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Human Monoclonal TLR4 Primary Antibody for ChIP, CyTOF - ABIN252522
Kessel, Toubi, Pavlotzky, Mogilner, Coran, Lurie, Karry, Sukhotnik et al.: Treatment with glutamine is associated with down-regulation of Toll-like receptor-4 and myeloid differentiation factor 88 expression and decrease in intestinal mucosal injury caused by ... in Clinical and experimental immunology 2008
Show all 75 Pubmed References
Dog (Canine) Monoclonal TLR4 Primary Antibody for BP, CyTOF - ABIN4360113
Rallabhandi, Bell, Boukhvalova, Medvedev, Lorenz, Arditi, Hemming, Blanco, Segal, Vogel: Analysis of TLR4 polymorphic variants: new insights into TLR4/MD-2/CD14 stoichiometry, structure, and signaling. in Journal of immunology (Baltimore, Md. : 1950) 2006
Show all 45 Pubmed References
Human Polyclonal TLR4 Primary Antibody for IHC (p), WB - ABIN4886746
Li, Qian, Ju, Wang: Upregulation of Toll-like receptor 2 expression in colorectal cancer infected by human cytomegalovirus. in Oncology letters 2014
Show all 29 Pubmed References
Dog (Canine) Monoclonal TLR4 Primary Antibody for FACS - ABIN252065
Konno, Wakabayashi, Akashi-Takamura, Ishii, Kobayashi, Takahashi, Kusumoto, Saitoh, Yoshizawa, Miyake: A molecule that is associated with Toll-like receptor 4 and regulates its cell surface expression. in Biochemical and biophysical research communications 2005
Show all 25 Pubmed References
Human Monoclonal TLR4 Primary Antibody for BP, CyTOF - ABIN4360167
Degraaf, Zasłona, Bourdonnay, Peters-Golden: Prostaglandin E2 reduces Toll-like receptor 4 expression in alveolar macrophages by inhibition of translation. in American journal of respiratory cell and molecular biology 2014
Show all 24 Pubmed References
Dog (Canine) Monoclonal TLR4 Primary Antibody for FACS - ABIN4360117
Mempel, Voelcker, Köllisch, Plank, Rad, Gerhard, Schnopp, Fraunberger, Walli, Ring, Abeck, Ollert et al.: Toll-like receptor expression in human keratinocytes: nuclear factor kappaB controlled gene activation by Staphylococcus aureus is toll-like receptor 2 but not toll-like receptor 4 or platelet ... in The Journal of investigative dermatology 2003
Show all 23 Pubmed References
Dog (Canine) Monoclonal TLR4 Primary Antibody for BP, CyTOF - ABIN4360119
Basak, Pathak, Bhattacharyya, Mandal, Pathak, Kundu et al.: NF-kappaB- and C/EBPbeta-driven interleukin-1beta gene expression and PAK1-mediated caspase-1 activation play essential roles in interleukin-1beta release from Helicobacter pylori ... in The Journal of biological chemistry 2005
Show all 23 Pubmed References
Dog (Canine) Monoclonal TLR4 Primary Antibody for FACS, ICC - ABIN4360164
Cognasse, Hamzeh, Chavarin, Acquart, Genin, Garraud: Evidence of Toll-like receptor molecules on human platelets. in Immunology and cell biology 2005
Show all 21 Pubmed References
Dog (Canine) Monoclonal TLR4 Primary Antibody for BP, ELISA - ABIN4360158
Scheel, Papavlassopoulos, Blunck, Gebert, Hartung, Zähringer, Seydel, Schromm: Cell activation by ligands of the toll-like receptor and interleukin-1 receptor family depends on the function of the large-conductance potassium channel MaxiK in human macrophages. in Infection and immunity 2006
Show all 18 Pubmed References
Human Monoclonal TLR4 Primary Antibody for FACS - ABIN4360193
Zanoni, Navone, Lunardi, Tridente, Bason, Sivori, Beri, Dolcino, Valletta, Corrocher, Puccetti: In celiac disease, a subset of autoantibodies against transglutaminase binds toll-like receptor 4 and induces activation of monocytes. in PLoS medicine 2006
Show all 16 Pubmed References
This study suggests that activated monocytes have an impact on brain vascular function through intercellular exosome signaling via Tlr4/MyD88.
