LAMP3 antibody (APC)
- Known as:
- LAMP3 (anti-) (Antigen presenting cellular)
- Catalog number:
- orb113240
- Product Quantity:
- 100 ul
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- LAMP3 antibody (APC)
Related genes to: LAMP3 antibody (APC)
- Gene:
- ANAPC1 NIH gene
- Name:
- anaphase promoting complex subunit 1
- Previous symbol:
- -
- Synonyms:
- MCPR, TSG24, APC1
- Chromosome:
- 2q13
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-13
- Date modifiied:
- 2016-10-05
- Gene:
- ANAPC2 NIH gene
- Name:
- anaphase promoting complex subunit 2
- Previous symbol:
- -
- Synonyms:
- APC2, KIAA1406
- Chromosome:
- 9q34.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-06
- Date modifiied:
- 2015-08-24
- Gene:
- ANAPC4 NIH gene
- Name:
- anaphase promoting complex subunit 4
- Previous symbol:
- -
- Synonyms:
- APC4
- Chromosome:
- 4p15.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-13
- Date modifiied:
- 2016-10-05
- Gene:
- ANAPC5 NIH gene
- Name:
- anaphase promoting complex subunit 5
- Previous symbol:
- -
- Synonyms:
- APC5
- Chromosome:
- 12q24.31
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-01
- Date modifiied:
- 2014-08-12
- Gene:
- ANAPC7 NIH gene
- Name:
- anaphase promoting complex subunit 7
- Previous symbol:
- -
- Synonyms:
- APC7
- Chromosome:
- 12q24.11
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-13
- Date modifiied:
- 2016-10-05
Related products to: LAMP3 antibody (APC)
Related articles to: LAMP3 antibody (APC)
- Recent studies reveal that inorganic nanoparticles (NPs) can alter allergic skin reactions in a contact hypersensitivity (CHS) mouse model. Specifically, negatively charged silica (SiO) NPs suppressed the response whereas manganese doped titanium dioxide (mTiO) exacerbated it. Mast cells are critically important in transducing the CHS response. In this study we investigated the effect of SiO and mTiO NPs on bone marrow derived mast cell (BMMC) activation markers, degranulation and cytokine release. Sensitized BMMC were exposed to NPs alone or NPs plus antigen. Cytokines (IL-6, IL-13, TNF-α) and degranulation (β-hexosaminidase) studies were performed. Flow cytometry was used to follow cell surface activation markers including FcεRI, CD63 (LAMP-3), and CD107a (LAMP-1). Transmission Electron Microscopy (TEM) studies were preformed to assess NP endocytosis. Results found that mTiO NPs were cytotoxic to BMMC in a dose- and time-dependent manner. SiO NPs showed minimal cytotoxicity up to 100 µg/ml. In the absence of antigen the NPs had limited effect on sensitized BMMC degranulation or cytokine release. However, in the presence of antigen, 30 min co-culture studies (NP plus antigen) showed that SiO NPs protect against degranulation, and they suppressed the expression of cell surface activation markers whereas mTiO NPs exacerbated these. - Source: PubMed
Publication date: 2026/05/21
Pineda Jessica PerezDeLouise Lisa A - We evaluated the biomarker potential of Sig27, a 27-gene panel originating from prostate cancer, in breast cancer (BC). Orthotopic BC tumors were generated in Balb/c mice using 4T1 cells expressing either empty vector (EV) or the gain-of-function PCSK9 mutant D374Y. Sig27 expression was analyzed in mouse tumors, 13,103 primary BCs, 60 metastases, and 780 normal breast tissues. Its prognostic value was assessed in BC, 20 other cancer types, and in tumor-associated macrophages (TAMs), regulatory T cells (Tregs), and exhausted CD8⁺ T cells (CD8Tex). Sig27 was significantly altered in D374Y vs. EV tumors and showed consistent dysregulation in primary and metastatic BCs. It stratified BC fatality risk comparably to OncotypeDX and MammaPrint. Notably, Sig27 predicted poor prognosis across 21 cancer types. In 2716 BCs, OncotypeDX and MammaPrint correlated with mitotic progression, while Sig27 was predominantly associated with immune regulation. In bulk RNA-seq datasets (n = 6734), Sig27 and its key genes (FPR3, LAMP3, and FAM65B) were strongly associated with multiple immune checkpoints (ICs). Single-cell RNA-seq data revealed their primary expression in TAMs, and to a lesser extent in Tregs and CD8Tex. These associations were enhanced in Sig27IM, formed by FPR3, LAMP3, and FAM65B. Their expression, along with Pd-l1, Lgals9, and Pvrig, was upregulated in D374Y tumors. Furthermore, Sig27 and Sig27IM predicted pathologic complete response in BC treated with PD1 and PD-L1 inhibitors; Sig27IM displayed robust correlations with established immune-signatures: CTL, Merck18, TIDE, and STAT1_sig. Collectively, Sig27 captures BC's immune properties, which likely contribute to its biomarker potential. - Source: PubMed
