NALCN (Sodium Leak Channel, Non-Selective)

Furthermore, immunohistochemical staining showed consistent protein-level changes in MMP11 and PYGL. These results illuminate the potential for a transcriptomic biomarker to differentiate benign from malignant melanocytic neoplasms and improve the accuracy of melanoma diagnosis.

Genetic elimination of either HNRNP L, the Nalf1 CARE motif, or the pore-forming subunit of the nonselective NALCN diminishes pain amplification in vivo. Collectively, these results illustrate that an element situated in a 3'UTR is required for neuropathic pain in female mice.

A coculture system of primary rat oligodendrocytes and neurons revealed that the mutant AR in oligodendrocytes affected the activity and synchronization of neurons. These findings suggest that dysregulated cell-to-cell communication plays a critical role in early SBMA pathology and that synaptic or ion channel-related proteins, such as contactin associated protein 2 (Cntnap2) and NALCN channel auxiliary factor 1 (Fam155a), are potential therapeutic targets for SBMA.

Genetic elimination of either HNRNP L, the Nalf1 CARE motif, or the pore-forming subunit of the nonselective NALCN diminishes pain amplification in vivo. Collectively, these results illustrate that an element situated in a 3'UTR is required for neuropathic pain in female mice.

Moreover, NALCN may play a role in glucose and glutamine uptake. NALCN facilitates immune cell aggregation in GC and has potential as a biomarker for immune infiltration.

This study identified novel genomic signatures that may improve risk stratification in early-stage node-negative CC, potentially guiding the selection of high-risk patients for adjuvant therapy.

In this first GWAS exploring propofol requirements, we discovered novel genetic associations suggesting new biologically relevant pathways for propofol and general anesthesia. The roles of the gene products of ROBO3/FEZ1, NALCN and KCNJ2 in propofol anesthesia warrant further studies.

Here, we provide FGFR4, NALCN, and NAV2 as novel high-risk candidate genes for familial endometriosis. Our results also support the association of endometriosis with high-grade serous carcinoma. Further studies are required to validate the findings and to reveal the exact pathogenesis mechanisms of endometriosis. Elucidating the genetic background of endometriosis defines the etiology of the disease and provides opportunities for expedited diagnostics and personalized treatments.

Recent work by Folcher et al (2023) reports a critical role for Na leak channel NALCN in metastatic prostate cancer. The study demonstrates that NALCN promotes metastatic spread to distant organs by controlling Ca signaling.

This signaling cascade promotes activity of the NACLN-colocalized proto-oncogene Src kinase, actin remodeling and secretion of proteolytic enzymes, thus increasing cancer cell invasive potential and metastatic lesions in vivo. Overall, our findings provide new insights into an ion signaling pathway specific for metastatic cells where NALCN acts as persistent invasion controller.