TAK-242 (resatorvid), a small molecule specific inhibitor of Toll-like receptor (TLR) 4 signaling, inhibits the production of lipopolysaccharide-induced inflammatory mediators by binding to the intracellular domain of TLR4. Previously, Cys747 in TLR4 was identified as the binding site of TAK-242. However, the mechanism by which TAK-242 inhibits TLR4 signaling after binding to TLR4 remains unknown. The present study demonstrated, using coimmunoprecipitation, that TAK-242 interferes with protein-protein interactions between TLR4 and its adaptor molecules. Among ten different human TLRs, TAK-242 selectively bound to TLR4. The time course of the inhibitory effect of TAK-242 on inflammatory mediator production corresponded to that of the binding of TAK-242 to TLR4. TAK-242 inhibited the association of TLR4 with TIR domain-containing adaptor protein (TIRAP) or TRIF-related adaptor molecule (TRAM) in HEK293 cells overexpressing TLR4, MD-2 and TIRAP or TRAM, respectively. TAK-242 inhibited the ...
Background. The Toll-like receptor 4 (TLR4) is an essential component of the innate immune response to various microorganisms. We investigated the association between TLR4 polymorphism and the risk of acquiring severe infections, in patients with human immunodeficiency virus (HIV)-1 infection.. Methods. The presence of TLR4 Asp299Gly and Thr399Ile single nucleotide polymorphisms (SNPs) was determined in a cohort of 199 HIV-1 infected patients and evaluated in relation to the occurrence of various infections.. Results. One hundred seventy-two patients were homozygous for the wild-type genotype; 22 patients (11%) were heterozygous for both SNPs; 4 were heterozygous for 1 polymorphism; 1 patient was heterozygous for the Asp299Gly SNP and homozygous for the Thr399Ile SNP. Of individuals with a nadir CD4 cell count of ,100 cells/mm3, those who carried both SNPs, compared with those who carried the wild-type genotype, demonstrated a ,3-fold increase in the odds ratio (OR) of any serious infection (OR, ...
Continuous inflammation in the colon often leads to chronic diseases such as inflammatory bowel disease (IBD) and colorectal cancer. Recent evidence strongly suggests the role of Toll-Like Receptors 2 and 4 in the etiology of aforementioned diseases. Therefore, pharmacological inhibition of TLR-2/TLR-4 has been a new promising strategy for preventing inflammation in IBD and colorectal cancer. In the current study, we have developed a novel polymer-drug complex (Ora-Curcumin) as a TLR-2/TLR-4 antagonist to modulate the gut innate immune system. Ora-Curcumin is a molecular complex of curcumin with a hydrophilic polymer Eudrgit® S100 prepared by nano-precipitation. Ora-curcumin is more water soluble (~1000 times) and stable than curcumin in aqueous buffers. It is water soluble only at pHs above 6.8. Therefore, once consumed orally, it is expected to be soluble and functionally available only at the luminal side of the colon where the pH reaches 6.8. In addition, Ora-Curcumin was potent TLR-4 ...
Despite advances in its treatment, the incidence of renal diseases has been consistently increasing. Hence, there is a need to understand the underlying molecular mechanisms of the progression of kidney diseases. Recent research implicates inflammation as an important mediator of renal injury. We hypothesized that inhibiting Toll-like receptor 4 (TLR4), an upstream modulator of several inflammatory pathways, would prevent the progression of renal diseases. First, we determined the mechanism by which AngiotensinII (AngII)-induced inflammation is modulated by TLR4 using an in vitro model of rat tubulo-epithelial cells. We blocked TLR4 using gene silencing strategy in NRK52E cells. In TLR4-silenced cells, the expression of TLR4 was decreased, activation of NF-κB was reduced, inflammation and oxidative stress were attenuated, suggesting a role for TLR4 in potentiating AngII-induced renal inflammation. We then focused on an in vivo acute kidney injury (AKI) model to elucidate the effect of TLR4 in AKI. We
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Despite the assumption that at least some TLR family members mediate innate immune response, very little information was available regarding their expression pattern in immunocompetent cells and no functional data are available for TLR other then TLR2 and TLR4. The existence of many of them may reflect specialized functions, redundancy, and/or differential expression and roles in different cell types. Herein, we have characterized the pattern of mRNA expression of the first five TLR.. We separated fresh human monocytes, NK cells, PMN, B cells, T lymphocytes, Th1 or Th2 lymphocytes, and monocyte-derived DC. Total RNA was extracted from the cells and analyzed by Northern blot to detect specific TLR transcripts. To note, TLR1, TLR2, and TLR4 probes allowed a signal detection on the filter only after a few hours of autoradiography. On the other hand, TLR3 and TLR5 probes required at least an overnight exposure of the filter to evidence a specific transcript, suggesting that distinct TLR transcripts ...
