LAMP3 Over-expression Lysate Product
- Known as:
- LAMP3 Over-expression Lysate Product
- Catalog number:
- GWB-8ACDC9
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- GenWay
- Gene target:
- LAMP3 Over-expression Lysate Product
Related genes to: LAMP3 Over-expression Lysate Product
- 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 Over-expression Lysate Product
(META) Human Metapneumovirus Type 16 (A1) Lysate(META) Human Metapneumovirus Type 18 (B2) Lysate(META) Human Metapneumovirus Type 20 (A2) Lysate(META) Human Metapneumovirus Type 27 (A2) Lysate(META) Human Metapneumovirus Type 3 (B1) Lysate(META) Human Metapneumovirus Type 4 (B2) Lysate(META) Human Metapneumovirus Type 5 (B1) Lysate(META) Human Metapneumovirus Type 8 (B2) Lysate(META) Human Metapneumovirus Type 9 (A1) Lysate0 day neonate eyeball cDNA. RIKEN full-length enriched library. clone E130107M17 product hypothetical protein. full insert seque - N_A Polyclonal0 day neonate head cDNA. RIKEN full-length enriched library. clone 4831434J02 product nuclear factor of activated T-cells. cytop - N_A Polyclonal0 day neonate head cDNA. RIKEN full-length enriched library. clone 4832421E02 product myocyte enhancer factor 2C. full insert se - N_A Polyclonal1,2,3,4-Tetrahydro-1,2-dimethyl-4,6-isoquinolinediol
(Major Product) CAS: 102830-16-0 Formula: C11H15NO21,2,3,4-tetrahydro-1,2-dimethyl-4,8-isoquinolinediol
(Minor Product) CAS: 102830-20-6 Formula: C11H15NO210 days embryo whole body cDNA. RIKEN full-length enriched library. clone 2610510L15 product poly(A)-specific ribonuclease (dead - N_A Polyclonal Related articles to: LAMP3 Over-expression Lysate Product
- 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 - Breast cancer brain metastasis (BCBrM) remains one of the most lethal manifestations of breast cancer. Its response to immunotherapy is severely limited by the blood-brain barrier, which restricts immune cell infiltration and antigen presentation, thereby creating an immunosuppressive microenvironment. To overcome these barriers, recent studies have focused on novel immune checkpoints, including the Lymphocyte-Activated Gene 3-Galectin 3 (LAG3-LGALS3) and T-Cell Immunoreceptor with Ig and ITIM Domains-Nectin Cell Adhesion Molecule 2 (TIGIT-NECTIN2) axes, as well as on the reprogrammed metastatic ecosystem driven by immunosuppressive cells such as Forkhead Box P3-positive (FOXP3⁺) Regulatory T (Treg) cells, Lysosomal-Associated Membrane Protein 3-positive (LAMP3⁺) tolerogenic dendritic cells (DCs), C-C Motif Chemokine Ligand 18-positive (CCL18⁺) M2-like macrophages, Regulator of G-Protein Signaling 5-positive (RGS5⁺) cancer-associated fibroblasts (CAFs), Galectin 1-positive (LGALS1⁺) and TANK-Binding Kinase 1-positive (TBK1⁺) microglia, and phosphorylated Signal Transducer and Activator of Transcription 3-positive (pSTAT3⁺) reactive astrocytes. In addition, targeted inhibition of tumor-derived N-acetyltransferase 8-like (NAT8L) and metabolites N-Acetylaspartate (NAA), suppression of the N-Methyl-D-Aspartate Receptor (NMDAR) signaling pathway in tumor cells, and interventions against γ-Aminobutyric Acid (GABA)ergic reprogramming in BCBrM cells. Moreover, targeted interventions against distinct immune escape pathways-such as the Ubiquitin-Conjugating Enzyme E2T (UBE2T)/Cell Division Cycle 42 (CDC42)/Cluster of Differentiation 276 (CD276) and C-C Motif Chemokine Ligand 2-C-C Motif Chemokine Receptor 2/C-C Motif Chemokine Receptor 4 (CCL2-CCR2/CCR4) axes-have shown promise in reshaping the immune microenvironment and enhancing the efficacy of conventional immunotherapy. Collectively, this perspective outlines evolving strategies in immune checkpoint modulation, cellular ecosystem reprogramming, and neuroimmune intervention, providing a forward-looking framework to enhance the efficacy of immunotherapy in BCBrM. - Source: PubMed
Publication date: 2026/04/02
Zou YutianWu JiadiYuan ZeHe XiaofangTang Hailin - Nemolizumab reduces pruritus and skin lesions in patients with atopic dermatitis (AD), yet some patients develop cutaneous adverse events (CAEs) with increased serum thymus- and activation-regulated chemokine (TARC); mechanisms are unclear. - Source: PubMed
Publication date: 2026/03/12
Honryo AkiraMasuda ToshihiroNakamizo SatoshiTakafuji TakuyaMinami FuukaYonekura SatoruUchibayashi MidoriInoue KenichiKiyonari HiroshiYamanaka MasafumiIrie HiroyukiNakashima ChisaNakajima SaekoOtsuka AtsushiAsahina RyotaKabashima Kenji