TLR4 rs10759932, but not TLR2 rs3804099 and rs3804100, was associated with risk of premalignant and/or malignant gastric cancer and H. pylori susceptibility.
Expression levels of TLR2 and TLR4 were associated with age. In particular, we observed that their expression increased during the suckling period and then clearly decreased once the infants reached 1 year of age.
The TLR4-HMGB1 pathway was up-regulated in the neurons and astrocytes inside focal cortical dysplasia type II brain lesions.
this study shows that signaling via toll-like receptor 4 and CD40 in B cells plays a regulatory role in the pathogenesis of multiple sclerosis through interleukin-10 production
the involvement of hTLR4 in different types of cancer
Expression of neutrophil TLR2, TLR4 and CD64 is increased in pulmonary tuberculosis patients.
Single-molecule experiments demonstrate that PRDX5 specifically binds to TLR4. PRDX5 binding induces a cellular mechanoresponse.
These results show that isofraxidin binds to and inhibits MD-2, thus preventing TLR4/MD-2 complex formation without altering TLR2 signalling. We demonstrated that isofraxidin promoted cell proliferation and inhibited the lipopolysaccharide induced inflammatory response through suppressing the activation of the TLR4/MD-2 axis and NF-kappaB signalling in human osteoarthritis chondrocytes.
SLAMF1 is required for TLR4-mediated TRAM-TRIF-dependent signaling in human macrophages.
In a cohort of 114 Greek COPD patients, we confirmed that the presence of TLR4-D299G or TLR4-T399I SNPs was significantly associated with an earlier COPD stage (p = 0.003 and p = 0.009, respectively). In comparison, the absence of any analyzed polymorphism, including those of TLR2-R753Q and genotypic MBL deficiency, was associated with a more severe disease phenotype, characterized by more frequent exacerbation.
Herpes simplex virus type 2 infection could stimulate AP-1 activation via TLR4-MyD88/TRIF axis, and then feedback to up-regulate TLR4 expression in human genital epithelial cells.
The findings of this study suggest that PSAP can promote glioma cell proliferation via the TLR4/NF-kappaB signaling pathway and may be an important target for glioma treatment.
these results show that palmitate induces TLR4dependent MIP-1alpha expression requiring the MyD88 recruitment and activation of MAPK, NF-kappaB/AP-1 and PI3K signaling. It implies that the increased systemic levels of free fatty acid palmitate in obesity/T2D may contribute to metabolic inflammation through excessive production of MIP-1a.
High expression of the HMGB1-TLR4 axis is closely associated with Parkinson disease development, progression, drug treatment effectiveness, staging, and disease duration and has great significance for PD diagnosis and treatment.
A relationship was identified between TLR4 methylation and subjective and physiological arousal during acute alcohol intoxication that depends on self-reported alcohol use.
Findings suggest that hyaluronan (HA) fragments interact with toll like receptor 4 (TLR4) and lead macrophage polarization to an M2-like phenotype via miR-935.
Association of TRPV1 and TLR4 through the interleukin-1 receptor domain potentiates TRPV1 activity by blocking activation-induced desensitization
NOD1 expression seems to be modulated by 5-HT and other immune receptors as TLR2 and TLR4. This study could clarify the relation between both the intestinal serotonergic system and innate immune system, and their implications in intestinal inflammation.
in human glioma U251 cells, TLR4 functions to reverse tumor differentiation, and it may be a target for glioma prevention and therapy.