Pattern recognition underpins innate immunity; the accurate identification of danger, including infection, injury, or tumor, is key to an appropriately targeted immune response. Pathogen detection is increasingly well defined mechanistically, but the discrimination of endogenous inflammatory triggers remains unclear. Tenascin-C, a matrix protein induced upon tissue damage and expressed by tumors, activates toll-like receptor 4 (TLR4)-mediated sterile inflammation. Here we map three sites within tenascin-C that directly and cooperatively interact with TLR4. We also identify a conserved inflammatory epitope in related proteins from diverse families, and demonstrate that its presence targets molecules for TLR detection, while its absence enables escape of innate immune surveillance. These data reveal a unique molecular code that defines endogenous proteins as inflammatory stimuli by marking them for recognition by TLRs.
Research proven purified goat polyclonal TLR-3 (Toll-like receptor3)/CD283 antibody. Designed for immune response research. Excellent for western blotting, DIRECT Elisa and related applications.
Lipopolysaccharide (LPS) tolerance is a state of refractoriness towards a second stimulation by LPS after a preceding stimulation. LPS is recognized by Toll-like receptor-4 (TLR-4), which belongs to a group of pattern recognition receptors mediating activation of innate immunity by microbial compone …
Introduction: Toll-like receptors (TLRs) are crucial for the recognition of pathogens which subsequently lead to the activation of inflammatory pathways. However, the mycoplasma lipopeptid and TLR-2/-6 ligand MALP-2 has been used in therapeutic applications, e.g. dermal wound healing. Since tissue regeneration requires the reestablishment of a functional vascular network we investigated the impact of the TLR-2/6 ligand MALP-2 on angiogenesis and reendothelialization.. Methods and results: Expression of TLR-2 and -6 in human endothelial cells was demonstrated by PCR, Western blot and immunofluorescence and significantly up regulated after stimulation with MALP-2 (100 ng/mL, qRT-PCR, Western blot). MALP-2 induced tube formation (Matrigel, P,0.05) and endothelial cell proliferation (BrdU-incorporation, P,0.01) in vitro which could be inhibited with neutralizing antibodies against TLR-2/-6. Furthermore, MALP-2 enhanced neovascularisation of matrigel implants in mice as determined by hemoglobin ...
Ation was dependent on TLR7. Thus, despite the fact that TLR8 is expressed on MedChemExpress Crenolanib murine microglia and astrocytes, it appears to only
Objective: This paper describes a case-control study and a meta-analysis conducted to determine whether the TLR4 Asp299Gly (rs4986790) and Thr399Ile (..
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Sigma-Aldrich offers abstracts and full-text articles by [Rong Chen, Liqiang Feng, Mo Ruan, Xinghui Liu, Sahil Adriouch, Hua Liao].
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TLR2 antibody (toll-like receptor 2) for ELISA, IHC-P, WB. Anti-TLR2 pAb (GTX31279) is tested in Human, Mouse samples. 100% Ab-Assurance.
摘 要:Toll样受体4(TLR4)是固有免疫系统中能够识别病原相关分子模式的受体家族成员,可识别革兰氏阴性菌的脂多糖(LPS)而在细菌感染性疾病的发生中起重要作用。近年来越来越多的研究发现,TLR4还广泛参与病毒感染性疾病的发生和病毒的免疫逃逸,由于其信号转导通路的独特性和细胞定位的可变性,再次引起人们极大的研究兴趣。该文将介绍TLR4的生物学特性、信号转导通路及TLR4与病毒感染的最新研究进展 ...
