TLR2 mAb FITC Conjugate;human (TL2.1)
- Known as:
- TLR2 mAb fluorecein Conjugate;H. sapiens (TL2.1)
- Catalog number:
- ASACSA-780FIE
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- TLR2 mAb FITC Conjugate;human (TL2.1)
Related genes to: TLR2 mAb FITC Conjugate;human (TL2.1)
- Gene:
- EEF1AKMT3 NIH gene
- Name:
- EEF1A lysine methyltransferase 3
- Previous symbol:
- FAM119B, METTL21B
- Synonyms:
- DKFZP586D0919
- Chromosome:
- 12q14.1
- Locus Type:
- gene with protein product
- Date approved:
- 2006-05-15
- Date modifiied:
- 2017-02-10
- Gene:
- METTL21EP NIH gene
- Name:
- methyltransferase like 21E, pseudogene
- Previous symbol:
- METTL21CP1
- Synonyms:
- -
- Chromosome:
- 13q33.1
- Locus Type:
- pseudogene
- Date approved:
- 2011-08-15
- Date modifiied:
- 2012-11-09
- 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
- Gene:
- VCPKMT NIH gene
- Name:
- valosin containing protein lysine methyltransferase
- Previous symbol:
- C14orf138, METTL21D
- Synonyms:
- VCP-KMT
- Chromosome:
- 14q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-01-28
- Date modifiied:
- 2016-01-05
Related products to: TLR2 mAb FITC Conjugate;human (TL2.1)
Related articles to: TLR2 mAb FITC Conjugate;human (TL2.1)
- Microglia perform the function of CNS macrophages and act as the primary immune cells in the brain. They surveil the environment, phagocytose cellular debris, maintain homeostasis and respond to tissue damage. While under physiological conditions they play a role in supporting neurons, activated microglia participate directly in the degeneration of neurons in the substantia nigra, as the hallmark of the Parkinsons disease (PD). Their detrimental effects result from direct phagocytosis of dopaminergic neurons as well as via neuroinflammation and release of toxic reactive oxygen and nitrogen species. This pathological shift is driven by a complex interplay of genetic predispositions, such as LRRK2 and GBA mutations, and environmental triggers like toxins and gut dysbiosis.A central mechanism of this neurodegeneration involves extracellular α-synuclein acting as a danger signal (DAMP), which activates microglial Toll-like receptors (e.g., TLR2) to initiate a severe inflammatory cascade. Furthermore, the extreme biophysical stability of aggregated α-synuclein overwhelms the microglial endolysosomal network, leading to lysosomal failure, "frustrated phagocytosis," and the active propagation of the disease via exosomal shedding. Relieving this maladaptive chronic neuroinflammation is a primary therapeutic goal. Modern strategies aim to break this vicious cycle through precise interventions like NLRP3 inflammasome inhibition and autophagy enhancement. Concurrently, advanced fluid biomarkers, such as seed amplification assays (SAA), alongside multidimensional neuroimaging techniques (PET, SPECT, MRI), are proving crucial for detecting these early microglial and pathological changes to guide personalized, disease-modifying therapies of PD. - Source: PubMed
Publication date: 2026/06/22
Debasa-Mouce ManuelOuro AlbertoDe Leon JoshuaGulkarov ShellyReiss Allison BBougea Anastasia - Lactiplantibacillus plantarum is a metabolically versatile lactic acid bacterium found in fermented foods and the human gastrointestinal tract. Its relatively large genome (3.0-3.6 Mb) features an open pan-genome with 1,436-2,100 core genes and over 13,000 cloud genes, enabling remarkable adaptation to diverse environments. This species encodes a diverse repertoire of CAZymes that degrade plant polysaccharides and host glycans, yielding short-chain fatty acids that modulate epithelial barrier integrity, host metabolism, and immune signaling. Pattern-recognition receptors (PRRs, including TLR2, TLR9, and NOD2) detect L. plantarum at the host interface, primarily through cell-surface molecules such as lipoteichoic acids, peptidoglycan, and exopolysaccharides. These interactions can influence NF-κB signaling, leading to either inflammatory or regulatory responses, depending on the specific strain. Certain strains also possess the glutamate decarboxylase system (GadB/GadC), which transforms dietary glutamate into gamma-aminobutyric acid (GABA), linking L. plantarum to the biology of the gut-brain axis. Despite substantial mechanistic evidence, clinical outcomes are inconsistent due to the significant variability among strains, marked differences in host microbiomes, and the absence of predictive multiomic markers for colonization and efficacy. This review consolidates current insights on genome organization, metabolic characteristics, and mechanisms of host interaction, with a specific focus on the challenges that continue to hinder the advancement of L. plantarum as a precision biotherapeutic. - Source: PubMed
