SEPTIN7 (Septin 7)

Immunohistochemical analysis did not uncover astrocyte or microglial activation, implying that myelin outfoldings per se do not induce secondary neuropathology. Together, our data reveal a critical function for CDC42 and CDC42EP1/CDC42EP2 in regulating myelin septin filaments, which facilitate structural integrity of myelin sheaths.

This review summarizes the current knowledge about the role of SEPT2 in tumors and supports its potential as a biomarker for certain types of tumors. After in-depth analysis, it provides new perspectives for oncology.

In addition, PFD attenuates the interaction of septin7-tubulin, thereby inhibiting microtubule polymerization. In summary, this study revealed a target and mechanistic insights into EC therapeutic strategies and identified a potential candidate agent for the treatment of EC.

Furthermore, we have demonstrated that decreased MYO6 protein leads to reduced expression of GIPC1, SEPT2, and SEPT7 in breast cancer cells. These findings contribute to a more comprehensive understanding of the pathways influencing breast cancer cell migration, a critical aspect of metastasis.

We genetically edited human natural killer cell line (NK92) and mouse primary CD8+ T-cells expressing the engineered protein, and we demonstrated improved penetration and cytotoxicity against various tumor spheroid models. Our proposed strategy to enhance immune cell infiltration is compatible with other methodologies and therefore, could be used in combination to further improve cell-based immunotherapies against solid tumors.

Western blotting confirmed biotinylation and enrichment of FAK and vinculin, known interactors of Hic-5 and paxillin, as well as several potentially unique proximity interactors of Hic-5 and paxillin, including septin 7 and ponsin, respectively. Further investigation into the functional relationship between the unique interactors and Hic-5 or paxillin may yield novel insights into their distinct roles in cell migration.

Our aim was to evaluate the association between serum calretinin concentration or genetic factors and the survival or outcome of cisplatin-based chemotherapy in MM...MIR335 rs3807348 was associated with a better response to chemotherapy (OR = 2.69 (1.17-6.18), p = 0.020). We showed that serum calretinin is associated with survival and chemotherapy treatment outcomes in MM and could serve as a predictive biomarker.

The results of presented study suggest that genetic variability could influence serum calretinin levels. These findings could contribute to a better understanding of calretinin regulation and potentially to earlier MM diagnosis.

Differential transcriptomic analysis between the low-risk/nevus group and 5 reference BRAF V600E atypical nevi shows comparable mRNA profiles, with similar BRAF transcript levels across different exons. The findings may suggest the BRAF fusions act through alteration of protein function, rather than RNA upregulation. Our study further expands the growing literature on this class of melanocytic tumors, demonstrates novel fusion partners, and provides novel insight on the transcriptomic level.

Septin-3 is a novel autoantibody target in patients with paraneoplastic cerebellar syndromes. Based on our findings, RC-IIFA with HEK293 cells expressing the septin-3/5/6/7/11 complex may serve as a screening tool to investigate anti-septin autoantibodies in serological samples with a characteristic staining pattern on neuronal tissue sections. Autoantibodies against individual septins can then be confirmed by RC-IIFA expressing single septins.

The fusion genes associated with HPV infection might explain biological disparities in HPV+ versus HPV- HNSCC and may be targets for the prevention and diagnosis of HNSCC. Future studies need to determine the functional impact of the identified fusion genes in HPV+ tumors.

Notably, we did not find evidence that deleting Septin2 or Septin9 in Schwann cells impairs myelin biogenesis, nerve conduction velocity or motor/sensory capabilities, at least at the assessed timepoints. Our data thus show that SEPTIN2 but not SEPTIN9 is required for the formation or stabilization of a septin multimer in PNS myelin in vivo; however, its functional relevance remains to be established.