Review





Similar Products

receptor 4 tlr 4  (MedChemExpress)
96
MedChemExpress receptor 4 tlr 4
Schematic representation of the potential roles and mechanisms of Cx43 in LPS-induced inflammation in hDPCs. LPS interacts with <t>TLR-4</t> on the cell membrane, leading to the phosphorylation and subsequent degradation of IκBα, which in turn facilitates the nuclear translocation of NF-κB, ultimately triggering inflammation in hDPCs. Additionally, LPS stimulates the activity of Cx43 hemichannels (HCs), promoting the extracellular release of ATP and HMGB1 through these channels. The released ATP may then bind to P2X7 receptors, further exacerbating LPS-induced inflammation via autocrine and paracrine pathways. Concurrently, the activation of Cx43 HCs by LPS may initiate their fusion with vesicles containing HMGB1 on the plasma membrane. This fusion results in the displacement of the Cx43 HC-HMGB1 complex from the cytoskeleton, allowing for the subsequent release of HMGB1 into the extracellular space. This released HMGB1 may then activate TLR-4 on neighboring cells, further promoting LPS-induced inflammation. Dashed lines in the schematic represent hypothetical inferences.
Receptor 4 Tlr 4, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/receptor 4 tlr 4/product/MedChemExpress
Average 96 stars, based on 1 article reviews
receptor 4 tlr 4 - by Bioz Stars, 2026-02
96/100 stars
  Buy from Supplier
toll-like receptor 4 (tlr-4)  (Manco Inc)
90
Manco Inc toll-like receptor 4 (tlr-4)
Schematic representation of the potential roles and mechanisms of Cx43 in LPS-induced inflammation in hDPCs. LPS interacts with <t>TLR-4</t> on the cell membrane, leading to the phosphorylation and subsequent degradation of IκBα, which in turn facilitates the nuclear translocation of NF-κB, ultimately triggering inflammation in hDPCs. Additionally, LPS stimulates the activity of Cx43 hemichannels (HCs), promoting the extracellular release of ATP and HMGB1 through these channels. The released ATP may then bind to P2X7 receptors, further exacerbating LPS-induced inflammation via autocrine and paracrine pathways. Concurrently, the activation of Cx43 HCs by LPS may initiate their fusion with vesicles containing HMGB1 on the plasma membrane. This fusion results in the displacement of the Cx43 HC-HMGB1 complex from the cytoskeleton, allowing for the subsequent release of HMGB1 into the extracellular space. This released HMGB1 may then activate TLR-4 on neighboring cells, further promoting LPS-induced inflammation. Dashed lines in the schematic represent hypothetical inferences.
Toll Like Receptor 4 (Tlr 4), supplied by Manco Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/toll-like receptor 4 (tlr-4)/product/Manco Inc
Average 90 stars, based on 1 article reviews
toll-like receptor 4 (tlr-4) - by Bioz Stars, 2026-02
90/100 stars
  Buy from Supplier
toll like receptor tlr 4  (Santa Cruz Biotechnology)
96
Santa Cruz Biotechnology toll like receptor tlr 4
Schematic representation of the potential roles and mechanisms of Cx43 in LPS-induced inflammation in hDPCs. LPS interacts with <t>TLR-4</t> on the cell membrane, leading to the phosphorylation and subsequent degradation of IκBα, which in turn facilitates the nuclear translocation of NF-κB, ultimately triggering inflammation in hDPCs. Additionally, LPS stimulates the activity of Cx43 hemichannels (HCs), promoting the extracellular release of ATP and HMGB1 through these channels. The released ATP may then bind to P2X7 receptors, further exacerbating LPS-induced inflammation via autocrine and paracrine pathways. Concurrently, the activation of Cx43 HCs by LPS may initiate their fusion with vesicles containing HMGB1 on the plasma membrane. This fusion results in the displacement of the Cx43 HC-HMGB1 complex from the cytoskeleton, allowing for the subsequent release of HMGB1 into the extracellular space. This released HMGB1 may then activate TLR-4 on neighboring cells, further promoting LPS-induced inflammation. Dashed lines in the schematic represent hypothetical inferences.
Toll Like Receptor Tlr 4, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/toll like receptor tlr 4/product/Santa Cruz Biotechnology
Average 96 stars, based on 1 article reviews
toll like receptor tlr 4 - by Bioz Stars, 2026-02
96/100 stars
  Buy from Supplier
primary anti tlr-4  (Cell Signaling Technology Inc)
95
Cell Signaling Technology Inc primary anti tlr-4
Schematic representation of the potential roles and mechanisms of Cx43 in LPS-induced inflammation in hDPCs. LPS interacts with <t>TLR-4</t> on the cell membrane, leading to the phosphorylation and subsequent degradation of IκBα, which in turn facilitates the nuclear translocation of NF-κB, ultimately triggering inflammation in hDPCs. Additionally, LPS stimulates the activity of Cx43 hemichannels (HCs), promoting the extracellular release of ATP and HMGB1 through these channels. The released ATP may then bind to P2X7 receptors, further exacerbating LPS-induced inflammation via autocrine and paracrine pathways. Concurrently, the activation of Cx43 HCs by LPS may initiate their fusion with vesicles containing HMGB1 on the plasma membrane. This fusion results in the displacement of the Cx43 HC-HMGB1 complex from the cytoskeleton, allowing for the subsequent release of HMGB1 into the extracellular space. This released HMGB1 may then activate TLR-4 on neighboring cells, further promoting LPS-induced inflammation. Dashed lines in the schematic represent hypothetical inferences.
Primary Anti Tlr 4, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/primary anti tlr-4/product/Cell Signaling Technology Inc
Average 95 stars, based on 1 article reviews
primary anti tlr-4 - by Bioz Stars, 2026-02
95/100 stars
