| 2000 |
BNC1 (brain Na+ channel 1) is required for normal low-threshold rapidly adapting mechanosensation; BNC1-null mice show markedly reduced sensitivity of rapidly adapting mechanoreceptors in hairy skin. BNC1 protein was localized to lanceolate nerve endings surrounding hair follicles by direct immunolocalization. Acid-evoked currents in sensory neurons and acid-stimulated nociceptor responses were normal in BNC1-null mice (negative result for pH-sensing role). |
Gene knockout (BNC1-null mice), electrophysiology of mechanoreceptors, immunolocalization of channel protein in nerve endings |
Nature |
High |
11069180
|
| 1999 |
BNC1 channel pore structure probed by TEA block: external TEA blocks activated BNC1 (Gly430Val/Thr mutants) in a steeply voltage-dependent manner consistent with multi-ion block within the pore. Mutation Gly430Phe introduced a new TEA binding site ~30% across the electric field, providing structural insight into the channel pore. |
Electrophysiology (patch clamp) with site-directed mutagenesis of pore-lining residue Gly430; quaternary ammonium blockers of varying size |
Biophysical journal |
High |
10049320
|
| 2002 |
BNC1 interacts with the PDZ-domain protein PICK1 via its C-terminus. Yeast two-hybrid and mammalian cell co-expression experiments showed that deletion of the BNC1 C-terminus or mutation of the PICK1 PDZ domain abolished the interaction. Co-expression of PICK1 altered the subcellular distribution of BNC1 channels in a PDZ-domain- and BNC1 C-terminus-dependent manner. |
Yeast two-hybrid assay, co-expression in mammalian cells, C-terminal deletion mutants, PDZ-domain point mutants, subcellular distribution imaging |
The Biochemical journal |
Medium |
11802773
|
| 2011 |
BNC1 (Basonuclin 1) is a direct transcriptional target of p63. Chromatin immunoprecipitation and reporter assays demonstrated that p63 directly binds the BNC1 promoter and induces BNC1 expression, linking p63 to regulation of ribosomal biogenesis and epithelial cell proliferative potential through BNC1. |
Chromatin immunoprecipitation (ChIP), luciferase reporter assay |
European journal of cancer |
Medium |
21741828
|
| 2012 |
BNC1 is required for maintenance of spermatogenesis in mice. Bnc1-null male mice are sub-fertile and show progressive age-dependent loss of germ cells leading to Sertoli-cell-only tubules, declining sperm count and motility. Bnc1 heterozygotes also showed dosage-sensitive reduction in sperm count and testis weight. |
Gene knockout (Bnc1-null mice) and heterozygote analysis; histology, sperm count, fertility assays |
Genesis |
High |
22266914
|
| 2013 |
HSF2BP, a testis-specific protein, binds BNC1 and inhibits its transcriptional activity by sequestering BNC1 to the cytoplasm. Co-expression of HSF2BP with BNC1 caused striking redistribution of BNC1 from nucleus to cytoplasm without affecting BNC1 expression level, identified by yeast two-hybrid screening and confirmed in mammalian cells. |
Yeast two-hybrid screening, co-immunoprecipitation/co-expression in mammalian cells, subcellular localization imaging, transcriptional activity reporter assay |
FEBS letters |
Medium |
23707421
|
| 2015 |
RNAi-mediated knockdown of BNC1 in breast cancer cell lines resulted in a significant increase in migratory and invasive potential, indicating BNC1 suppresses cell migration and invasion. |
RNAi knockdown in breast cancer cell lines, migration and invasion assays |
Clinical epigenetics |
Low |
26052355
|
| 2019 |
BNC1 regulates cell heterogeneity in human pluripotent stem cell-derived epicardium. Single-cell RNA sequencing revealed that BNC1-high and TCF21-high epicardial subpopulations define distinct cell fates; knockdown of BNC1 during epicardial establishment resulted in a homogeneous TCF21-high population, demonstrating BNC1 is required for maintaining epicardial cell heterogeneity and fate specification. |
Single-cell RNA sequencing of hPSC-derived epicardium, RNAi knockdown of BNC1, differentiation assays into cardiac fibroblasts and smooth muscle cells |
Development |
Medium |
31767620
|
| 2020 |
BNC1 directly binds the promoters of spermatogenesis genes Klhl10, Tex14, and Spatc1 in mouse testis (by ChIP-seq). BNC1 physically associates with the germ cell-specific transcription factor TAF7L both in vitro and in testis (by biochemical analysis). A BNC1 truncation mutation disabled nuclear translocation of the BNC1/TAF7L complex, thereby disrupting spermatogenesis-specific gene expression and causing testicular premature aging. |
Chromatin immunoprecipitation sequencing (ChIP-seq), co-immunoprecipitation (in vitro and in testis), genome-wide expression profiling, mouse truncation mutation model |
