Rabbit Anti-Human CD282, N-terminus
- Known as:
- Rabbit Antibody toHuman CD282, N-terminus
- Catalog number:
- 129-10141
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Rabbit Anti-Human CD282 N-terminus
Related genes to: Rabbit Anti-Human CD282, N-terminus
- Gene:
- TLR2 NIH gene
- Name:
- toll like receptor 2
- Previous symbol:
- -
- Synonyms:
- TIL4, CD282
- Chromosome:
- 4q31.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-06-25
- Date modifiied:
- 2016-10-25
Related products to: Rabbit Anti-Human CD282, N-terminus
Related articles to: Rabbit Anti-Human CD282, N-terminus
- The scavenger receptor CD36 is a versatile receptor that regulates various inflammatory processes by interacting with different ligands in concert with other receptors in a context- and cell-type-specific manner. While CD36 is injurious in acute adult stroke, it is beneficial in acute perinatal stroke. This differing acute response may be influenced by the maturation-dependent availability of CD36 receptor partners in the brain, such as Toll-like receptors (TLRs), the developmental state of the blood-brain barrier, and leukocyte subtypes during injury. Here, we further explore CD36-TLR2 interactions in neonatal brain injury by examining whether CD36 similarly affects gene expression and leukocyte trafficking via the blood-CSF barrier/choroid plexus after transient middle cerebral artery occlusion and direct TLR2 stimulation in wild type and CD36 knockout mice. We then examine the consequences of CD36 deficiency for long-term injury outcomes after neonatal stroke. We demonstrate that CD36 deficiency affects long-term behavior performance under physiological conditions and a shift in the role of CD36 from beneficial during acute injury to detrimental in the chronic phase following neonatal stroke. We further show that CD36 contributes to sustained immune responses, as indicated by long-term alterations in microglial phenotypes, and influences long-term functional outcomes. Collectively, these findings underscore the complex time-dependent roles of CD36 and provide insight into the mechanisms by which it modulates ischemic injury in neonatal mice. - Source: PubMed
Di Martino ElenaRayasam AdityaMottahedin AminFaustino JoelMahuvakar ShivaniEk JoakimMallard CarinaVexler Zinaida S - Mycoplasma pneumoniae pneumonia (MPP) can cause serious extrapulmonary complications, including life-threatening thrombosis. This study aimed to elucidate the roles of neutrophils and neutrophil extracellular traps (NETs) in vascular endothelial cell (EC) activation in pediatric MPP-associated thrombosis. We analyzed the relationship between neutrophils and thrombosis in children with MPP and used mouse models of neutrophilia (Csf3 plasmid injection), neutropenia (Csf3 deficient, Csf3-/-), and defective NETs formation (Pad4 deficient, Pad4-/-). The effects of neutrophils and NETs on EC activation were further examined in vivo, in vitro, and in human samples. Elevated neutrophil count was observed in patients with thrombosis and functioned as a potential diagnostic marker as well as a risk factor for MPP-associated thrombosis. EC activation was enhanced in MPP mice with neutrophilia but attenuated in neutropenic or Pad4-/- mice. NETs activated ECs through TLR2 and JAK/STAT3 signaling, and inhibition of NETs formation (Cl-amidine), TLR2 (C29), and JAK (upadacitinib) each attenuated this response. Strong correlations among neutrophils, NETs, EC activation, and thrombosis were observed in pediatric patients. These findings suggest that neutrophils promoted thrombosis in MPP via NETs-mediated EC activation involving TLR2 and JAK/STAT3 signaling. This study provides mechanistic insights into the inflammatory-thrombotic processes in MPP-associated thrombosis and offers a rationale for further investigation of neutrophils, NETs, TLR2, and JAK/STAT3 signaling in this context. - Source: PubMed
Publication date: 2026/09/22
Huang XiaZhu YifanGuo YunLv TianGu HaiyanLuo YingyingLi DanSun HangZhao DeyuLiu Feng - (Ai) is an herb that is known to have anti-inflammatory and anti-diabetic effects. This research was carried out with the aim of determining the effect of Ai extract on the inflammatory process as part of the innate immune response that occurs in type 2 diabetes mellitus. - Source: PubMed
Publication date: 2026/08/28
