mProX™ Human TLR4 Stable Cell Line

Product Information

Target Family

Immune Checkpoint

Target Protein Species

Human

Host Cell Type

HEK293;CHO-K1;HAECs

Target Classification

Immune Checkpoint Cell Lines

Target Research Area

CNS Research;Ocular Research

Related Diseases

Macular Degeneration, Age-Related, 10; Pertussis

Gene ID

Human:7099

UniProt ID

Human:O00206

Product Properties

Biosafety Level

Level 1

Activity

Yes

Quantity

10⁶ cells per vial

Applications

TLR4, a toll-like receptor, has various applications in different fields. In the field of comparative genomics, TLR4 has been studied in the family Equidae, specifically in the order Perissodactyla, to analyze the diversity and evolution of immunity-related genes. In the study, twelve TLR genes were identified and their sequences were confirmed in equids. Phylogenetic reconstruction of the TLR gene family in Perissodactyla revealed six sub-families, with TLR4 clustering together with TLR5. Another application of TLR4 is in vaccine development. A multi-epitope vaccine candidate for SARS-CoV-2 was designed using the reverse vaccinology approach, based on the spike protein (S) and membrane protein (M). The vaccine candidate was predicted to induce both cellular and humoral immune responses and interact with immune receptors such as TLR2 and TLR4. TLR4 is also involved in the pathogenesis of diseases like refractory epilepsy and lupus nephritis. In refractory epilepsy, alterations in DNA 5-hydroxymethylation patterns in the hippocampus were observed, and TLR4 was found to be associated with gene expression changes. In lupus nephritis, the Nrf2/HMGB1/TLR4/NF-Œ∫B signaling pathway was investigated as a potential regulatory pathway, and the expression of TLR4+CXCR4+ plasma cells subset was analyzed. Lastly, TLR4 has been studied in the context of retinal ischemia-reperfusion injury, where overexpression of S100A4 was found to inhibit the TLR4/NF-Œ∫B pathway and endoplasmic reticulum stress, leading to neuroprotection against retinal I/R injury.

Protocols

Please visit our protocols page.

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FAQ

chat Alex Williams (Verified Customer)

How does TLR4 mediate immune responses to bacterial infections? Jul 10 2022

chat Patrick Liam (Creative Biolabs Scientific Support)

TLR4 recognizes bacterial components like lipopolysaccharides, triggering immune responses and playing a crucial role in the body's defense against gram-negative bacteria. Jul 10 2022

chat Alex Brown (Verified Customer)

What is the significance of TLR4 in metabolic diseases? Mar 03 2023

chat Patrick Liam (Creative Biolabs Scientific Support)

TLR4 is implicated in the regulation of energy balance and insulin resistance, linking nutrition, lipids, and inflammation, and could be a target in treating metabolic disorders. Mar 03 2023

Published Data

Fig.1 The measurement of Toll-like receptor 4 (TLR4) small interfering RNA (siRNA) knockdown efficiency was carried out via RT-PCR.

Human aortic endothelial cells underwent transfection with TLR4 and scrambled siRNA (Sc si), followed by the utilization of one microgram of total RNA for cDNA synthesis. Subsequently, PCR was conducted, employing 50-100 ng of cDNA, to detect TLR4 and GAPDH mRNA using sequence-specific primers. The TLR4 mRNA levels were found to be suppressed when compared to those of the scrambled control, while the transfection had no impact on the GAPDH mRNA levels. Densitometric analysis was then performed on TLR4 mRNA knockdown in endothelial cells, revealing a significant decrease in the TLR4/GAPDH mRNA ratio when compared to that of the scrambled control. Each panel and bar represent results from four separate experiments, with error bars indicating the average ± SD of two band intensities (n = 4 separate experiments; * P < 0.05).

Ref: Dasu, Mohan R., et al. "The biological effects of CRP are not attributable to endotoxin contamination: evidence from TLR4 knockdown human aortic endothelial cells." Journal of lipid research 48.3 (2007): 509-512.

Pubmed: 17158793

DOI: 10.1194/jlr.C600020-JLR200

Research Highlights

Yeong Ha, Jae. et al. "Periodontitis promotes bacterial extracellular vesicle-induced neuroinflammation in the brain and trigeminal ganglion." PLoS pathogens, 2023.
Extracellular vesicles (EVs), also known as outer membrane vesicles, released by Gram-negative bacteria, particularly the periodontopathogen Aggregatibacter actinomycetemcomitans (Aa), have garnered considerable interest due to their role in various inflammatory diseases. Recent research has shown that Aa EVs can cross the blood-brain barrier and their extracellular RNA cargo can induce the release of proinflammatory cytokines in the brain. To explore the link between periodontal disease (PD) and neuroinflammatory diseases, a study was conducted using a mouse model of ligature-induced PD. It was found that when Aa EVs were administered to PD mice through intragingival injection or EV-soaked gel, there was a significant increase in the production of proinflammatory cytokines in the brain. This effect was confirmed by experiments using TLR-reporter cell lines and MyD88 knockout mice, which demonstrated that Aa EVs activated TLR4 and TLR8 signaling pathways, ultimately leading to the release of proinflammatory cytokines through the MyD88 pathway. Additionally, the direct retrograde transfer of Aa EVs from axon terminals to the cell bodies of trigeminal ganglion (TG) neurons and their subsequent activation was observed when EVs were injected through the epidermis and gingiva. It was also found that Aa EVs altered the action potential of TG neurons. These findings suggest that EVs from periodontopathogens like Aa may play a crucial role in neuroinflammatory diseases, neuropathic pain, and other systemic inflammatory symptoms associated with periodontitis.
Yeong Ha, Jae. et al. "Periodontitis promotes bacterial extracellular vesicle-induced neuroinflammation in the brain and trigeminal ganglion." PLoS pathogens, 2023.
Pubmed: 37871107 DOI: 10.1371/journal.ppat.1011743

Fu, Hongfang. et al. "Unraveling the protective mechanisms of Chuanfangyihao against acute lung injury: Insights from experimental validation." Experimental and therapeutic medicine, 2023.
The effectiveness of Chuanfangyihao (CFYH) in treating acute lung injury (ALI) has been well-documented in clinical practice. However, the specific mechanism by which CFYH exerts its effects remains unclear. To address this gap in knowledge, the present study aimed to elucidate the pharmacological mechanism of action of CFYH in ALI through experimental validation. Using a rat model of ALI induced by lipopolysaccharide (LPS), the study evaluated the lung damage and pathological changes, as well as measured the levels of inflammatory and cell death markers. The results showed that CFYH attenuated pulmonary edema and decreased the expression of inflammation-related molecules such as IL-6, TNF-Œ±, and TLR4. Additionally, CFYH was found to inhibit programmed cell death in ALI. These findings provide insight into the predominant mechanism of action of CFYH in alleviating ALI.
Fu, Hongfang. et al. "Unraveling the protective mechanisms of Chuanfangyihao against acute lung injury: Insights from experimental validation." Experimental and therapeutic medicine, 2023.
Pubmed: 37869635 DOI: 10.3892/etm.2023.12234