TLR4 knockout (KO) mice displayed increased anxiety-like behavior and reduced social interaction compared to wild type control mice.In addition, the phosphorylation levels at Thr75 and Ser97 in DARPP-32 were increased in the frontal cortex of TLR4 KO male mice.
Early TLR4-driven aerobic glycolysis was later coupled with mitochondrial biogenesis.
LUBAC regulates TLR4-mediated B cell responses.
Mycobacterium tuberculosis GrpE-stimulated dendritic cells induced the proliferation of GrpE-specific Th1-type effector/memory CD4(+)/CD8(+)CD44(high)CD62L(low) T cells from the spleen of Mtb-infected mice in a TLR4-dependent manner.
Elucidated the mechanism of tumor suppression by TLR4-activated bone marrow-derived DCs (BMDCs) isolated from BALB/c mice.
PPI can specifically stimulate TLR4.
Cognitive dysfunction induced by Porphyromonas gingivalis is mediated by activation of the TLR4 signaling pathway.
It findings indicate that core fucose is essential for CD14-dependent TLR4 and TLR2 signalling in murine macrophage activity, leading to DSS-induced experimental colitis.
Results suggest that Toll-like receptors (TLRs) blockage could be a potential candidate for therapeutic interventions to reduce malaria-induced pathology both in the mother and the fetus.
TLR4-dependent stimulation of macrophage phagocytosis requires mTORC1-directed SREBP-1a-dependent lipid synthesis.
Elimination of TLR4 receptors prevents autophagy dysfunctions in the structural synaptic connections induced by binge alcohol drinking.
Study demonstrates that TLR4 deficiency mice are protected from Ang-II induced renal injury by a robust antioxidant mechanism which is associated with attenuation of pro-inflammatory cytokines and macrophage activation. These data show that TLR4 plays a role in the recruitment of bone marrow-derived fibroblasts into the kidney via TGF-beta activation and TLR4 deficiency their accumulation to decrease renal fibrosis.
To regulate both TLR4-MyD88 and mTOR-autophagy pathways.
The TLR4 mediates HFD induced increase in body weight, inflammation and aortic lipid accumulation through, at least partly, the PPARgamma/ABCG1 signaling pathway.
Our findings demonstrate that alkali burn promotes the TLR4-MyD88-caspase-8 axis to cause imbalanced NLRP3/NLRP6, and DS exacerbates ocular surface damage via magnifying this imbalance.
Sca1(+)Lin(-)CD117(-) mouse bone marrow-derived mesenchymal stem cells regulate immature dendritic cell maturation by inhibiting TLR4-IRF8 signaling via the Notch-RBP-J pathway.
Blocking TLR4/Akt/mTOR might be an underlying basis for the anti-inflammatory effect of 20C.
It was also indicated that UA suppressed Tolllike receptor 4 (TLR4), myeloid differentiation factor 88 and nuclear factorkappaB protein expression in mice with diabetesinduced nephropathy
Two single nucleotide polymorphisms had significant effects on the milk production for Chinese Holstein, and these SNP could be used for molecular marker-assisted selection of milk production.
PGE2 downregulates LPS-induced inflammatory responses via the TLR4-NF-kappaB signaling pathway in bovine endometrial epithelial cells.
Based on the impact of both candidate genes,TLR4 and CACNA2D1, on udder health, linear or generalized linear mixed models was applied for testing the associations of SNPs located in the genes and clinical mastitis
a single nucleotide polymorphism of the bovine toll like receptor 4 gene (TLR4) in New Zealand (NZ) Holstein-Friesian x Jersey (HF x J) cross dairy cows was associated with milk production traits
STA3 facilitates TLR4-dependent IL-6 and IL-8 production via IL-6 receptor-positive feedback in endometrial cells.
Studied genetic diversity of the Toll-like receptor gene TLR4 in Czech Red and Czech Red Pied cattle. Found 8 SNPs, which were grouped into 18 haplotypes.