  Buy from Supplier
tlr 4  (Cell Signaling Technology Inc)
96
Cell Signaling Technology Inc tlr 4
Schematic representation of the potential roles and mechanisms of Cx43 in LPS-induced inflammation in hDPCs. LPS interacts with <t>TLR-4</t> on the cell membrane, leading to the phosphorylation and subsequent degradation of IκBα, which in turn facilitates the nuclear translocation of NF-κB, ultimately triggering inflammation in hDPCs. Additionally, LPS stimulates the activity of Cx43 hemichannels (HCs), promoting the extracellular release of ATP and HMGB1 through these channels. The released ATP may then bind to P2X7 receptors, further exacerbating LPS-induced inflammation via autocrine and paracrine pathways. Concurrently, the activation of Cx43 HCs by LPS may initiate their fusion with vesicles containing HMGB1 on the plasma membrane. This fusion results in the displacement of the Cx43 HC-HMGB1 complex from the cytoskeleton, allowing for the subsequent release of HMGB1 into the extracellular space. This released HMGB1 may then activate TLR-4 on neighboring cells, further promoting LPS-induced inflammation. Dashed lines in the schematic represent hypothetical inferences.
Tlr 4, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/tlr 4/product/Cell Signaling Technology Inc
Average 96 stars, based on 1 article reviews
tlr 4 - by Bioz Stars, 2026-02
96/100 stars
  Buy from Supplier
tlr  (Cell Signaling Technology Inc)
95
Cell Signaling Technology Inc tlr
Schematic representation of the potential roles and mechanisms of Cx43 in LPS-induced inflammation in hDPCs. LPS interacts with <t>TLR-4</t> on the cell membrane, leading to the phosphorylation and subsequent degradation of IκBα, which in turn facilitates the nuclear translocation of NF-κB, ultimately triggering inflammation in hDPCs. Additionally, LPS stimulates the activity of Cx43 hemichannels (HCs), promoting the extracellular release of ATP and HMGB1 through these channels. The released ATP may then bind to P2X7 receptors, further exacerbating LPS-induced inflammation via autocrine and paracrine pathways. Concurrently, the activation of Cx43 HCs by LPS may initiate their fusion with vesicles containing HMGB1 on the plasma membrane. This fusion results in the displacement of the Cx43 HC-HMGB1 complex from the cytoskeleton, allowing for the subsequent release of HMGB1 into the extracellular space. This released HMGB1 may then activate TLR-4 on neighboring cells, further promoting LPS-induced inflammation. Dashed lines in the schematic represent hypothetical inferences.
Tlr, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/tlr/product/Cell Signaling Technology Inc
Average 95 stars, based on 1 article reviews
tlr - by Bioz Stars, 2026-02
95/100 stars
  Buy from Supplier
toll-like receptor (tlr)4  (Morishita Jintan)
90
Morishita Jintan toll-like receptor (tlr)4
Schematic representation of the potential roles and mechanisms of Cx43 in LPS-induced inflammation in hDPCs. LPS interacts with <t>TLR-4</t> on the cell membrane, leading to the phosphorylation and subsequent degradation of IκBα, which in turn facilitates the nuclear translocation of NF-κB, ultimately triggering inflammation in hDPCs. Additionally, LPS stimulates the activity of Cx43 hemichannels (HCs), promoting the extracellular release of ATP and HMGB1 through these channels. The released ATP may then bind to P2X7 receptors, further exacerbating LPS-induced inflammation via autocrine and paracrine pathways. Concurrently, the activation of Cx43 HCs by LPS may initiate their fusion with vesicles containing HMGB1 on the plasma membrane. This fusion results in the displacement of the Cx43 HC-HMGB1 complex from the cytoskeleton, allowing for the subsequent release of HMGB1 into the extracellular space. This released HMGB1 may then activate TLR-4 on neighboring cells, further promoting LPS-induced inflammation. Dashed lines in the schematic represent hypothetical inferences.
Toll Like Receptor (Tlr)4, supplied by Morishita Jintan, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/toll-like receptor (tlr)4/product/Morishita Jintan
Average 90 stars, based on 1 article reviews
toll-like receptor (tlr)4 - by Bioz Stars, 2026-02
90/100 stars
  Buy from Supplier
toll- like receptor 4 (tlr- 4) elisa  (Elabscience Biotechnology)
90
Elabscience Biotechnology toll- like receptor 4 (tlr- 4) elisa
Schematic representation of the potential roles and mechanisms of Cx43 in LPS-induced inflammation in hDPCs. LPS interacts with <t>TLR-4</t> on the cell membrane, leading to the phosphorylation and subsequent degradation of IκBα, which in turn facilitates the nuclear translocation of NF-κB, ultimately triggering inflammation in hDPCs. Additionally, LPS stimulates the activity of Cx43 hemichannels (HCs), promoting the extracellular release of ATP and HMGB1 through these channels. The released ATP may then bind to P2X7 receptors, further exacerbating LPS-induced inflammation via autocrine and paracrine pathways. Concurrently, the activation of Cx43 HCs by LPS may initiate their fusion with vesicles containing HMGB1 on the plasma membrane. This fusion results in the displacement of the Cx43 HC-HMGB1 complex from the cytoskeleton, allowing for the subsequent release of HMGB1 into the extracellular space. This released HMGB1 may then activate TLR-4 on neighboring cells, further promoting LPS-induced inflammation. Dashed lines in the schematic represent hypothetical inferences.
Toll Like Receptor 4 (Tlr 4) Elisa, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/toll- like receptor 4 (tlr- 4) elisa/product/Elabscience Biotechnology
Average 90 stars, based on 1 article reviews
toll- like receptor 4 (tlr- 4) elisa - by Bioz Stars, 2026-02
90/100 stars
  Buy from Supplier

