Transfected Stable Cell Lines
Reliable | High-Performance | Wide Rage
Precision reporter, kinase, immune receptor, biosimilar, Cas9, and knockout stable cell lines for diverse applications.
| Cat.No. | Product Name | Price |
|---|---|---|
| CSC-DC011280 | Panoply™ Human PANX1 Knockdown Stable Cell Line | Inquiry |
| CSC-SC011280 | Panoply™ Human PANX1 Over-expressing Stable Cell Line | Inquiry |
| Cat.No. | Product Name | Price |
|---|---|---|
| AD11787Z | Human PANX1 adenoviral particles | Inquiry |
| LV20940L | human PANX1 (NM_015368) lentivirus particles | Inquiry |
| Cat.No. | Product Name | Price |
|---|---|---|
| SHH370396 | shRNA set against Mouse PANX1 (NM_019482.2) | Inquiry |
| SHH370400 | shRNA set against Rat PANX1 (NM_199397.2) | Inquiry |
| SHR064201 | shRNA set against Rat Olr479_predicted(NM_001000305.1) | Inquiry |
| SHR086896 | shRNA set against Mouse Panx1(NM_019482.2) | Inquiry |
| SHR086988 | shRNA set against Human PANX1(NM_015368.3) | Inquiry |
| SHW017043 | shRNA set against Danio rerio PANX1A (NM_200916) | Inquiry |
| Cat.No. | Product Name | Price |
|---|---|---|
| CDFH013667 | Human PANX1 cDNA Clone(NM_015368.3) | Inquiry |
| CDFH013668 | Human PANX1 cDNA Clone(NM_015368.3) | Inquiry |
| MiUTR1H-07490 | PANX1 miRNA 3'UTR clone | Inquiry |
| MiUTR1M-08881 | PANX1 miRNA 3'UTR clone | Inquiry |
| CDCB178518 | Danio rerio PANX1A ORF Clone (NM_200916) | Inquiry |
| CDCB183023 | Rabbit PANX1 ORF clone (XM_008262563.1) | Inquiry |
| CDCL145803 | Human Panx1 ORF clone (NM_019482.2) | Inquiry |
| CDCR299359 | Human PANX1 ORF Clone(NM_015368.3) | Inquiry |
| CDCR382320 | Rat Panx1 ORF Clone(NM_199397.2) | Inquiry |
| CDCS413943 | Human PANX1 ORF Clone (BC016931) | Inquiry |
Upregulation of pro-inflammatory cytokines, such as interleukin (IL)-1 beta, is the key for tumor necrosis factor (TNF)-alpha triggered inflammation in endothelial cells, while there is still unsatisfied understanding of molecular mechanisms driving their production, processing, or release. Pannexin 1 was recently implicated to be an intermediary of the TNF-alpha/IL-1beta inflammatory pathway in the human umbilical vein endothelial cell (HUVEC) line. Besides the role as a nucleotide and metabolite channel of PANX1 channel, its permeability for ions of various sizes and charges has also been suggested in previous work. The revelation of its strategically placed positive residues in the recent structural reports detailing PANX1 subunit and channel composition may imply its preference towards passing negatively charged molecules, such as Cl- and ATP. In the subsequent studies also revealed that the purported tunnels are additionally lined with a set if negatively charged amino acids (aspartate and glutamate), which could facilitate cation or Ca2+ transport. This put forward the possibility that various possible open configurations in response to different stimuli may be the result of preference towards supporting alternate permeability to anions or cations. Another possibility may be to account for indirect regulation of Ca2+ influx by PANX1, for example by modulating the activity of a Ca2+ transporter, exchange, or channel. The crosstalk of PANX1 and NMDAR, which is also known as N-methyl-D-aspartate receptors, present and functional on peripheral endothelial cells, has also been suggested to be involved in the current context.
In peripheral and nervous system pathologies, PANX1-mediated inflammatory signaling, such as the release of ATP and other nucleotides, inflammasome activation and cytokine release, have some implications. IL1B transcription up-regulated by PANX1 implicated in many of these pathologies may represent a potential therapeutic target. Those exciting new findings about the role of PANX1 in inflammation may connect it to TNF-alpha and NF-κB,thus laying the groundwork for unraveling the complexities of inflammatory disease pathogenesis and treatment in endothelial cells as well as other cells expressing PANX1.
In neurological diseases, such as Alzheimer's disease, multiple sclerosis, neuropathic pain, and brain trauma, neuroinflammation is a major component of central nervous system (CNS) injuries. Release of pro-inflammatory cytokines and chemokines at the damage sites can be initiated by activation of innate immune cells, for the functionality alteration of nearby tissues and mediation of leukocytes recruitment to the injury site. ATP is a molecule released for inflammation response trigger and serves as a chemotactic and endogenous danger signal, and extracellular ATP activates multiple purinergic receptors that have been shown to promote neuroinflammation in a variety of CNS diseases. PANX1 channels may work as the principal conduits of ATP release from dying cells and innate immune cells in the brain.
Figure 1. Panx1 deficiency protects mouse kindneys from ischemia-reperfusion injury (IRI). (Jakub Jankowski, et al. 2018)
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