C20orf75
- Known as:
- C20orf75
- Catalog number:
- Y213847
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- C20orf75
Related genes to: C20orf75
- Gene:
- LRRN4 NIH gene
- Name:
- leucine rich repeat neuronal 4
- Previous symbol:
- C20orf75
- Synonyms:
- dJ1056H1.1, NLRR4
- Chromosome:
- 20p12.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-07-17
- Date modifiied:
- 2014-11-19
Related products to: C20orf75
Related articles to: C20orf75
- Cervical cancer progression is intricately linked to dysregulated cell death pathways, particularly PANoptosis, a coordinated form of programmed cell death. However, prognostic biomarkers and immunological implications of PANoptosis-related genes (PRGs) in cervical cancer remain underexplored. - Source: PubMed
Publication date: 2025/11/22
Tong YuehongDeng WeiXu LiliLi YaoZhang Keke - Myocardial infarction-associated transcript (MIAT), an intergenic long noncoding RNA (lncRNA), is conserved between rodents and humans and is directly linked to maladaptive cardiac remodeling in both patients and mouse models with various forms of heart failure (HF). We previously reported attenuation of cardiac stress, apoptosis, and fibrosis in a murine model of myocardial infarction (MI) with global MIAT ablation. Our transcriptomic profiling and mechanistic studies further revealed MIAT-induced activation of maladaptive genes, such as Hoxa4, Fmo2, Lrrn4, Marveld3, and Fat4. However, the source of MIAT and its contribution to MI and HF remain unknown. In this study, we generate a novel cardiomyocyte (CM)-specific MIAT conditional knockout mouse model, which exhibits improved cardiac function after MI. We further report that CM-specific MIAT ablation is sufficient to reduce cardiac damage, apoptosis, and fibrosis following chronic MI. Mechanistically, CM-specific MIAT deletion in mice leads to decreased expression of proapoptotic and pathological profibrotic genes, such as p53, Bak1, Col3a1, Col6a1, Postn, and Snail1 after chronic MI. These results enable us to begin to dissect cell-specific contributions to MIAT signaling and bolster the idea that MIAT plays a direct pathological role in CMs after MI. - Source: PubMed
Publication date: 2025/02/20
Hayasaka TaikiKawaguchi SatoshiSepúlveda Marisa NTeoh Jian-PengMoukette BrunoAonuma TatsuyaMadhur Meena SDesai Ankit ALiangpunsakul SuthatConway Simon JKim Il-Man - This study explored the role of leucine-rich repeat neuronal 4 (LRRN4) in ovarian carcinogenesis using the p53- and Rb-defective human fallopian tube epithelial cell line FE25. We evaluated the expression of LRRN4 in FE25 cells with and without LRRN4 knockdown by short hairpin RNA (shRNA) and studied its effects on cell proliferation, cell cycle, migration, invasion, chemotherapeutic sensitivity, apoptosis, and xenograft formation. The results showed that FE25 shRNA-LRRN4 cells exhibited more aggressive malignant behaviors than FE25 cells, including faster proliferation and increased cell distribution in the G2/M phase, Akt pathway activation, cell migration, and cell invasion, as well as decreased sensitivity to chemotherapeutic drugs. FE25 shRNA-LRRN4 cells exhibited reduced levels of apoptosis and decreased expression of cleaved caspase 3, 7, 8, and 9, indicating reduced apoptotic activity. Additionally, FE25 shRNA-LRRN4 cells showed decreased LRRN4 and CK7 expression and increased WT1 expression, suggesting a potential role for LRRN4 in ovarian carcinogenesis. FE25 shRNA-LRRN4 generated a xenograft in mice with increased levels of and expression compared to their levels in cells. Overall, this study suggests that LRRN4 may play a role in ovarian carcinogenesis by promoting aggressive malignant behavior in FE25 cells through the activation of the Akt pathway. These findings provide insights into the potential molecular mechanisms underlying ovarian cancer and may have implications for the development of new therapeutic targets for this disease. - Source: PubMed
Publication date: 2023/08/15
Chang Yu-HsunWu Kun-ChiWang Kai-HungDing Dah-Ching - Profibrotic properties of pleural mesothelial cells may play an important role in the fibrosis activity in idiopathic pulmonary fibrosis (IPF). The purpose of this study was to compare the expression of pleural mesothelial cell markers in IPF and cryptogenic organizing pneumonia (COP), with an assumption that increased expression implies increase in fibrosis. - Source: PubMed
Publication date: 2023/08/07
Loloci GjustinaKim Yu MinChoi Won-IlJang Hye JinPark Sang JoonKwon Kun Young - Identification of genetic risk factors for Parkinson disease (PD) has to date been primarily limited to the study of single nucleotide variants, which only represent a small fraction of the genetic variation in the human genome. Consequently, causal variants for most PD risk are not known. Here we focused on structural variants (SVs), which represent a major source of genetic variation in the human genome. We aimed to discover SVs associated with PD risk by performing the first large-scale characterization of SVs in PD. - Source: PubMed
Publication date: 2023/02/03
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