Journal of molecular cell biology |
High |
31065688
|
| 2020 |
BNC1 directly binds BNC1-binding elements in the promoter regions of Ybx2 and Papolb to induce their transcription, promoting spermatogenesis. Confirmed by ChIP of mouse testicular tissue and luciferase reporter assays. Loss of BNC1 led to germ cell apoptosis and decreased YBX2 and PAPOLB protein levels. |
Chromatin immunoprecipitation (ChIP) of mouse testicular tissue, luciferase reporter assay in HEK293 cells, Bnc1 knockdown in CRL-2196 cells, mouse truncation mutation model |
Reproductive sciences |
Medium |
33211273
|
| 2022 |
BNC1 deficiency in oocytes triggers ferroptosis via the NF2-YAP pathway, causing premature follicular activation and excessive follicular atresia leading to primary ovarian insufficiency (POI). Pharmacologic inhibition of YAP signaling or ferroptosis significantly rescued the POI phenotype in Bnc1-mutant mice. |
Targeted Bnc1 mutation mouse model, pharmacologic rescue experiments (YAP inhibitor, ferroptosis inhibitor), lipid metabolism and redox homeostasis assays in oocytes |
Nature communications |
High |
36198708
|
| 2024 |
BNC1 deficiency in spermatogonia causes mitochondrial dysfunction (lower mitochondrial membrane potential, higher ROS) and apoptosis via downregulation of the CREB/SIRT1/FOXO3 signaling pathway. Nicotinamide riboside or metformin reversed mitochondrial dysfunction and inhibited apoptosis in Bnc1-knockdown spermatogonia by stimulating CREB/SIRT1/FOXO3 signaling. |
Bnc1 truncation mutation mouse model, Bnc1 knockdown in spermatogonia, mitochondrial membrane potential assay, ROS measurement, pharmacologic rescue (nicotinamide riboside, metformin), CREB/SIRT1/FOXO3 pathway analysis |
Biology of reproduction |
Medium |
38079523
|
| 2023 |
BNC1 physically interacts with PRMT1 (protein arginine methyltransferase 1) to co-activate proliferative/cell-cycle gene programs in squamous cell carcinoma (SCC). ChIP-seq identified direct BNC1 transcriptional targets; BNC1 inhibition suppressed proliferation and increased migration via FRA1, while also repressing IRF6-dependent differentiation. PRMT1 inhibition selectively blocked BNC1-dependent proliferative gene activation without affecting BNC1's repression of promigratory genes. |
RNA-seq, ChIP-seq, protein interactome analysis, RNAi knockdown, PRMT1 inhibitor treatment in SCC xenografts |
bioRxiv (preprint)preprint |
Medium |
37034732
|
| 2025 |
BNC1 physically interacts with PRMT1 to activate cell cycle genes in SCC. BNC1 activates proliferation genes while repressing a FRA1-dependent promigratory program and an IRF6-dependent differentiation program, thus controlling the proliferation-differentiation-migration axis in squamous epithelium. PRMT1 inhibition blocks proliferative gene activation without affecting repression of promigratory genes. |
RNA-seq, ChIP-seq, physical interaction assays, PRMT1 inhibitor treatment, SCC xenograft experiments |
The Journal of investigative dermatology |
Medium |
40962202
|
| 2025 |
HSF2BP directly binds to BNC1 (C-terminal hydrophobic domain essential), suppressing BNC1 transcriptional activity and leading to reduced activation of TGF-β/SMAD3 signaling in lung adenocarcinoma cells. Co-immunoprecipitation confirmed the physical interaction; overexpression and knockdown experiments in LUAD cell lines and in vivo mouse models established the HSF2BP→BNC1→TGF-β/SMAD3 regulatory axis. |
Co-immunoprecipitation, lentiviral overexpression/knockdown in LUAD cell lines, in vivo subcutaneous tumorigenesis in mice, RT-qPCR, Western blot, flow cytometry, ELISA |
Scientific reports |
Medium |
41083582
|
| 2025 |
BNC1 suppresses CCL20 expression by directly binding to the CCL20 promoter, thereby reducing JAK-STAT signaling activation and promoting apoptosis in gastric cancer cells. Overexpression of BNC1 inhibited proliferation, migration, and invasion both in vitro and in vivo. |
Transcriptome sequencing, promoter-binding assays, overexpression/knockdown in gastric cancer cell lines, in vivo mouse model |
PeerJ |
Low |
40444282
|
| 2024 |
BNC1 reduces glioma cell proliferation and enhances ferroptosis through the TCF21/PI3K signaling pathway. BNC1 protein was shown to interact with TCF21 protein; BNC1 enhanced TCF21 expression in vivo (bioluminescence imaging). SiTCF21 or enhanced TCF21 expression both declined BNC1-mediated ferroptosis effects, placing BNC1 upstream of TCF21 in this pathway. |
Cell proliferation assays, ferroptosis assays, co-immunoprecipitation (BNC1-TCF21 interaction), siRNA knockdown of TCF21, bioluminescence imaging in mouse glioma model, ferroptosis inhibitor/agonist pharmacology |
Tissue & cell |
Low |
39603023
|