ANK2 (Ankyrin 2)

Notably, we highlight the potential regulatory role of ANK2 in the progression of CRC. This research provides theoretical support and new directions for early screening, diagnostic biomarker identification, and targeted therapy strategies for CRC.

These findings suggest that SHANK2 plays a crucial role in tumor malignant potential through the Hippo pathway suppression and highlight its usefulness as a prognostic factor and potential therapeutic target in GC.

KANK2 serves as a valuable biomarker for diagnosis and prognosis in various cancers, and its expression is intricately linked to multiple molecular and cellular processes, offering potential therapeutic targets for future research.

Our data suggest that the cholesterol synthetic flow and CoA content may be limited in statin-sensitive cancer cells. We also suggest that CoA synthesis and cholesterol storage may fluctuate with atorvastatin treatment in statin-sensitive cancer cells.

The study also introduces a multivariate prognostic model incorporating SHANK2, providing a novel perspective on glioma prognosis. While the retrospective nature of the study presents limitations, our results suggest that SHANK2 expression could serve as a valuable biomarker for glioma prognosis and inform future therapeutic strategies.

BBP-671 crosses the blood brain barrier to correct the neuron-specific CoA deficiency and improve motor function in a mouse model of pantothenate kinase associated neurodegeneration. The central role of CoA and acetyl-CoA in intermediary metabolism suggests that pantothenate kinase activators may be useful in modifying neurological metabolic disorders.

Significant differences exist in overall gene expression between the thyroid tissues of patients with PTC and those of healthy people. Furthermore, the differential genes ANK2, TLE1, and TCF4 are expected to be reliable molecular markers for the mechanism study and diagnosis of PTC.

Therefore, our findings indicate that Prickle ensures neuron-glial interaction within neuropils through regulating cell adhesion between neurons and ensheathing glia. Dysregulation of this process may represent a conserved pathogenic mechanism underlying PRICKLE1-associated epilepsy.