Ask about this productRelated genes to: SLC15A4 Blocking Peptide
- Gene:
- SLC15A4 NIH gene
- Name:
- solute carrier family 15 member 4
- Previous symbol:
- -
- Synonyms:
- PHT1, PTR4
- Chromosome:
- 12q24.33
- Locus Type:
- gene with protein product
- Date approved:
- 2003-09-09
- Date modifiied:
- 2016-10-05
Related products to: SLC15A4 Blocking Peptide
Related articles to: SLC15A4 Blocking Peptide
- SLC15A4 is a transporter protein known to be involved in immune regulation, but its role in cancer is not well understood. This study aimed to thoroughly investigate SLC15A4 across different cancers, focusing on its expression levels, link to patient survival, genetic changes, biological functions, and connection to the immune environment and treatment response. We combined large-scale data analysis from public databases with lab experiments in breast cancer (BRCA) cells. Our results showed that SLC15A4 is often present at high levels in tumors, and this high level was strongly linked to poorer patient survival. It was also connected to the presence of immune cells and how sensitive tumors were to certain drugs, suggesting it could serve both as a survival predictor and a player in the immune environment. Our in vitro experiments demonstrate distinct SLC15A4 expression levels in different BRCA cell lines, and computer-based screening pinpointed potential drugs that could block it. In conclusion, SLC15A4 is an important indicator of patient outcomes and a promising target for new treatments, especially in BRCA and lower-grade glioma (LGG). - Source: PubMed
Publication date: 2026/04/06
Lyu XiaodanLin ZimingLin YaZhu ShuangfeiWang PengpengZhu HanwenXu HuaeLiu Pingyu - Neurodevelopmental disorders (NDDs), including autism spectrum disorder (ASD), are genetically complex and often linked to structural genomic variations such as copy number variants (CNVs). Current diagnostic strategies face challenges in interpreting the clinical significance of such variants. - Source: PubMed
Publication date: 2025/07/24
Rincic MartinaBrecevic LukrecijaLiehr ThomasGotovac Jercic KristinaDoder InesBorovecki Fran - E26 transformation-specific variant transcription factor 7 (ETV7) is implicated in various cancers, but its role in oral squamous cell carcinoma (OSCC) remains undefined. This study explores the clinicopathological significance and molecular mechanisms of ETV7 upregulation in OSCC. - Source: PubMed
Publication date: 2025/07/26
Yong Xiang ZhiDi Li JianTang Yu XingHe Rong QuanLi PingTao Ren ChuanChen Gang - SLC15A4, an endolysosomal solute carrier family transporter, plays a critical role in TLR7/8/9-induced immune responses through assembling a complex with the downstream adaptor TASL in a conformation-dependent manner. Despite its close functional association and promising therapeutic potential in infections, tumors, and autoimmune diseases, the development of conformation-specific antibodies for human SLC15A4 (hSLC15A4) remains challenging. Here, using a systematic screening and validation approach, we identify a pair of conformation-selective antibodies, clones 107 and 235, targeting the endolysosomal lumen surface of hSLC15A4 with opposite conformation-regulatory activities. Specifically, clone 107 selectively binds to hSLC15A4 in a TASL binding-incompetent luminal-open state; whereas clone 235 stabilizes hSLC15A4 in a TASL binding-competent cytoplasmic-open state. Our research identifies antibodies that recognize distinct conformations of hSLC15A4, potentially enabling modulation of the TLR7/8/9 pathway and contributing to the development of targeted therapies and research tools selectively targeting hSLC15A4. - Source: PubMed
Publication date: 2025/08/08
Zhu YalanZhang XuyuanZhang QixiangSun PanpanLiu KexinNie XiaohuaMa JunxiaoZhang LiweiGao YinaWang YongLiu SongqingGao AngZhang LiguoGao Pu - Impaired N6-methyladenosine (mA) modification has been implicated in regulating various inflammatory diseases, but its role in psoriasis remains unclear. Here, mA modification and its methyltransferase METTL3 are revealed to be upregulated in psoriatic macrophages, while the demethylase ALKBH5 is downregulated. Conditional knockout of Mettl3 in macrophages alleviated psoriasis-like symptoms in mice, whereas knockout of Alkbh5 exacerbated them. Both in vivo and in vitro, Mettl3 deficiency inhibited IMQ-induced M1 macrophage polarization, while Alkbh5 deficiency promoted M1 polarization. The regulation of macrophage polarization by mA is likely mediated by targeting Slc15a3. SLC15A3 enhances the recruitment of TASL, a recently identified endolysosomal IRF5 adaptor, which functions similarly to the IRF3 adaptors STING and MAVS at the endoplasmic reticulum (ER) and mitochondria, respectively, to augment IRF5 signaling via SLC15A4. The findings underscore the critical role of mA RNA modification in psoriasis pathogenesis and unveil a novel regulatory mechanism of TASL-IRF5 signaling through mA modification, suggesting potential new therapeutic targets for psoriasis treatment. - Source: PubMed
Publication date: 2025/07/18
Huang TaoChen ShijunDing KeYuan LiyanLv WeiqiChen KechenLiu YuchenMa DongzhaoZhang XinWang XiaoboLuo GuanzhengYang BinLin YingRong Zhili