Ask about this productRelated genes to: LANCL2 antibody
- Gene:
- LANCL2 NIH gene
- Name:
- LanC like 2
- Previous symbol:
- GPR69B
- Synonyms:
- TASP
- Chromosome:
- 7p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-06-02
- Date modifiied:
- 2016-10-05
Related products to: LANCL2 antibody
Related articles to: LANCL2 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 - Prostate cancer remains a major health concern, ranking as the second leading cause of cancer-related deaths in men in the United States. The dissemination of tumor cells from the prostate, their entry into circulation, and subsequent skeletal metastasis involve complex mechanisms that are not fully elucidated. Notably, disseminated tumor cells demonstrate a remarkable ability to home to the hematopoietic stem cell niche within bone marrow, where they may remain dormant for years. Key signaling pathways implicated in dormancy include TGF-β, BMP4/BMP7, GAS6/TAM receptors, and Wnt5a, each influencing cell cycle arrest, survival, and phenotype adaptation. Recent research has explored analogies between dormancy mechanisms in cancer and plant biology, particularly focusing on phytohormones such as abscisic acid and gibberellins, which regulate plant stress responses and developmental dormancy. While plants utilize PYR1/PYL/RCAR receptors for abscisic acid, mammals rely on LANCL2 and PPARγ. This study evaluated the effects of abscisic acid, gibberellic acid, and the ABA agonist pyrabactin on human and murine prostate cancer cell lines. Results demonstrated that gibberellic acid lacked proliferative effects and could not counteract ABA-induced growth arrest. In contrast, pyrabactin potently induced growth arrest and apoptosis, activating SMAC/Diablo cell death pathways independently of LANCL2 and PPARγ signaling. Further, the activity of abscisic acid and pyrabactin depended on cellular uptake via SLC4AE2 and SLC4A3 anion exchangers; downregulation of these transporters partially reversed their inhibitory effects. These findings suggest a mechanistic parallel between phytohormone-induced dormancy in plants and regulated dormancy and apoptosis in PCa, opening new avenues for therapeutic targeting of dormancy pathways in cancer metastasis. - Source: PubMed
Rodriguez AgustinaJung YounghunParajuli Keshab RajTaichman Russell S - Neuroinflammation is a key pathological hallmark of Alzheimer's disease (AD). Investigational and FDA approved drugs targeting inflammation already exist, thus drug repurposing for AD is a suitable approach. BT-11 is an investigational drug that reduces inflammation in the gut and improves cognitive function. BT-11 is orally active and binds to lanthionine synthetase C-like 2 (LANCL2), a glutathione-s-transferase, thus potentially reducing oxidative stress. We investigated the effects of BT-11 long-term treatment on the TgF344-AD rat model of AD. BT-11 (1) reduced spatial memory deficits, and hippocampal Abeta plaque load, and increased neuronal levels in males, and reduced microglia numbers in females, and (2) induced transcriptomic changes in signaling receptor, including G-protein coupled receptor pathways in both males and females, with changes in neurotrophic factors only in males. We detected LANCL2 in hippocampal nuclear and cytoplasmic fractions with potentially different post-translational modifications, suggesting distinct functions based on its subcellular localization. LANCL2 was present in oligodendrocytes, indicating a role in oligodendrocyte function. To our knowledge, these last two findings have not been reported. Overall, our data support that targeting LANCL2 with BT-11 improves cognition and reduces AD-like pathology potentially by modulating G-protein signaling. LANCL2's localization in oligodendrocytes suggest a possible role oligodendrocyte function that warrants further investigation. Our studies contribute to the field of new immunomodulatory AD therapeutics and establish LANCL2 as a promising therapeutic target meriting further mechanistic investigation. - Source: PubMed
Publication date: 2025/12/23
Birnbaum Emily MXie LeiSerrano PeterRockwell PatriciaFigueiredo-Pereira Maria E - Gastric cancer (GC) constitutes a significant global public health burden due to its high morbidity rates and poor prognosis, underscoring the critical need for identifying novel therapeutic targets and elucidating their mechanisms. As a key member of the lanthionine synthetase C-like enzyme family, LANCL2 has shown aberrant expression in multiple malignancies. However, its biological significance in GC remains unclear. To this end, a series of exploration and research were conducted. Through integrated analyses of multi-omics databases and experimental validation, LANCL2 was up-regulated in STAD at both mRNA and protein levels. Moreover, elevated LANCL2 is closely associated with poor prognosis, and the constructed nomogram exhibited reliable predictive performance for 1, 3, and 5-year overall survival (OS) in the GC cohort. In addition, the genetic alteration status of LANCL2 was associated with new neoplasm event post initial therapy indicator, MSIsensor score, tumor mutation burden (TMB), and survival prognosis. Functional enrichment analysis indicated that LANCL2 is primarily associated with the regulation of immune checkpoints, the cell cycle and DNA repair. Furthermore, the expression of LANCL2 displayed significant correlations with immune infiltration, m6A methylation, ferroptosis, tumor cell stemness and drug reactivity. Finally, in vitro studies confirmed that silencing or overexpression of LANCL2 can significantly influence the changes of proliferation and cell cycle of GC cells. Overall, this study indicated LANCL2 as a critical regulator in GC pathogenesis, and highlighted its potential as a prognostic biomarker for gastric cancer management. - Source: PubMed
Publication date: 2025/05/25
Fang XidongLiu MengxiaoRen QianLi RenpengWu GuozhiYuan HaoZheng YaGou XiWang YupingZhou Yongning - Deoxynivalenol (DON) and octyl gallate (OG) are prevalent compounds in the environment and food. DON is frequently detected in cereals such as corn and wheat, while OG is commonly employed as a food additive. As a result, human exposure to these substances is inevitable. Given this, the objective of this experiment was to investigate the impact of co-exposure to DON (10 μg/kg) and OG (10 μg/kg) on intestinal inflammation. The RAW264.7 macrophage cell line was utilized to analyze cytokine levels as well as proteomic and metabolomic changes. In the quantitative real-time PCR experiments, the DON group showed significant difference compared to the control group (* < 0.05) and the DON-OG group (# < 0.05) regarding cytokine levels such as IL-10, TNF-α, Il6, Il1b, Ccl2, Il12α, Nos2, Cxcl1, and Cxcl2. In the animal experiment, C57BL/6 mice were utilized to monitor body weight, the presence of bloody stools, and diarrhea. Additionally, the colonic tissues of the mice underwent pathological analysis. The results indicated that cells treated with both DON and OG displayed lower levels of inflammation compared to those treated with DON alone. Furthermore, proteomic and metabolomic analyses revealed that the regulation of the Lancl2 protein and the mTOR signaling pathway contributed to the milder inflammatory response observed in the DON-OG group. These findings were further corroborated by the pathological analysis of the colonic tissues from the mice. In the combined exposure of DON and OG, OG partially mitigated the intestinal inflammation induced by DON. - Source: PubMed
Publication date: 2025/02/06
Dongye ChenxinChen XiangrongZhao YanfangLi HuijuanAbdallah Mohamed FLi TianliangChen Xiangfeng