Publication date: 2026/08/21
Chen YongRizwan MuhammadNawaz AsifWaheed Muhammad IhteshamWaqas MuhammadUllah Mati - Diabetes mellitus (DM) increases the risk of oral candidiasis by impairing immunity and enhancing virulence. Although GG (LGG) has antifungal potential, its effect in diabetes remains unclear. This study evaluated the efficacy of LGG against and in diabetic rats. - Source: PubMed
Vaishnavi Vedam Venkata KanthiBanik UrmilaChuah CandyParasuraman Subramani - Microglia are the resident immune cells of the central nervous system (CNS) that maintain tissue homeostasis and contribute to the pathogenesis of neuroinflammatory disorders. As innate immune cells, microglia can acquire memory-like states that exert long-term effects on CNS function and disease susceptibility. Increasing evidence highlights a dynamic interaction between the gut microbiota and the CNS, shaping microglial maturation and responsiveness throughout life. In addition to soluble microbial metabolites, gut-derived extracellular vesicles (EVs), including vesicles of microbial origin, have emerged as important mediators of microbiota-host communication capable of modulating brain homeostasis and inflammatory signaling; however, their role in programming microglial immune memory remains unclear. - Source: PubMed
Publication date: 2026/08/06
Lajqi TrimKöstlin-Gille NataschaBirdir CahitHebel JanineMiftari IlirBauer ReinhardZarogiannis Sotirios GFunaya CharlottaGille ChristianDietz-Ziegler Stefanie - Post-acute sequelae of SARS-CoV-2 infection (PASC) is a major public health consequence of COVID-19. Persistent PASC symptoms affect multiple physiological systems, including the nervous system. The etiology of PASC is unknown; however, brain-mediated symptoms may arise from dysregulated neuroinflammatory processes. We have reported that intra-cisterna magna (ICM) administration of the SARS-CoV-2 spike (S)1 antigen in rats induces behavioral alterations, prolonged neuroinflammation, and reduced brain corticosterone. Inappropriate neuroinflammation triggered by immune challenge suppresses motivated behaviors, including voluntary wheel running (VWR), and disrupts diurnal rhythms. Accordingly, this study tested the hypothesis that S1 reduces VWR distance and changes diurnal activity patterns. Given evidence that regular physical activity reduces inflammation, we also determined whether VWR attenuates the neuroinflammatory effects of S1. Male Sprague-Dawley rats were housed with either locked (sedentary) or unlocked (VWR) running wheels. After 12 days, rats received ICM S1 or vehicle and remained undisturbed while VWR was recorded for 17 days. S1-treated rats ran less and showed disrupted diurnal VWR patterns compared with vehicle controls. Eighteen days post-ICM injections, sedentary S1-treated rats, but not VWR rats, exhibited persistent elevation of hypothalamic gene expression of IL1β, MhcII, Tlr2, and Tlr4. In contrast, VWR S1-treated rats, but not sedentary S1-treated rats, had elevated hypothalamic corticosterone 18 days post-injection. Taken together, S1 in the brain produces behavioral symptoms of PASC and prolonged neuroinflammation. Despite reductions in total running distance after S1, VWR was sufficient to block the persistent upregulation of neuroinflammatory genes. Brain corticosterone may contribute to the impacts of S1 and VWR. - Source: PubMed
Publication date: 2026/08/10
Kelley TelFrank Matthew GBall Jayson BHopkins ShelbyNguyen Tina HThompson Robert SMaier Steven FFleshner Monika