in glioma. - Source: PubMed
Publication date: 2025/08/29
Yuan YunboLi JunhongWang MengpingYuan QiuyunLiu YanhuiYang WanchunChen Mina - - Source: PubMed
Publication date: 2025/04/11
Xie WenjiaXi YuqingDong DaoqianLiu ShuaiMa ZhengliangPeng LiangyuXia TianjiaoGu Xiaoping