Antiviral inte immunity depends on the combition of parallel pathways triggered by virus detecting proteins in the Toll-like receptor (TLR) family and…
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TLR2 (толл-подобный рецептор 2, CD282) - мембранный белок, входящий в группу толл-подобных рецепторов, обеспечивающих функционирование врождённого иммунитета. TLR2 так же как TLR1 распознаёт патоген-связанные молекулярные структуры грам-положительных бактерий, включая пептидогликаны, липотейхоевую кислоту, некоторые компоненты микобактерий и зимозан клеточной стенки дрожжей. ...
Oh, Djin-Ye; Baumann, Konstantin; Hamouda, Osamah; Eckert, Jana K; Neumann, Konrad; Kücherer, Claudia; Bartmeyer, Barbara; Poggensee, Gabriele; Oh, Nari; Pruss, Axel; Jessen, Heiko; Schumann, Ralf R Abstract Objectives: Toll-like receptors (TLRs) play an important role in the innate immune response to pathogens. TLR7 recognizes RNA of various viruses including HIV. The objective of this study…
BACKGROUND: Inflammation and matrix degradation are the hallmarks of high-risk atherosclerosis that leads to myocardial infarction and stroke. Toll-like receptors (TLRs), key players in innate immunity, are upregulated in atherosclerotic lesions, but their functional role in human atherosclerosis is unknown. We explored the effects of blocking TLR-2, TLR-4, and myeloid differentiation primary response gene 88 (MyD88), a signaling adaptor shared by most TLRs and interleukin-1 receptor (IL-1R), in an in vitro model of human atherosclerosis. METHODS AND RESULTS: Carotid endarterectomies were obtained from patients with symptomatic carotid disease. Cells were isolated via enzymatic tissue dissociation and cultured in the presence or absence of TLR signaling blockers. A dominant-negative form of MyD88 (MyD88(DN)) decreased the production of monocyte chemotactic protein-1/CCL2 (P=0.000), IL-8/CXCL8 (P=0.006), IL-6 (P=0.002), matrix metalloproteinase-1 (MMP-1; P=0.002), and MMP-3 (P=0.000), as well as nuclear
Upon ligand engagement, TLRs elicit an intracellular signaling cascade that eventually leads to the expression of genes encoding antimicrobial, inflammatory, and immunomodulatory proteins [1]. Through a focused effort, four TLR adaptor proteins containing TIR homology domains were identified about ten years ago and demonstrated to play specific roles in the activation of TLR signaling [2], [3], [4], [5], [6], [7], [8]. The TIR adaptors enable signaling through TLRs by interacting with the TIR domain in the cytoplasmic tail of TLRs [1]. Among the 10 human TLRs, all except TLR3 are dependent on the TIR adaptor protein MyD88 (myeloid differentiation primary response gene 88) for signaling [1]. The MyD88 pathway activates the transcription factor NF‐κB to induce pro‐inflammatory gene expression. On the other hand, TLR3 depends on TRIF (TIR‐domain‐containing adapter inducing IFN‐β) for downstream signaling, and TLR4 can signal both through MyD88 and TRIF. Like the MyD88 pathway, the TRIF ...
The recent discovery of an ancient family of toll-like receptors (TLRs) in the immune system has substantially enhanced the potential for a variety of therapies, for both failing immune systems, which leaves the body open to infection or over-active ones, which can lead to chronic inflammation. Signaling by Toll-Like Receptors provides a comprehensive review of important techniques in molecular biology, cell biology, biochemistry, genetics, and immunology and their critical application to the study of toll-like receptor structure, biological function, and the intracellular signaling triggered by these receptors, as well as the high promise for uncovering effective pharmaceutica ...
TY - JOUR. T1 - Toll-like receptor 2 (TLR2)-TLR9 crosstalk dictates IL-12 family cytokine production in microglia. AU - Holley, Monica M.. AU - Zhang, Yongqing. AU - Lehrmann, Elin. AU - Wood, William H.. AU - Becker, Kevin G.. AU - Kielian, Tammy L. PY - 2012/1/1. Y1 - 2012/1/1. N2 - Microglia are the resident mononuclear phagocytes of the CNS parenchyma and represent an initial line of defense against invading microorganisms. Microglia utilize Toll-like receptors (TLRs) for pathogen recognition and TLR2 specifically senses conserved motifs of gram-positive bacteria including lipoproteins, lipoteichoic acids, and peptidoglycan (PGN) leading to cytokine/chemokine production. Interestingly, primary microglia derived from TLR2 knockout (KO) mice over-expressed numerous IL-12 family members, including IL-12p40, IL-12p70, and IL-27 in response to intact S. aureus, but not the less structurally complex TLR2 ligands Pam3CSK4 or PGN. The ability of intact bacteria to augment IL-12 family member ...
