ArticleCells2023
The Src-Family Kinases SRC and BLK Contribute to the CLDN6-Adhesion Signaling.
Article in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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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.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Stage-Dependent Transcriptional Reprogramming of B-Cell Receptor Signaling and Antigen Presentation During Bovine Leukemia Virus-Driven Lymphomagenesis.Animal genetics · 2026Article
- A Novel Tight Junction-Nuclear Receptor Signaling Pathway Regulating Cancer Progression.Pathology international · 2025Review
- PEAK1 maintains tight junctions in intestinal epithelial cells and resists colitis by inhibiting autophagy-mediated ZO-1 degradation.Nature communications · 2025Article
- The phenotypic and genetic association between endometriosis and immunological diseases.Human reproduction (Oxford, England) · 2025Article
- Extrajunctional CLDN10 cooperates with LAT1 and accelerates clear cell renal cell carcinoma progression.Cell communication and signaling : CCS · 2024Article
- Claudins: from gatekeepers of epithelial integrity to potential targets in hepato-pancreato-biliary cancers.Frontiers in oncology · 2024Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell adhesion molecules, including integrins, cadherins, and claudins (CLDNs), are known to activate Src-family kinases (SFKs) that organize a variety of physiological and pathological processes; however, the underlying molecular basis remains unclear. Here, we identify the SFK members that are coupled with the CLDN6-adhesion signaling. Among SFK subtypes, BLK, FGR, HCK, and SRC were highly expressed in F9 cells and concentrated with CLDN6 along cell borders during epithelial differentiation. Immunoprecipitation assay showed that BLK and SRC, but not FGR or HCK, form a complex with CLDN6 via the C-terminal cytoplasmic domain. We also demonstrated, by pull-down assay, that recombinant BLK and SRC proteins directly bind to the C-terminal cytoplasmic domain of CLDN6 (CLDN6C). Unexpectedly, both recombinant SFK proteins recognized the CLDN6C peptide in a phosphotyrosine-independent manner. Furthermore, by comparing phenotypes of F9:
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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.