
-   Administration of human umbilical cord mesenchymal stem cell (HucMSC)-derived exosome reduced inflammation and ferroptosis following traumatic brain injury (TBI) by activating the long non-coding RNA (lncRNA) TUBB6/nuclear factor erythroid 2-related factor 2 (Nrf2) pathway. Knockdown of TUBB6 resulted in a partial failure of exosome-mediated neuroprotection post-TBI, suggesting TUBB6's involvement in inflammatory and ferroptotic processes [PMID: 38030103].
-   In the mdx mouse model of Duchenne muscular dystrophy, it was observed that the gene expression of beta-tubulin tubb6 is elevated as compared to wild-type. The overexpression of tubb6 in wild-type fibers reproduces the microtubule and Golgi element (GE) alterations seen in mdx muscle, indicating a role for tubb6 in the disorganization observed in dystrophic muscle. This suggests a model where GE mispositioning and lack of dystrophin-driven microtubule guidance contribute to the pathophysiology of Duchenne muscular dystrophy [PMID: 31620435].
-   Sea buckthorn sterol (SBS) increased the Tubb6 gene expression in a rat model of acute liver injury induced by carbon tetrachloride (CCl4). The increase of TUBB6 expression probably related to the decrease in the TNF-alpha level caused by SBS. In the liver tissues of these rats, Tubb6 expression was regulated by SBS as part of a response that included both mitigation of metabolic damage and anti-lipid peroxidation effects. The protective mechanism against liver injury involved the inhibition of inflammation and the restoration of expression in metabolic pathways [PMID: 35408620].

## Summary

TUBB6, encoding beta-tubulin isotype 6, is a component of microtubules critical for maintaining cytoskeleton structure, intracellular transport, and cellular division processes. Upregulation of TUBB6 in liver tissue can occur in response to toxic injuries, such as hepatocarcinogenesis induced by hepatitis B virus or CCl4-induced acute liver injury, which are conditions associated with cellular stress and damage. The elevated Tubb6 expression assists in reinforcing the microtubule network, supporting cellular organization and ensuring proper intracellular trafficking, which is particularly important in hepatocytes given their metabolic and detoxification roles.

Dysregulation of Tubb6 in liver diseases and toxicities, such as hepatocarcinogenesis and acute liver injury, potentially corresponds to the cell's need to adapt to stress or injury. In the context of an acute liver injury induced by carbon tetrachloride (CCl4), the induced expression of Tubb6 may aid in the restructuring of damaged cytoskeleton, thus promoting cell survival and recovery in hepatocytes. Increased levels of TUBB6 can counteract the cytoskeleton disorganization caused by toxic insults, thereby restoring cellular integrity and facilitating repair mechanisms. Upregulation of Tubb6 in the liver tissue of transgenic mice, which serves as a model for hepatitis B virus-induced hepatocarcinogenesis, could be related to a compensatory response where enhanced beta-tubulin isotype expression is needed for increased cellular turnover and the maintenance of cytoskeletal integrity in the face of viral-induced damage and cellular transformation processes.