This Bovine Toll-like receptor 3 (TLR3) ELISA Kit employs a two-site sandwich ELISA to quantitate TLR3.,TLR3; CD283;,TLR 3 is a member of the Toll-like receptor family of pattern recognition receptors of the innate immune system. Discovered in 2001,TLR3 recognizes double-stranded RNA, a form of genetic information carried by some viruses such as reoviruses. Upon recognition, TLR 3 induces the activation of NF-kB to increase production of type I interferons which signal other cells to increase their antiviral defenses. Double-stranded RNA is also recognised by the cytoplasmic receptors RIG-I and MDA-5.The structure of TLR3 was reported in June 2005 by researchers at The Scripps Research Institute. TLR3 forms a large horseshoe shape that contacts with a neighboring horseshoe, forming a
Specific families of pattern recognition receptors are responsible for detecting microbial pathogens and generating innate immune responses. Toll-like receptors (TLRs) are membrane-bound receptors identified as homologs of Toll in Drosophila. Mammalian TLRs are expressed on innate immune cells, such as macrophages and dendritic cells, and respond to the membrane components of Gram-positive or Gram-negative bacteria. Pathogen recognition by TLRs provokes rapid activation of innate immunity by inducing production of proinflammatory cytokines and upregulation of costimulatory molecules. TLR signaling pathways are separated into two groups: a MyD88-dependent pathway that leads to the production of proinflammatory cytokines with quick activation of NF-{kappa}B and MAPK, and a MyD88-independent pathway associated with the induction of IFN-beta and IFN-inducible genes, and maturation of dendritic cells with slow activation of NF-{kappa}B and MAPK. Source: KEGG:Toll-like Receptor Signaling ...
The innate immune system is the first line of defense against invading pathogens. Recognition of microbial ligands by the innate immune system relies on germ-line encoded, evolutionarily conserved receptors called pattern recognition receptors (PRRs). Toll-like receptors (TLRs) are one such family of PRRs and are involved in innate defenses to a variety of microbes. At the core of TLR signaling pathways are Toll interleukin-1 receptor (TIR) domain containing adapter proteins. Much of the specificity of TLR pathways arise from the differential use of these adapter proteins. The TLR signaling cascade that ensues upon ligand recognition is marked by finely orchestrated molecular interactions between the receptor and the TIR domain containing adapter proteins, as well as various downstream kinases and effector molecules. Conserving the structural integrity of the TLR components is thus essential for maintaining a robust host defense system. Sometimes, changes in a protein can be brought about by single
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to circumvent innate immunity was demonstrated (Cirl et al. 2008, Nature Medicine 14, 399-406). This involves a bacterial TIR domain-containing protein (Tcp) that is secreted by bacterial pathogens and inhibits Toll-like receptor (TLR) signalling. ,p, Toll-like receptors have a central role in innate immunity. They recognise molecules from microbial pathogens and trigger an immune response through a signalling domain called TIR. Bacterial Tcps contain a TIR domain that mimics the TIR domain of Toll-like receptors. TLR signalling is interrupted when MyD88, a downstream component of TLR signalling, binds to the TIR domain of a bacterial Tcp instead of to the TIR domain of a Toll-like receptor. This way, secreted Tcps impair the release of cytokines and, subsequently, prevent an inflammatory response. ,p, Our data show that bacterial Tcps or the TIR domains contained in Tcps can be used to modulate cytokine responses of innate immune cells as is desirable in the treatment of autoimmune diseases. ...
The identification of the bacterial endotoxin receptors for innate immunity, most notably TLR4 (Toll-like receptor 4), has sparked great interest in therapeutic manipulation of the innate immune system. In the present mini-review, several natural and synthetic molecules that modulate the TLR4-mediated LPS (lipopolysaccharide) signalling in animals and humans are considered, and their mechanisms of action are discussed. The process of LPS sensing and signal amplification in humans is based on the sequential action of specific receptors situated in the extracellular side of the innate immunity cells, which bind and transfer LPS to TLR4: LBP (LPS-binding protein), CD14, MD-2 (myeloid differentiation protein 2). We classified the compounds active on TLR4 pathway depending on the specific molecular targets (LPS, LBP, CD14, MD-2 or TLR4). Small molecules developed by our group are described that inhibit LPS-stimulated TLR4 activation by selectively targeting the LPS-CD14 interaction. These compounds ...
