LYVE1 Antibody
- Known as:
- LYVE1 Antibody
- Catalog number:
- GWB-BSP845
- Product Quantity:
- 20ug
- Category:
- -
- Supplier:
- GenWay
- Gene target:
- LYVE1 Antibody
Ask about this productRelated genes to: LYVE1 Antibody
- Gene:
- LYVE1 NIH gene
- Name:
- lymphatic vessel endothelial hyaluronan receptor 1
- Previous symbol:
- XLKD1
- Synonyms:
- LYVE-1
- Chromosome:
- 11p15.4
- Locus Type:
- gene with protein product
- Date approved:
- 2001-03-21
- Date modifiied:
- 2015-07-22
Related products to: LYVE1 Antibody
Related articles to: LYVE1 Antibody
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Publication date: 2026/09/16
Zhang WanyuXu DingkangSong DengpanGao Qiang - Macrophages are heterogeneous tissue-resident immune cells distributed throughout the body. The majority of tissue-resident macrophages are seeded in the peripheral tissues during embryogenesis, and these embryonic precursors form tissue-specific macrophages dependent on their specific microenvironment. The skin is the first line of immune defence and contains various uniquely differentiated tissue-resident macrophage populations, including Langerhans cells in the epidermis, perivascular and sensory nerve-associated macrophages in the dermis, and LYVE1 + and CD169 + macrophages in the hypodermis. Cutaneous melanoma is the most aggressive skin cancer, and macrophages are abundant immune cells found in these tumours. Due to the diversity of macrophage subsets in the skin, macrophages have highly heterogeneous roles in melanoma lesions, including exerting both tumour-suppressing and promoting functions. Additionally, macrophage subsets in the tumour-draining lymph node play important roles in tumour immunity and progression. A comprehensive understanding of the different macrophage subsets in both tumour and tumour-draining lymph nodes may lead to improved therapeutic outcomes for cutaneous melanoma. - Source: PubMed
Publication date: 2026/09/16
Weninger Felix G PKeith Yuki Honda - Sepsis arises from heterogeneous host-cell states that influence bacterial clearance, yet single-cell transcriptomic approaches do not directly connect microbial signals with host transcriptional programs. This study introduces single-cell host-bacterial 16S co-sequencing (scH16S-seq), which couples host transcriptomes with barcode-resolved bacterial 16S-derived UMI signals to resolve bacterial signal-enriched host-cell states. Applied to Klebsiella pneumoniae (KP) sepsis, scH16S-seq mapped cell-associated bacterial 16S-derived signals to discrete CD38 myeloid states, including Acod1 monocyte-derived macrophages, Lyve1 interstitial macrophages, and hypoxic neutrophils sharing inflammatory, hypoxic, and metabolically stressed programs. Increased myeloid CD38 expression is also observed across human sepsis cohorts. Mechanistically, KP induces CD38-associated NADdepletion, mitochondrial bioenergetic failure, reduced ATP, and impaired lysosomal acidification. CD38 inhibition, NAD-related metabolic intervention, or Cd38 deficiency restores NAD homeostasis and mitochondrial function, whereas blockade of mitochondrial ATP synthesis or V-ATPase-dependent acidification attenuates lysosomal and antibacterial rescue. Lyz2-Cre-mediated Cd38 deletion improves bacterial control and sepsis outcomes in vivo. Together, scH16S-seq resolves KP 16S signal-enriched myeloid states and identifies a targetable CD38-NAD-mitochondrial-lysosomal axis linking immunometabolic dysfunction to impaired antibacterial defense in sepsis. - Source: PubMed
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