Fig. 5
- ID
- ZDB-FIG-250227-12
- Publication
- Deebani et al., 2025 - Knockdown of zebrafish tmem242 enhances the production of ROS that signals to increase f9a expression resulting in DIC-like condition
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Tmem242 role in hemostasis. The model elucidates the regulatory mechanism by which Tmem242 modulates the expression of the coagulation factor gene, f9a. The schematic drawing portrays the physiological state in the presence of Tmem242 (a) compared with the consequences of tmem242 knockdown (b). Upon Tmem242 depletion, inhibition of ATP synthase activity occurs, culminating in increased ROS production. Subsequently, the heightened ROS levels induce upregulation of sirt6 expression, which in turn, promotes increased expression of nrf2, which in this study was found to be an activator for f9a transcription. Consequently, elevated levels of f9a mRNA results in increased F9a protein production, which along with the other coagulation factors contributes to the observation of abnormal hemostatic function resembling the characteristics of DIC pathology. |