TLR3 Polyclonal Antibody
- Known as:
- TLR3 Polyclonal Antibody
- Catalog number:
- ASACSA-790E
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- TLR3 Polyclonal Antibody
Related genes to: TLR3 Polyclonal Antibody
- Gene:
- TLR3 NIH gene
- Name:
- toll like receptor 3
- Previous symbol:
- -
- Synonyms:
- CD283
- Chromosome:
- 4q35.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-06-25
- Date modifiied:
- 2019-04-23
Related products to: TLR3 Polyclonal Antibody
Related articles to: TLR3 Polyclonal Antibody
- Porcine reproductive and respiratory syndrome (PRRS) caused by PRRS virus (PRRSV) leads to significant economic losses for the global swine industry. Screening and identification of PRRSV-regulated host proteins, followed by the development of long-acting anti-PRRSV therapeutics targeting these genetically stable host factors, represents a mainstream research direction in this field. Glucose-6-phosphate transporter (G6PT) is a core regulator of glucose uptake. However, its role in PRRSV infection remains unknown. Here, we report for the first time that PRRSV infection significantly upregulated the expression of G6PT in MARC-145 cells, a monkey kidney cell line, and in porcine alveolar macrophage (PAM)-Tang, a PAM-derived immortalized cell line. Functionally, overexpression of G6PT facilitated PRRSV replication, while knockdown of G6PT inhibited PRRSV replication. These findings indicated that G6PT contributed to efficient PRRSV propagation. Mechanistically, G6PT suppressed retinoic acid-inducible gene I (RIG-I)- and Toll-like receptor 3 (TLR3)-mediated type I interferon transcription in a manner independent of its canonical G6P transport activity. Furthermore, G6PT overexpression upregulated key glycolytic enzymes, including hexokinase 2 (HK2) and pyruvate kinase M2 (PKM2). In conclusion, we propose that PRRSV hijacks G6PT to promote its replication by suppressing innate immunity and enhancing aerobic glycolysis, identifying G6PT as a potential novel target for anti-PRRSV drug development. - Source: PubMed
Publication date: 2026/06/19
Shi XibaoWang KeqiWang YuyaoPeng SiyuWang LanChen HaoZhang XiaozhuanWang AipingZhang Gaiping - Stevens-Johnson syndrome (SJS) is a rare and severe mucocutaneous disorder often triggered by medications or infections. Our previous research identified that four key genes, Ikzf1, Ptger3, Mavs, and Tlr3 are involved in SJS susceptibility and the conjunctival epithelial innate immune response, demonstrating their role in regulating interferon-stimulated genes. However, the interplay among these regulatory factors remains unclear. This study aimed to elucidate the crosstalk mechanisms between the pathways regulated by these four genes in conjunctival epithelial cells. We constructed a comprehensive gene regulatory network using transcriptomic data from murine conjunctival epithelial cells under 16 distinct conditions, including polyI:C stimulation across wild-type, knockout, and transgenic backgrounds for the key genes. A targeted network analysis systematically identified numerous candidate genes mediating the crosstalk between the regulatory pathways initiated by Ikzf1, Ptger3, Mavs, and Tlr3. The identified candidates suggest the involvement of diverse signaling pathways previously unlinked to SJS pathology. Our findings suggest that the pathogenesis of SJS may arise not from the dysfunction of isolated genes but from the disruption of a balance maintained by intricate pathway crosstalk. - Source: PubMed
Publication date: 2026/06/18
Watanabe MakotoUeta MayumiNishigaki HiromiMizushima KatsuraNaito YujiKinoshita ShigeruSotozono ChieTakayama Jun - Macrophages are primary regulators of the innate immune system, integrating pattern recognition receptor (PRR) signaling and cytokine production to shape early inflammatory processes. However, the molecular mechanisms governing macrophage-driven responses in chickens remain poorly understood, despite their importance in controlling major infectious diseases. Among these pathways, interleukin (IL)-1β functions as a central mediator of inflammatory signaling, yet its integration with Toll-like receptor (TLR) pathways in chicken macrophages remains unclear. Here, lipoteichoic acid (LTA)-Toll-like receptor (TLR)2, poly(I:C)-TLR3, and lipopolysaccharide (LPS)-TLR4 pathways were investigated in the chicken macrophage-like cell line HD11 and an IL1β-deficient HD11 mutant, with PBMC-derived macrophages included for comparison. HD11 cells exhibited minimal responsiveness to LTA-TLR2 stimulation, whereas LPS-TLR4 stimulation elicited a limited response primarily characterized by strong induction of IL-1β and IL-8 but minimal or undetectable IL-6, tumor necrosis factor (TNF)-α, IL-18, and interferon (IFN)-β. In contrast, poly(I:C)-TLR3 stimulation induced IL-1β, IL-18, and IFN-β with limited induction of other cytokines. A genetically engineered CRISPR/Cas9 IL1B knockout (KO) HD11 model has been established to evaluate molecular interactions of the inflammatory response, which appears to be modulated by IL-1β in a TLR ligand-specific context. The present study highlights distinct pattern recognition profiles on chicken macrophages that may offer a molecular basis for IL-1β-targeted signaling networks and immunomodulation in chickens. - Source: PubMed
Publication date: 2026/06/12
Roh SeungyoonDalgaard Tina SørensenTran Ngo Thuy BaoPark Tae SubYun Cheol-Heui - - Source: PubMed
Publication date: 2026/06/10
Takada KazuhideHayakawa SatoshiKomine-Aizawa Shihoko - The ocular surface is a frontline mucosal immune barrier that protects the eye from pathogens while preserving immune tolerance essential for vision. Breakdown of this innate immune homeostasis can trigger chronic ocular surface inflammation, exemplified by Stevens - Johnson syndrome/toxic epidermal necrolysis with severe ocular complications (SJS/TEN with SOC) and atopic keratoconjunctivitis (AKC). - Source: PubMed
Publication date: 2026/06/17
Ueta Mayumi