Stradb is a gene whose functions are being explored through various research. While specific essential functions, common aliases, and associated pathways aren't clearly detailed in the provided references, its role in multiple biological contexts is emerging. It may be involved in pathways related to drug-induced toxicity, stress responses, and cell-function regulation, highlighting its overall biological importance in understanding physiological and pathological processes [1,2].

In HepG2 cells treated with high concentrations of clopidogrel, the target mRNA STRADB was downregulated, suggesting its involvement in clopidogrel-induced hepatotoxicity as miR-26a-5p, which targets STRADB, was also modulated [1]. In a study on acute psychological stress in healthy women, STRADB was among the genes downregulated in the experimental group experiencing stress induction compared to the control group [2]. In primary lung fibroblasts, STRADB was identified as a target gene of miR-455-3p, which was induced by TGF-β1, indicating its potential role in lung-related functions and diseases [3]. In ovarian cancer cells treated with disodium pentaborate decahydrate, STRADB was downregulated, suggesting its possible connection to the anti-cancer properties of this compound through the PI3K/AKT/mTOR pathway [4].

In conclusion, STRADB seems to be involved in processes related to drug-induced hepatotoxicity, psychological stress responses, lung-fibroblast function, and ovarian cancer cell regulation. Although no KO/CKO mouse model-based findings were in the references, these studies on cell lines and human samples indicate that STRADB may play a significant role in these disease-associated biological processes, and further functional studies, potentially including gene-knockout models, could help to clarify its exact functions and implications in these areas.