LAMP3 antibody (FITC)
- Known as:
- LAMP3 (anti-) (fluorecein)
- Catalog number:
- orb13924
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- LAMP3 antibody (FITC)
Related genes to: LAMP3 antibody (FITC)
- 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 (FITC)
Related articles to: LAMP3 antibody (FITC)
- 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 - The immune system is a major driver in pancreatic cancer development. Several prospective cohort studies have found associations for single immune system-derived proteins such as IL6 or CRP, but results are inconclusive, and Omics-based research is scarce. Hence, we aimed to investigate associations of a comprehensive protein panel with the risk of pancreatic cancer. Within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort, 92 immune proteins were measured in baseline blood samples of 406 incident pancreatic cancer cases and 406 sex- and age-matched controls, using the Olink Immuno-Oncology panel. Multivariable adjusted conditional logistic regression was used to estimate odds ratios (OR, 95% CI) for protein levels in association with pancreatic cancer risk. Eight biomarkers were associated with pancreatic cancer risk (MMP12, LAMP3, CD28, IL-6, IL-12, FASLG, PD-L2, and PDCD1) but only MMP12 was significantly associated after multivariable adjustments for confounders and the seven proteins, with OR = 1.56 (95% CI: 1.20-2.03) for a doubling in protein concentration. After correction for multiple testing, none of the proteins were associated with risk. Restricting analyses to cases diagnosed within the first 4 years and 4-8 years after recruitment resulted in OR of 1.89 (95% CI: 1.28-2.80) and 1.37 (95% CI: 1.01-1.86) for MMP12, respectively. Higher levels of MMP12 were associated with pancreatic cancer risk specifically in those diagnosed shortly after recruitment, while other immune-related factors were not associated with risk. Further cohort studies are needed to confirm our initial findings. - Source: PubMed
Publication date: 2026/06/23
Katzke Verena AChen YueDutta SrimantiCanzian FedericoAndersen Julie Louise MunkRostgaard-Hansen Agnetha LinnBouteille LéaRebours VincianeTruong ThérèseSchulze Matthias BBendinelli BenedettaPala ValeriaSimeon VittorioTumino RosarioSacerdote CarlottaVermeulen RoelKolijn P MartijnElias Sjoerd GCrous-Bou MartaSánchez Maria-JoséJimenez-Zabala AnaHuerta José MaríaGuevara MarcelaWareham NickBreeur MarieJohansson MattiasYarmolinsky JamesCampa DanieleKaaks Rudolf - Immune-related adverse events (irAEs) induced by immune checkpoint inhibitors (ICIs) share symptomatic and therapeutic similarities with chronic inflammatory diseases (CIDs). However, the molecular distinctions between irAEs and CIDs remain unclear. Herein, we systematically compared irAEs and CIDs across multiple tissues using large-scale multi-omics profiling. - Source: PubMed
Publication date: 2026/06/19
Kang JunhoAn JinhyeonChoi Jung Kyoon