FREE FULLTEXT Lester, Richard T; Yao, Xiao-Dan; Ball, T Blake; McKinnon, Lyle R; Kaul, Rupert; Wachihi, Charles; Jaoko, Walter; Plummer, Francis A; Rosenthal, Kenneth L Free Access Article Outline Abstract Objectives: Toll-like receptors (TLR) are important in pathogen recognition and may play a role in HIV disease. We evaluated the effect of chronic untreated and…
The innate immune system detects highly conserved, relatively invariant structural motifs of pathogens. Toll-like receptors (TLRs) have been identified as the primary innate immune receptors. TLRs distinguish between different patterns of pathogens and activate a rapid innate immune response; however, TLRs can also be activated by host-derived molecules. In addition to being expressed in immune cells, TLRs are expressed in other tissues, such as those of the cardiovascular system. TLRs could, therefore, be a key link between cardiovascular disease development and the immune system. Indeed, evidence that TLR activation contributes to the development and progression of atherosclerosis, cardiac dysfunction in sepsis, and congestive heart failure, is convincing. Although much has been learned about TLR activation in cellular components of the cardiovascular system, the role individual TLR family members have in the pathophysiology of cardiovascular diseases and hence in clinical practice remains to be
In his studies, he used proteinase-producing fungi as the environmental trigger for asthma. Laboratory mice that lacked toll-like receptor 4 did not mount a robust allergic airway disease when challenged by proteinase, viable fungi or other triggers but did have a normal Th2 immunity.. "Why do our bodies do this?" said Corry. The answer is both simple and complicated. The system developed to allow organisms to survive infection with deadly organisms such as fungi. How it achieves that is complicated.. In this "survival mode," the immune system generates symptoms that can themselves create disease.. Against the insidious onslaught of organisms such as fungi, which can kill if left unchecked, asthma may be a better alternative, said Corry.. "If you don¹t fight fungi off, they will get you," he said.. Others who took part in this research include Valentine Ongeri Millien, Wen Lu, Joanne Shaw, Xiaoyi Yuan, Garbo Mak, M.D., Luz Roberts, Li-Zhen Song J. Morgan Knight, Chad J. Creighton, Amber Luong, ...
Toll-like receptor 4 (TLR4), along with its accessory protein myeloid differentiation factor 2 (MD-2), builds a heterodimeric complex that specifically recognizes lipopolysaccharides (LPS), which are present on the cell wall of Gram-negative bacteria, activating the innate immune response. Some TLR4 modulators are undergoing preclinical and clinical evaluation for the treatment of sepsis, inflammatory diseases, cancer and rheumatoid arthritis. Since the relatively recent elucidation of the X-ray crystallographic structure of the extracellular domain of TLR4, research around this fascinating receptor has risen to a new level, and thus, new perspectives have been opened. In particular, diverse computational techniques have been applied to decipher some of the basis at the atomic level regarding the mechanism of functioning and the ligand recognition processes involving the TLR4/MD-2 system at the atomic level. This review summarizes the reported molecular modeling and computational studies that ...
Toll-like receptor 2 (TLR2)is a member of the TLR family, which plays a central role in the innate immune response to a wide variety of microorganisms. Animal studies have shown thatTLR2-knockout mice are more susceptible to septicemia due to Staphylococcus sure us and Listeria monocyto genes,meningitis due to Streptococcus pneumoniae,and infection with Mycobacterium tuberculosis,suggesting that functional TLR2polymorphisms may impair host response to a certain spectrum of microbial pathogens. In humans, 2 polymorphisms in the exon part of TLR2, which attenuatereceptor signaling, enhance the risk of acute severe infections, tuberculosis, and leprosy. Because gram-positive bacteria have became the first cause of severe infections, including septic shock, knowledge of the role that alteration or lack of TLR2function plays in the pathogenesis of infectious diseases could contribute to the design of new the rapeuticstrategies, including prevention, pharmacologicalintervention, and vaccine ...
