LAMP3 Antibody (OAAF03804)
- Known as:
- LAMP3 Antibody (OAAF03804)
- Catalog number:
- oaaf03804
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- LAMP3 Antibody (OAAF03804)
Related genes to: LAMP3 Antibody (OAAF03804)
- Gene:
- LAMP3 NIH gene
- Name:
- lysosomal associated membrane protein 3
- Previous symbol:
- -
- Synonyms:
- LAMP, TSC403, DC-LAMP, DCLAMP, CD208
- Chromosome:
- 3q27.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-29
- Date modifiied:
- 2016-10-05
Related products to: LAMP3 Antibody (OAAF03804)
Related articles to: LAMP3 Antibody (OAAF03804)
- The tumor microenvironment (TME) of thyroid cancer is a complex immunological ecosystem whose composition and interactions critically influence disease progression and therapy resistance. Single-cell RNA sequencing (scRNA-seq) has emerged as a transformative tool to dissect this landscape at unprecedented resolution, moving beyond bulk-tissue analyses to delineate cell-type- specific immune dysfunction, stromal crosstalk, and immunosuppressive niche formation. This review synthesizes how scRNA-seq has elucidated key immunopathological mechanisms in thyroid cancer, including the establishment of dominant immunosuppressive networks involving exhausted CD8⁺ T cells, regulatory T cells, tolerogenic dendritic cells (e.g., LAMP3⁺ DCs), and tumor-associated macrophages. We highlight the discovery of recurrent immunomodulatory signaling axes-such as MIF-(CD74 +CXCR4), CCL20-CCR6, and NECTIN2-TIGIT-that orchestrate immune evasion and represent potential pharmacologic targets. Furthermore, we discuss how single-cell-derived insights are fueling the development of immune-centric biomarkers and prognostic models with implications for predicting response to immune checkpoint inhibition and other immunotherapies. However, translational advancement is hampered by the correlative nature of current findings, technical artifacts, and profound inter-tumoral heterogeneity. We argue that future efforts must prioritize the functional validation of inferred immune interactions through spatial multi-omics and experimental models, and leverage scRNA-seq data to define therapeutically actionable immune subtypes of the TME. Bridging this gap will be essential to translate deep immunological profiling into tailored immunomodulatory strategies that improve outcomes for patients with thyroid cancer. - Source: PubMed
Publication date: 2026/07/16
Li HongxueChen YuQi XiangxiuHe JingniZhao HangLiu ZhenWang Lidong - Hypopharyngeal squamous cell carcinoma (HPSCC) is a rare, highly aggressive malignancy, with recurrence playing a pivotal role in treatment failure and cancer-related mortality. The tumor microenvironment (TME) characteristics and molecular mechanisms driving recurrence in HPSCC remain poorly defined. - Source: PubMed
Publication date: 2026/07/13
Cai ZhimouZhang JinhongDing YaodongXu ZhenglinLiu ZhiQiang ZhiweiLu ZhaoyueChen LinWen WeipingLei Wenbin - Metastasis is a major determinant of treatment failure and mortality in thyroid cancer, yet the interplay between malignant evolution and the immune microenvironment remains poorly characterized. Immunotherapy offers promise, but its efficacy requires a deeper understanding of tumor-associated immune infiltration and checkpoint regulation. In this study, we constructed a high-resolution transcriptomic atlas of the thyroid cancer ecosystem by analyzing 55,005 single cells from paired primary tumors and lymph node metastases. By integrating chromosomal copy number variation (CNV) inference with consensus nonnegative matrix factorization (cNMF), we deciphered the intrinsic heterogeneity of malignant epithelial cells, revealing distinct transcriptional programs and developmental trajectories driving the metastatic cascade. The metastatic niche exhibited significant reprogramming of the immunosuppressive landscape, characterized by the enrichment of FOXP3⁺ regulatory T (Treg) cells, LAMP3⁺ dendritic cells (DCs), and CCL18⁺ M2-like macrophages. Notably, while canonical checkpoints PD-1 and PD-L1/2 showed minimal expression, ligand-receptor interaction analysis identified the LAG3-LGALS3 axes as dominant immune evasion pathways mediating the crosstalk between CD8⁺ T cells and the tumor stroma. In conclusion, this study comprehensively maps the coevolution of malignant thyrocyte plasticity and the immunosuppressive metastatic niche. By uncovering the specific role of LAMP3⁺ DCs and identifying LAG3/TIGIT as critical alternative checkpoints, our findings challenge the utility of conventional PD-1 blockade in this context and provide a robust molecular rationale for developing next-generation immunotherapeutic strategies tailored to thyroid cancer. Although limited by a modest sample size, these findings provide a foundation for further investigation of the metastatic immune landscape in thyroid cancer. - Source: PubMed