Handayani TriPrijanti Ani RKrisnamurti Desak G BDwijayanti AdistiFachri WilzarHakim Rani W - Serum amyloid A (SAA) is an acute-phase protein that can increase in plasma concentration by up to 1000-fold during infection and inflammation. Clinical studies have identified significantly elevated SAA levels in pneumonia (MPP), correlating with disease severity, lung injury, and prognosis. Emerging evidence indicates that SAA is not merely a passive inflammatory biomarker but an active contributor to MPP pathogenesis, which engages receptors such as formyl peptide receptor 2 (FPR2), Toll-like receptor 2 (TLR2), Toll-like receptor 4 (TLR4), and the receptor for advanced glycation end products (RAGE) to intensify the inflammatory response. The proposed Community-Acquired Respiratory Distress Syndrome (CARDS) toxin-NLR family pyrin domain containing 3 (NLRP3)-Interleukin-1 (IL-1)-SAA amplification loop synthesizes evidence from disparate experimental systems into a coherent mechanistic hypothesis; however, this pathway has not been experimentally verified in a single integrated model, and each component has been demonstrated independently rather than as a functional loop. SAA has demonstrated diagnostic and predictive value in MPP, with reported area under the curve(AUC) values of 0.942 for MPP diagnosis and 0.735 -0.872 for predicting refractory MPP(RMPP) across studies with variable designs; however, detailed performance metrics, including 95% confidence intervals (CIs), study populations, and sample sizes are limited by inconsistent reporting in the source literature. SAA is induced within 4-6 hours post-infection, more rapidly than C-reactive protein (CRP), procalcitonin (PCT), and interleukin-6 (IL-6); however, its limited specificity requires interpretation alongside clinical findings and other biomarkers. Moreover, SAA plays context-dependent roles in various pulmonary diseases, such as chronic airway diseases, interstitial lung diseases, acute infectious pneumonias, and acute lung injury. The dual nature of SAA-protective at low levels but pathogenic when persistently elevated-presents a therapeutic challenge: balancing acute-phase host defense with the prevention of chronic inflammatory damage. This review consolidates current knowledge on SAA structural biology, high-density lipoprotein (HDL)-associated regulation, receptor-mediated signaling, and clinical applications in MPP. It also examines SAA roles across pulmonary diseases, cellular sources, mechanisms of action, and emerging therapeutic strategies targeting SAA-mediated pathways. - Source: PubMed
Publication date: 2026/09/07
Zhang FengqinZhang Yingqian - Aminoacyl-tRNA synthetases (aaRSs) generate the aminoacyl-tRNA pool required for protein synthesis, yet selected family members also participate in nutrient sensing, stress adaptation, metabolite-dependent protein modification and extracellular immune communication. This dual biology creates a recurrent interpretive problem in cancer: an aaRS signal can reflect canonical translational demand in tumor cells, a mitochondrial program specific to immune cells, protein modification driven by lactate or amino acids, an interferon-responsive state, a secreted ligand or extracellular vesicle cargo. This review provides a mechanistic, critically appraised synthesis rather than a catalog of the aaRS family. We reconnect aminoacylation, codon-dependent translation and aaRS-specific translational stress with tumor biology and then apply a source-resolved framework based on cellular source, molecular form, localization, receiving pathway and immune output. Mechanistic strength and clinical maturity are graded independently, with direct evidence of immune function recorded separately. Representative mechanisms include substrate-specific AARS1/AARS2 lactylation, context-dependent LARS1 programs driven by codon demand, LARS2-dependent mitochondrial translation in tumor-infiltrating regulatory T cells (TI-Tregs) and regulatory B cells (Bregs), activation of Toll-like receptor 2/6 (TLR2/6) by the unique domain embedded in CARS1 (UNE-C1), WARS1 tryptophanylation intrinsic to CD8+ T cells, KARS1 and GARS1 circuits that depend on molecular form, and additional QARS1, MARS1, RARS1 and VARS1 mechanisms. Several modules show strong preclinical immune causality and human association, but none has prospective clinical validation in treated patients. aaRS-informed biomarkers and therapeutic targeting should therefore be developed as complementary, context-dependent strategies. - Source: PubMed
Publication date: 2026/09/07
Zhao ZhipengLi RudongWang SiyiWu XuhuiSun Pengda