Publication date: 2026/05/18
Su YingyingDong YingZhang TaoTang Damu - The ATP-binding cassette subfamily A member 3 (ABCA3) protein in the limiting membrane of lamellar bodies in alveolar type 2 (AT2) cells transports phospholipids required for pulmonary surfactant assembly. ABCA3 deficiency results from biallelic pathogenic variants in ABCA3 and causes progressive neonatal respiratory failure or childhood interstitial lung disease (chILD). Palliative care or lung transplantation are the only current definitive treatments for progressive respiratory failure due to ABCA3 deficiency. Complementing dysfunctional ABCA3 by gene addition has therapeutic potential. Previous studies show that repairing or complementing ABCA3 in induced pluripotent stem cell (iPSC)-derived AT2 cells rescues lamellar body morphology and surfactant phospholipid composition. Pathogenic variants disrupt ABCA3 function through altered protein trafficking (type 1) or by impaired phospholipid transport (type 2) into lamellar bodies. Here we tested ABCA3 gene complementation using a human pulmonary epithelial cell line (A549) with a genomically silenced ABCA3 locus (ABCA3 KO). Using this line, we generated additional cell lines that stably express individual ABCA3 variant cDNA constructs from a single genomic locus: L101P (type 1), E292V (type 2), E690K (type 2), or wild-type (WT) ABCA3. Lentiviral-mediated delivery of WT ABCA3 to each cell line partially rescued localization to LAMP3 + vesicles, lamellar body-like structure morphology, and cell proliferation. A functional assay measuring NF-κB signaling suggested that ABCA3 complementation ameliorated aberrant inflammatory signaling in E292V or E690K (type 2) mutant lines, but not in L101P (type 1) or knockout lines. These studies highlight the therapeutic potential of gene complementation as well as differences between ABCA3 pathogenic variants that may influence genetic therapy outcomes. - Source: PubMed
Publication date: 2026/03/09
Cooney Ashley LLamer ShakaylaYang PingWegner Daniel JWhite Frances VCole F SessionsWohlford-Lenane ChrisHennessey ErinBawa PushpinderKotton Darrell NSinn Patrick LWambach Jennifer AMccray Paul B - - Source: PubMed
Publication date: 2026/05/05
Ono-Minagi HitomiBurbelo Peter DAtyeo NatalieAfione Sandra AZheng ChangyuChiorini John A - Laryngeal squamous cell carcinoma (LSCC) is typically diagnosed at advanced stages, highlighting the critical need for early intervention. By integrating single-cell and bulk RNA-seq data from LSCC, vocal cord leukoplakia (VCL), and LSCC precursors, we characterized dynamic remodeling of the tumor microenvironment during LSCC pathogenesis. We identified transcriptional program gene modules that reflect malignant epithelial cells (maEpCs). The infiltration of POSTN fibroblasts progressively increases from normal tissue to VCL and further to LSCC, accompanied by enhanced intercellular communication. These fibroblasts interact with maEpCs and endothelial cells via ligands such as MIF, promoting epithelial-mesenchymal transition, cancer stemness, and angiogenesis. Blocking MIF reversed cancer-associated fibroblast-driven invasion and angiogenesis. Here, we further revealed that an immunosuppressive microenvironment arises as early as the precancerous stage, with VCL exhibiting CD8 T cell exhaustion and abundant LAMP3 dendritic cells that correlate positively with Tregs and exhausted CD8 T cells, promoting early immune escape. Additionally, LSCC was uniquely enriched for a pro-tumor SPP1 macrophage subset with low phagocytic activity and high angiogenic potential, linked to poor prognosis. Our findings uncover key mechanisms driving LSCC malignant progression, offer insights for early diagnosis and prognosis assessment, and highlight MIF as a promising therapeutic target. - Source: PubMed
Publication date: 2026/03/28
Cai ZhimouLi YunZhang JinhongLuo ShiyunQiang ZhiweiLu ZhaoyueChen LinLei Wenbin