Csnk2b, encoding a regulatory subunit of casein kinase 2, is involved in multiple biological processes. It modulates the transcriptional activity of interferon regulatory factor 1 (IRF1), enhancing the binding of IRF1 to chromatin for the transcription of key antiviral genes, and also affects AFAP1 transcription [2]. It is also associated with the ATF6 signaling pathway in intestinal epithelial cells during endoplasmic reticulum stress [5].

Csnk2b variants are linked to neurodevelopmental disability (NDD) and epilepsy. Most individuals with Csnk2b variants have developmental delay and generalized epilepsy within the first 2 years, but there is a broad spectrum of phenotypic severity, from early normal development with pharmacoresponsive seizures to profound intellectual disability with intractable epilepsy [1]. Heterozygous pathogenic variants in Csnk2b are associated with Poirier-Bienvenu neurodevelopmental syndrome (POBINDS), characterized by facial dysmorphisms, seizures, intellectual disability, and behavioral disturbances [4]. In addition, CSNK2B is highly expressed in colorectal cancer tissues and promotes CRC cell viability and tumorigenesis by activating the mTOR signaling pathway [3]. In hepatocellular carcinoma, miR-1205 suppresses cell proliferation by directly targeting CSNK2B [6].

In conclusion, Csnk2b plays essential roles in regulating antiviral responses, endoplasmic reticulum stress-related inflammation, and is significantly associated with neurodevelopmental disorders and certain cancers. Understanding its functions through various studies helps to better comprehend the underlying biological mechanisms and provides potential targets for related disease treatment.