ArticleThe Journal of biological chemistry2011
Pathways regulating the trafficking and turnover of pannexin1 protein and the role of the C-terminal domain.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 42 citations in OpenAlex.
- Cross-Presentation and Activation of CD8+ T Cells: The Role of Pannexin-1 in Dendritic Cells.International journal of molecular sciences · 2026Article
- NADPH acts as an endogenous P2X7 receptor modulator to gate neuroinflammatory responses of microglia.Acta pharmacologica Sinica · 2026Article
- ATP increases murine neuroblastoma cell size through a PANX1- and macropinocytosis-dependent mechanism.Biology open · 2025Article
- Pannexins in the vasculature.American journal of physiology. Heart and circulatory physiology · 2025Review
- Noncanonical function of Pannexin1 promotes cellular senescence and renal fibrosis post-acute kidney injury.Nature communications · 2025Article
- Pannexin1 channels in the liver: an open enemy.Frontiers in cell and developmental biology · 2023Review
- Article
- A Lack of GD3 Synthase Leads to Impaired Renal Expression of Connexins and Pannexin1 inInternational journal of molecular sciences · 2022Article
- Effects of Drugs Formerly Suggested for COVID-19 Repurposing on Pannexin1 Channels.International journal of molecular sciences · 2022Article
- Pannexin1 channels-a potential therapeutic target in inflammation.Frontiers in cell and developmental biology · 2022Review
- Connexin therapeutics: blocking connexin hemichannel pores is distinct from blocking pannexin channels or gap junctions.Neural regeneration research · 2021Review
- A novel motif in the proximal C-terminus of Pannexin 1 regulates cell surface localization.Scientific reports · 2019Article
- Enhanced Macrophage Pannexin 1 Expression and Hemichannel Activation Exacerbates Lethal Experimental Sepsis.Scientific reports · 2019Article
- The weak voltage dependence of pannexin 1 channels can be tuned by N-terminal modifications.The Journal of general physiology · 2018Article
- Therapeutic strategies targeting connexins.Nature reviews. Drug discovery · 2018Review
- Interaction Between Pannexin 1 and Caveolin-1 in Smooth Muscle Can Regulate Blood Pressure.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
- Revisiting multimodal activation and channel properties of Pannexin 1.The Journal of general physiology · 2018Review
- A Germline Variant in the PANX1 Gene Has Reduced Channel Function and Is Associated with Multisystem Dysfunction.The Journal of biological chemistry · 2016Article
- Connexins, Pannexins, and Their Channels in Fibroproliferative Diseases.The Journal of membrane biology · 2016Review
- Chemotherapeutic drugs induce ATP release via caspase-gated pannexin-1 channels and a caspase/pannexin-1-independent mechanism.The Journal of biological chemistry · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Pannexin1 (Panx1) is an integral membrane protein comprised of three species as follows: an unglycosylated core-Gly0, a high mannose-Gly1, and a complex glycosylated Gly2 species. Although Panx1 channels mediate several cellular responses, the domain regulating its oligomerization and cell surface trafficking and the mechanisms governing its internalization and degradation have not been identified. This study characterizes the role of the Panx1 C-tail domain by truncating the polypeptide at residue 307 and expressing the mutant in BICR-M1R(k) and HEK-293T cells. Enzymatic digestion and immunolabeling assays revealed that the Panx1(T307)-RFP was glycosylated primarily to the high mannose species consistent with its retention in the endoplasmic reticulum. Co-expression of Panx1(T307)-RFP with Panx1 followed by co-immunoprecipitation assays revealed that the mutant and Panx1 could interact, whereas biotinylation assays showed that this interaction inhibited Panx1 from maturing into the Gly2 species and reaching the cell surface. Additional inhibitor studies indicated that the degradation of the mutant was via proteasomes, whereas Panx1 was degraded by lysosomes. Analysis of the pathways important in Panx1 internalization revealed partial co-distribution of Panx1 with many molecular constituents of the endocytic machinery that include clathrin, AP2, dynamin II, caveolin-1, and caveolin-2. However, co-immunoprecipitation assays together with the disruption of lipid rafts by methyl-β-cyclodextrin suggest that Panx1 does not engage this endocytic machinery. Furthermore, dominant-negative and pharmacological studies revealed that Panx1 internalization was dynamin II-independent. Collectively, these results indicate that the oligomerization and trafficking of Panx1 are regulated by the C-terminal domain, whereas internalization of long lived Panx1 channels occurs in a manner that is distinct from classical endocytic pathways.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.