Mouse Anti-Human Dectin-1
- Known as:
- Mouse Antibody toHuman Dectin-1
- Catalog number:
- 129-10231
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Mouse Anti-Human Dectin-1
Related products to: Mouse Anti-Human Dectin-1
Related articles to: Mouse Anti-Human Dectin-1
- Spinocerebellar Ataxia type 2 (SCA2) and Amyotrophic Lateral Sclerosis type 13 (ALS13) are triggered by polyglutamine expansion in Ataxin-2 (ATXN2). To understand these neurodegenerative disorders at the molecular level, the brains of 10-month-old -CAG100-knockin mice were analyzed as microglial, astroglial and neuronal fractions via global RNA sequencing. Data were validated by comparison with the spinal cord oligonucleotide microarray profile or filtered by RNA-seq consistency. Here, we show that the mutation causes a massive inflammatory response in microglia and a reciprocal loss of neuronal transcripts in glial fractions, suggesting severe synapse loss. Beyond these general neurodegenerative signs, we identify pathognomonic changes in the machinery for protein translation and RNA splicing. Glial fractions showed upregulation of (to 2082%), , , , , , , , and as an unspecific neuroinflammatory signature, versus downregulation of axonal (to <19%), and synaptic , , , and mRNAs correlating with circuit disconnection. In all fractions, reductions in , , and were noted versus disease-specific inductions of ribosomal subunits, presumably mirroring the partial loss-of-function of ATXN2 as RNA translation modulator. Selective accumulations of embryonic factors and versus downregulation of adult specify the mutation impact on splicing and translation elongation. As a potential underpinning of toxic gain-of-function, the proteostasis transcript appeared increased in astroglial and microglial fractions. These transcriptome data suggest altered ribosomal and spliceosome machinery, with massive microgliosis versus mild astrogliosis, at the core of SCA2 and ALS13. - Source: PubMed
Publication date: 2026/04/15
Auburger GeorgKandi Arvind ReddyVutukuri RajkumarAlmaguer-Mederos Luis-EnriqueGispert SuzanaSen Nesli-EceKey Jana - Microglial polarization imbalance between pro-inflammatory M1 and anti-inflammatory M2 phenotypes is a key mechanism in epilepsy-related neuroinflammation. This study explores the role of C-type lectin domain containing 7A (Clec7a) in M1 microglial polarization in epilepsy. An AAV-shClec7a was injected intra-hippocampally into Sprague-Dawley rats prior to induction of status epilepticus (SE) using lithium-pilocarpine. CLEC7A expression was assessed via qRT-PCR and Western blot. Histopathology was evaluated using H&E and Nissl staining. M1 markers and cytokines were analyzed by qRT-PCR/Western blot. The effects of Clec7a silencing were examined in kainic acid-stimulated BV2 cells and primary microglia. CLEC7A was significantly upregulated in epileptic models. AAV-shClec7a reduced Racine score, seizure frequency and duration, alleviated hippocampal damage, and suppressed M1 polarization and neuroinflammation, evidenced by decreased IBA1, iNOS, IL-1β, IL-6, and TNF-α, and increased IL-10 levels. Silencing Clec7a in vitro also inhibited M1 polarization and inflammation, and suppressed TLR4/MyD88/NF-κB pathway activation. Overexpression of Nfkb reversed the inhibition of M1 polarization induced by Clec7a silencing. Meanwhile, TLR4 inhibitor TAK-242 reversed Clec7a-induced M1 polarization. Clec7a is upregulated in epilepsy and promotes M1 polarization and neuroinflammation, mediated at least partially through the TLR4/MyD88/NF-κB signaling pathway. - Source: PubMed
Publication date: 2026/04/21
Dai FangfangChen Yan-Hui - Psoriasis, a chronic inflammatory skin disease affecting 2-3% of the global population, is driven by dysregulated immune responses. Despite advancements in biologic therapies, treatment challenges persist due to high recurrence rates. This study aimed to identify immune-related hub genes and elucidate their clinical implications in psoriasis pathogenesis and therapy. - Source: PubMed
Publication date: 2026/04/20
Sun YuzhenZhou ZiguangMao YuLiu NiuLi YanfengFang Weiyuan - Macrophage-associated immune responses play a critical role in acute kidney injury (AKI). Clec7a, primarily expressed on activated myeloid cells, functions as a pattern recognition receptor essential for regulating immune homeostasis. However, its specific effects and roles during AKI remain unclear. To investigate the role of Clec7a in AKI, we used a cisplatin-induced acute kidney injury (cis-AKI) model. We administered the Clec7a antagonist laminarin (LAM) and performed macrophage depletion. Additionally, we utilized siRNA to silence Clec7a and transferred Clec7a-expressing primary peritoneal macrophages (PPMs) to mice to explore potential therapeutic targets. Chromatin immunoprecipitation (ChIP) assays were conducted to demonstrate the physical binding of NF-κB/P65 to the Clec7a promoter. Our findings revealed an increase in Clec7a-expressing macrophages in the cis-AKI model. Blocking Clec7a signaling with LAM alleviated cisplatin-induced renal inflammation, an effect also observed with the knockdown of Clec7a in transferred PPMs. Notably, this study shows that Clec7a activation by its agonist d-Zymosan induces renal inflammation and up-regulates iNOS in C57BL/6 mice. Furthermore, both TLR4 and NF-κB inhibitors were able to antagonize LPS-induced Clec7a expression. ChIP assays confirmed the physical binding of NF-κB to the Clec7a promoter, indicating the regulatory effect of the TLR4/NF-κB signaling pathway on Clec7a expression. The synergistic signaling crosstalk between Clec7a-Syk and TLR4/NF-κB promotes and sustains the inflammatory phenotypes of M1 macrophages, contributing to damage in AKI. These findings provide novel insights into the pivotal role of Clec7a in renal inflammation and suggest its potential as a therapeutic target for AKI. - Source: PubMed
Zhang WeiXue FengShi XueFu HaiyangShi WeipingGuan ChenXu Yan - The molecular mechanisms linking immune cell signaling to osteoclastogenesis remain incompletely defined. Here, we identify an Annexin A1 (AnxA1)-Dectin-1 axis as a key driver of osteoclast differentiation. Dectin-1 (CLEC7A), a myeloid C-type lectin receptor best known for β-glucan recognition, is shown to bind the endogenous ligand AnxA1 on pre-osteoclasts, thereby promoting their maturation. In Dectin-1 deficient mice, reduced osteoclast numbers resulted in increased bone volume, whereas β-glucan-induced Dectin-1 activation enhanced osteoclastogenesis. Within the bone marrow niche, AnxA1 was abundantly expressed on B220+ B cells, and γ-irradiation markedly increased its surface translocation both in vitro and in vivo. γ-irradiated B220+ B cells exhibited strong Dectin-1 binding capacity and robustly stimulated osteoclast differentiation in a Dectin-1-dependent manner. These findings establish the AnxA1-Dectin-1 interaction as a critical immune-skeletal communication pathway, revealing a mechanism by which radiation exposed immune cells can accelerate bone resorption. Targeting this axis offers a potential strategy to mitigate radiation-induced bone degradation and preserve skeletal homeostasis. - Source: PubMed
Publication date: 2026/04/02
Guliyeva GulnazTakile Flora Nguemedjio FokoStallfort VerenaDerer AnjaFrey BenjaminGupta PoojaWeber ManuelTrumet LeahSchett GeorgBozec AlineGrötsch Bettina