TLR4 polymorphisms are associated with lower reproductive Performance.
As a pilot study, the present results revealed that identified SNPs in IL8 and TLR4 genes can be used as a genetic marker and predisposing factor for resistance/susceptibility to digital dermatitis in dairy cows. However, TLR4 gene may be a potential candidate for such disease.
Transcription levels of TLR2, TLR4, and CD14 in Holstein cows with retained placenta significantly decreased between the first and the seventh day postpartum.
Bovine viral diarrhea virus type 2 infection modulates TLR4 responsiveness in differentiated myeloid cells.
TLR2 and TLR4 mediate innate response against Cryptosporidium parvum in bovine intestinal epithelial cells.
TLR4 polymorphisms are associated with susceptibility to Mycobacterium avium ssp. paratuberculosis infection in Holsteins
positive correlation between lower neutrophil apoptosis and higher expression of TLR2 and TLR4 with the formation of NETs and change in surface architecture.
Studied SNPs in the bovine toll-like receptor 4 (TLR4) and monocyte chemo attractant protein-1(CCL2) genes.
Studied bovine TLR4 gene in mastitis resistance by association as well as expression profiling analysis in crossbred cattle.
Findings indicate that intervertebral disc (IVD) cells constitutively express TLR4.
Data suggest that granulosa cells from dominant follicles express functional TLR2 and TLR4; granulosa cells appear to participate in innate immunity by responding to bacterial lipopolysaccharides/lipopeptides via TLR2 and TLR4 signaling pathways.
The expressions of host TLR2 and 4 genes were significantly higher in acidosis-resistant steers compared to those in acidosis-susceptible steers.
TLR4 and downstream adaptor molecules, transcription factors and cytokines were up-regulated when endometrial epithelial cells were stimulated with LPS
Data from an in vitro co-culture model suggest that an early response of endometrium in uterine infection is up-regulation of expression of TLR4 and CD14 (monocyte differentiation antigen CD14).
TLR2, 3, 4, and 8 mRNA expression is strongly upregulated and correlates with the progression of atherosclerosis in the aorta. Fluvastatin significantly inhibited this progress and reduced inflammation via TLR downregulation.
The expression of TLR4 protein and mRNA, the level of activated NF-kappaB (p65) were respectively detected.
Lipopolysaccharide upregulates the expression of rabbit TLR2 and 4 in the uterine body and horn, and the expression of TLR4 in the ovary.
Polydatin might have a protective effect on lung ischemia/reperfusion injury by down-regulating TLR4 and NF-kappaB expression, then inhibiting the release of mediators of inflammation as ICAM-1.
SNPs associated with incidence of digestive disorders
TLR4 expression is upregulated in the brain after experimental subarachnoid haemorrhage
The elevated expression of TLR4 was detected after SAH and peaked on day 3 and 5. TLR4 is increasingly expressed in a parallel time course to the development of cerebral vasospasm in a rabbit experimental model of SAH.
Data suggest that expression of TLR4 in intestinal mucosa can be regulated by dietary factors; here, flaxseed oil down-regulates expression of TLR4 in piglet model of necrotizing enterocolitis.
Actinobacillus pleuropneumoniae induces alveolar Macrophages to produce proinflammatory cytokines via upregulation of TLR4 and NF-kappaB.
The TWEAK-independent Fn14 activation augments TLR4-mediated inflammatory responses in the intestine of piglets.
These results further confirm the involvement of the TLR4 signaling pathway in resistance to E. coli F18 in Meishan weaned piglets.
Data suggest expression of TLR4 and NFKB (nuclear factor kappa B) are regulated by dietary factors affecting innate immunity; here, Lactobacillus acidophilus in feed down-regulates expression of TLR4 and NFKB in mononuclear cells after LPS challenge.
At 30 days after autotransplantation of a pig kidney, mRNA expression increases for TLR4.