Publication date: 2026/07/10
Xu ShuhangSu YaorongZhang SenminHuang DongyeWu SongSong CailuZhong WenhuanXie LanChen Wenkuan - Retinal degenerative diseases are a leading cause of irreversible blindness. Their pathogenesis is intricately linked to oxidative stress-induced dysfunction of retinal pigment epithelial (RPE) cells and subsequent retinal degeneration. Macroautophagy/autophagy, a critical cellular degradation pathway, plays a vital role in maintaining RPE homeostasis, yet its dysregulation in retinal degenerative diseases remains poorly understood. In this study, we observed that sodium iodate (NaIO), an oxidative stress inducer, triggered lysosomal dysfunction via lysosomal membrane permeabilization (LMP), thereby impairing autophagic flux in RPE cells and exacerbating retinal degeneration. RNA sequencing identified (lysosomal-associated membrane protein 3) as a downregulated gene following NaIO treatment. Functionally, LAMP3 overexpression alleviated NaIO-induced LMP, improved lysosomal function, and alleviated autophagic impairment. Furthermore, upregulation of LAMP3 reduced oxidative stress and apoptosis in RPE cells, while alleviating retinal degeneration in a NaIO-induced mouse model. Mechanistically, our data suggested that NaIO upregulated the transcription factor SNAI1, which acts as a transcriptional repressor of . SNAI1 knockdown increased LAMP3 expression, thereby facilitating the recovery of lysosomal function and the alleviation of autophagic impairment. Collectively, our findings indicate that the SNAI1-LAMP3 axis contributes to the regulation of the autophagy-lysosomal pathway in retinal degeneration, highlighting a potential therapeutic target for delaying disease progression. AMD: age-related macular degeneration; AO: acridine orange; Baf A1: bafilomycin A; BAX: BCL2-associated X protein; BCL2: B cell leukemia/lymphoma 2; BSA: bovine serum albumin; CCK-8: cell counting kit-8; ChIP: chromatin immunoprecipitation; CM-HDCFDA: chloromethyl-2',7'-dichlorodihydrofluorescein diacetate; CTSD: cathepsin D; DAPI: 4',6-diamidino-2-phenylindole; DEGs: differentially expressed genes; DHE: dihydroethidium; EdU: 5-ethynyl-2'-deoxyuridine; ERG: electroretinography; GSEA: gene set enrichment analysis; H&E: hematoxylin and eosin; HsRPE: human primary retinal pigment epithelial; JC-1: 5,5',6,6'-tetrachloro-1,1',3,3'-tetraethylbenzimidazolylcarbocyanine iodide; LAMP1: lysosomal-associated membrane protein 1; LAMP2: lysosomal-associated membrane protein 2; LAMP3: lysosomal-associated membrane protein 3; LGALS3: lectin, galactose binding, soluble 3; LLOMe: leu-leu methyl ester; LMP: lysosomal membrane permeabilization; MAP1LC3B/LC3B: microtubule-associated protein 1 light chain 3 beta; MMP: mitochondrial membrane potential; NAC: N-acetyl-L-cysteine; NaIO: sodium iodte; NC: negative control; OCT: optical coherence tomography; PCA: principal component analysis; PI: propidium iodide; qRT-PCR: quantitative real-time polymerase chain reaction; Rapa: rapamycin; ROS: reactive oxygen species; RP: retinitis pigmentosa; RPE: retinal pigment epithelium; RPE65: retinal pigment epithelium 65; siRNA: small interfering RNA; SNAI1: snail family zinc finger 1; SQSTM1/p62: sequestosome 1; TJP1/ZO-1: tight junction protein 1; ZNF135: zinc finger protein 135. - Source: PubMed
Publication date: 2026/07/10
Ji YukeSun YananHuang XiaoshengLiang JiaFang DongYang WeihuaFeng LujiaZhang Shaochong - Limited therapeutic options are available for patients with advanced-stage mycosis fungoides (MF), and the 5-year survival rate is 25%. Due to its critical role in MF pathogenesis, the IL4/IL13 pathway presents a promising target for treatment. Here, we analyzed blocking of IL4Rα, the common subunit of the IL4 and IL13 receptors, within the advanced-stage MF cutaneous tumor microenvironment (TME). - Source: PubMed
Publication date: 2026/06/25
Gaydosik Alyxzandria MWang AlysonDas JishnuLapolla BrigitAkilov Oleg EGeskin Larisa JFuschiotti Patrizia