https://www.selleckchem.com/pr....oducts/acalabrutinib
Mechanistically, MKL1 interacted with NF-κB to activate miR-155 transcription in macrophages. In conclusion, our data suggest that MKL1 may contribute to pathological hypertrophy via regulating macrophage-derived miR-155 transcription.Cervical cancer is the fourth most prevalent cancer in women, which decreases quality of life of the patients. Traditional interventions have failed to improve the overall survival period of patients due to high tumor recurrence after treatment or late diagnosis. Fortunately, preliminary evidence sug
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