Data suggest TLR2, TLR4, and calcium signaling in enterocytes play principal roles in mucosal immunity against enterotoxigenic Escherichia coli; probiotic Lactobacillus delbrueckii and its extracellular polysaccharides appear to stimulate TLR2/TLR4.
TLR2 is required for the suppression of TLR4 signaling activation.
The current study screened for single nucleotide polymorphisms (SNPs) in the TLR4 gene and tested their association with Salmonella fecal shedding.
The role of TLR2, TLR4 and RP105/MD1 in the immunoregulatory effect of acidic exopolysaccharides from Lactobacillus plantarum N14, is reported.
Data suggest expression of TLR4 in liver can be regulated by dietary factors; here, supplementation with aspartate down-regulates expression of TLR4 in liver in a model of liver disease.
Fish Oil attenuates the activation of the HPA axis induced by LPS challenge. So it may be associated with decreasing the production of brain or peripheral proinflammatory cytokines through inhibition of TLR4 and NOD signaling pathways in weaned pigs.
Single nucleotide polymorphisms in TLR4 is associated with immune response to gram-negative bacterial infections.
The complete coding sequence of TLR4 gene in Min pig and 3 variants with single point mutations were obtained.
The relationship between TLR4 single nucleotide polymorphisms and the transcription levels of cytokines indicate that they are related to the modulation of the cytokine mediated immune response in pigs.
An alteration from cysteine to tryptophan at position 506 (C506W) caused loss of ability to induce nuclear factor-kappaB activation after lipid A stimulation.
These findings showed that TLR4 takes part in airway mucosal defense systems as a unique exogenous potentiator of electrolyte-water secretion from acinar cells, and that NO/cGMP/cGKsignaling is involved in this rapid TLR4 signaling pathway.
Three new alleles were isolated for exon 1 of the TLR4 gene.
similarity in TLR4 staining in macrophages, epithelium and vascular endothelium among dog, pig and cattle
A high level of conservation of TLR4 gene size and sequence, especially for the two last exons and particularly in the sequence corresponding to the LRRs and TIR domain, is observed between species
expression of TLR 2, 4 and 6 as transcript and protein in the placenta (chorioallantois) of 14 foals born alive
This study provides the basis for comparative investigations into the impact of different stimuli on the cellular expression of TLRs 2, 4 and 6 in order to find out if TLRs are involved in the pathogenesis of endometrial diseases and may help to understand as to why some mares develop persistent endometritis.
The research findings suggest that Th17 cells are involved in active equine inflammatory bowel disease, and that TLR4 expression was increased in affected horses.
A low steady expression of TLR4, MD-2 and CD14 mRNA was demonstrated for the intestinal samples with no variation between the intestinal segments analysed.
In the present study, the authors show that TLR4 expression is significantly decreased following the exogenous expression of BPV-1 E2 and E7 in primary equine fibroblasts.
evidence that pulmonary intravascular macrophages are equipped with TLR4 to handle and rapidly respond to circulating endotoxins
TLR4/MD-2 complex is responsible for recognition of Rhodococcus spheroides lipopolysaccharide as an agonist in equine cells.
The protein encoded by this gene is a member of the Toll-like receptor (TLR) family which plays a fundamental role in pathogen recognition and activation of innate immunity. TLRs are highly conserved from Drosophila to humans and share structural and functional similarities. They recognize pathogen-associated molecular patterns that are expressed on infectious agents, and mediate the production of cytokines necessary for the development of effective immunity. The various TLRs exhibit different patterns of expression. This receptor has been implicated in signal transduction events induced by lipopolysaccharide (LPS) found in most gram-negative bacteria. Mutations in this gene have been associated with differences in LPS responsiveness. Multiple transcript variants encoding different isoforms have been found for this gene.
, homolog of Drosophila toll
, lipopolysaccharide response
, Toll-like receptor4 protein
, Toll-like receptor 4-like protein