Image Search Results


Schematic representation of the potential roles and mechanisms of Cx43 in LPS-induced inflammation in hDPCs. LPS interacts with TLR-4 on the cell membrane, leading to the phosphorylation and subsequent degradation of IκBα, which in turn facilitates the nuclear translocation of NF-κB, ultimately triggering inflammation in hDPCs. Additionally, LPS stimulates the activity of Cx43 hemichannels (HCs), promoting the extracellular release of ATP and HMGB1 through these channels. The released ATP may then bind to P2X7 receptors, further exacerbating LPS-induced inflammation via autocrine and paracrine pathways. Concurrently, the activation of Cx43 HCs by LPS may initiate their fusion with vesicles containing HMGB1 on the plasma membrane. This fusion results in the displacement of the Cx43 HC-HMGB1 complex from the cytoskeleton, allowing for the subsequent release of HMGB1 into the extracellular space. This released HMGB1 may then activate TLR-4 on neighboring cells, further promoting LPS-induced inflammation. Dashed lines in the schematic represent hypothetical inferences.

Journal: Frontiers in Oral Health

Article Title: Blockade of connexin43-containing hemichannel attenuates the LPS-induced inflammatory response in human dental pulp cells by inhibiting the extracellular flux of ATP and HMGB1

doi: 10.3389/froh.2024.1496819

Figure Lengend Snippet: Schematic representation of the potential roles and mechanisms of Cx43 in LPS-induced inflammation in hDPCs. LPS interacts with TLR-4 on the cell membrane, leading to the phosphorylation and subsequent degradation of IκBα, which in turn facilitates the nuclear translocation of NF-κB, ultimately triggering inflammation in hDPCs. Additionally, LPS stimulates the activity of Cx43 hemichannels (HCs), promoting the extracellular release of ATP and HMGB1 through these channels. The released ATP may then bind to P2X7 receptors, further exacerbating LPS-induced inflammation via autocrine and paracrine pathways. Concurrently, the activation of Cx43 HCs by LPS may initiate their fusion with vesicles containing HMGB1 on the plasma membrane. This fusion results in the displacement of the Cx43 HC-HMGB1 complex from the cytoskeleton, allowing for the subsequent release of HMGB1 into the extracellular space. This released HMGB1 may then activate TLR-4 on neighboring cells, further promoting LPS-induced inflammation. Dashed lines in the schematic represent hypothetical inferences.

Article Snippet: The main experimental reagents used in this study included LPS from Sigma (USA), reverse transcription kit and SYBR Premix Ex TaqTM Kit from Novagen (China), phosphorylated NF-κB antibody (p-NF-κB) from CST (USA), NF-κB antibody from Abcam (USA), Toll-like receptor 4 (TLR-4) from Santa (USA), Gap19, Gap26, and HMGB1 from MCE (USA), ATP reagent and ATP detection kit from Bi Yun Tian (China), ELISA kit from Wuhan Sevier (China), and ethidium bromide (EB) and LY from Sigma (USA).

Techniques: Membrane, Phospho-proteomics, Translocation Assay, Activity Assay, Activation Assay, Clinical Proteomics