To locate the ligand binding site on TLR3, we analyzed ,50 mutations within the TLR3-ECD. Remarkably, only 2 of the 50 residues tested resulted in abrogation of both the activation of TLR3 by pI:pC and the direct binding of pI:pC to purified TLR3-ECD protein. These two residues, H539 and N541, are conserved from zebrafish to humans (Fig. 10, which is published as supporting information on the PNAS web site) and position the ligand binding site on the glycan-free surface of the ECD at LRR20.. Replacing His-539 with an alanine has little effect on TLR3 responsiveness, whereas substitution of a negatively charged carboxyl group for an imidazole ring at this site results in a total loss of function. This finding suggests that a negative charge from a backbone phosphate group on dsRNA occupies a position in close proximity to residue 539 in the ligand-receptor complex. In the WT protein a protonated imidazole ring of His-539 would neutralize the negative charge of the phosphate, but in the H539E ...
CpG-oligonucleotides (CpG-ODN), which induce signaling through Toll-like receptor 9 (TLR9), are currently under investigation as adjuvants in therapy against infections and cancer. CpG-ODN function as Th-1 adjuvants and are able to activate dendritic cells. In humans TLR9 has been described to be strongly expressed in B-lymphocytes, monocytes, plasmacytoid dendritic cells and at low levels in human respiratory cells. We determined whether a direct interaction of bacterial DNA with the tumor cells themselves is possible and investigated the expression and function of TLR9 in human malignant solid tumors and cell lines. TLR9 expression by malignant tumor cells, would affect treatment approaches using CpG-ODN on the one hand, and, on the other hand, provide additional novel information about the role of tumor cells in tumor-immunology. The expression of TLR9 in HOPE-fixed non-small lung cancer, non-malignant tissue and tumor cell lines was assessed using immunohistochemistry, confocal microscopy, in situ
As we learn more about the biology of the Toll-like receptors (TLRs), a wide range of molecules that can activate this fascinating family of pattern recognition receptors emerges. In addition to conserved pathogenic components, endogenous danger signals created upon tissue damage are also sensed by TLRs. Detection of these types of stimuli results in TLR mediated inflammation that is vital to fight pathogenic invasion and drive tissue repair. Aberrant activation of TLRs by pathogenic and endogenous ligands has also been linked with the pathogenesis of an increasing number of infectious and autoimmune diseases, respectively. Most recently, allergen activation of TLRs has also been described, creating a third broad class of TLR stimulus that has helped to shed light on the pathogenesis of allergic disease. To date, microbial activation of TLRs remains best characterized. Each member of the TLR family senses a specific subset of pathogenic ligands, pathogen associated molecular patterns (PAMPS), and a
Toll-like receptors (TLRs) have been described as sensors for pathogen-associated molecular patterns crucial for the initiation of an innate immune response. These mechanisms were developed long before the adaptive immune system evolved. The latest additions to the growing list of TLR ligands are he …
Statins enhance toll-like receptor 4-mediated cytokine gene expression in astrocytes: implication of Rho proteins in negative feedback regulation.: Toll-like re
Toll-like Receptors (TLRs) are not only crucial for the initiation of immune response, but also play a key role in several inflammatory diseases. This..
This webpage describes Toll-Like Receptors present in mice and humans and their corresponding ligands, adapter proteins, and accessory molecules. The website also provides a comprehensive distribution list of TLRs expression in both mouse and human cells. BioLegend develops and manufactures world-class, cutting-edge immunological reagents for biomedical research, offered at an outstanding value.
Effect of a Mushroom (Coriolus versicolor) Based Probiotic on the Expression of Toll-like Receptors and Signal Transduction in Goat Neutrophils
BOMFIM, G. F.... Toll-like receptor 4 inhibition reduces vascular inflammation in spontaneously hypertensive rats. Life Sciences 122 n. p. 1-7 FEB 1 2015. Artigo Científico.
Viral induction of AID is independent of the interferon and the Toll-like receptor signaling pathways but requires NF-,IMG SRC="/math/kgr.gif" ALT="{kappa}" BORDER="0", ...
邓守龙.,Kun Yu.,Qian Wu.,Yan Li.,Xiao-Sheng Zhang.,...&连正兴.(2016).Toll-Like Receptor 4 Reduces Oxidative Injury via Glutathione Activity in Sheep.Oxidative Medicine and Cellular Longevity,2016,Article No. 9151290 ...
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