ArticleThe Journal of biological chemistry2018
The ubiquitin-specific protease USP8 deubiquitinates and stabilizes Cx43.
Article in The Journal of biological chemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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
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Who cites it
19 citing papers in PubMed, 35 citations in OpenAlex.
- Systemic and cardiac pathology induced by a clinically relevant USP8 activating mutation.Disease models & mechanisms · 2026Article
- Spatiotemporal recruitment of the ubiquitin-specific protease USP8 directs endosome maturation.eLife · 2024Article
- The roles of connexins and gap junctions in the progression of cancer.Cell communication and signaling : CCS · 2023Review
- Molecular mechanism of lncRNA SNHG12 in immune escape of non-small cell lung cancer through the HuR/PD-L1/USP8 axis.Cellular & molecular biology letters · 2022Article
- Usp8 promotes tumor cell migration through activating the JNK pathway.Cell death & disease · 2022Article
- Knockdown of USP8 inhibits prostate cancer cell growth, proliferation, and metastasis and promotes docetaxel's activity by suppressing the NF-kB signaling pathway.Frontiers in oncology · 2022Article
- METTL3 Regulates Ossification of the Posterior Longitudinal Ligament via the lncRNA XIST/miR-302a-3p/USP8 Axis.Frontiers in cell and developmental biology · 2021Article
- Depleting deubiquitinating enzymes promotes apoptosis in glioma cell line via RNA binding proteins SF2/ASF1.Biochemistry and biophysics reports · 2020Article
- Myocardial infarction affects Cx43 content of extracellular vesicles secreted by cardiomyocytes.Life science alliance · 2020Article
- Antagonistic Functions of Connexin 43 during the Development of Primary or Secondary Bone Tumors.Biomolecules · 2020Review
- The ubiquitin-specific protease USP8 directly deubiquitinates SQSTM1/p62 to suppress its autophagic activity.Autophagy · 2020Article
- Regulation of gap junction intercellular communication by connexin ubiquitination: physiological and pathophysiological implications.Cellular and molecular life sciences : CMLS · 2020Review
- Down-Regulation of USP8 Suppresses HER-3 Positive Gastric Cancer Cells Proliferation.OncoTargets and therapy · 2020Article
- Down-regulation of USP8 Inhibits Cholangiocarcinoma Cell Proliferation and Invasion.Cancer management and research · 2020Article
- Ubiquitin-specific protease 8 (USP8/UBPy): a prototypic multidomain deubiquitinating enzyme with pleiotropic functions.Biochemical Society transactions · 2019Review
- Two de novo GJA1 mutation in two sporadic patients with erythrokeratodermia variabilis et progressiva.Molecular genetics & genomic medicine · 2019Article
- Inhibition of USP2 eliminates cancer stem cells and enhances TNBC responsiveness to chemotherapy.Cell death & disease · 2019Article
- Review
- Protein⁻Protein Interactions with Connexin 43: Regulation and Function.International journal of molecular sciences · 2018Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Connexin-43 (Cx43, also known as GJA1) is the most ubiquitously expressed connexin isoform in mammalian tissues. It forms intercellular gap junction (GJ) channels, enabling adjacent cells to communicate both electrically and metabolically. Cx43 is a short-lived protein which can be quickly degraded by the ubiquitin-dependent proteasomal, endolysosomal, and autophagosomal pathways. Here, we report that the ubiquitin-specific peptidase 8 (USP8) interacts with and deubiquitinates Cx43. USP8 reduces both multiple monoubiquitination and polyubiquitination of Cx43 to prevent autophagy-mediated degradation. Consistently, knockdown of
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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.