Casein kinase I delta (CKIδ) is involved in lymphocyte physiology

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Summary

The casein kinase I isoform delta (CKIδ) plays an important role in vesicular trafficking, chromosome segregation, cell cycle progression, cytokinesis, developmental processes, and circadian rhythm. In this study we examined the distribution pattern of CKIδ and quantified its kinase activity in various tissues of BALB/c mice. Whereas CKIδ is ubiquitously expressed, differences in the kinase activity were detected in organs with comparable CKIδ protein levels. To elucidate the role of CKIδ in splenocytes, which displayed the highest kinase activity, the cell type-specific distribution of CKIδ within the spleen was investigated. Immunohistochemical analysis revealed a strong CKIδ immunolabeling in lymphoid cells of the white pulp, while in the red pulp CKIδ immunoreactivity was found in cells of various haematopoietic lineages. Furthermore, high CKIδ kinase acitivity was observed in isolated lymphocytes and granulocytes of young BALB/c mice. In lymphocytes the CKIδ activity increased upon mitogenic stimulation, whereas upon γ-irradiation CKIδ protein and activity levels were diminished. Interestingly, the comparison of CKIδ activity in p53+/+ and p53−/− lymphocytes revealed a higher activity in p53+/+ lymphocytes. In addition, we observed an increased immunostaining in cells of hyperplastic B follicles and advanced B-cell lymphomas in p53-deficient mice. Thus, our results indicate that CKIδ plays several roles in lymphocyte physiology.

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Cited by (27)

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    The function of CK1δ in lymphoid neoplasms was first described using a mouse model leading to the observation that the expression level of CK1δ is increased in cells of hyperplastic B follicles and advanced B cell lymphomas in p53-deficient mice. Later, CK1δ mRNA and protein levels were also analyzed in 18 lymphoma cell lines and strong expression of CK1δ could be found in all analyzed cell lines (Maritzen et al., 2003; Winkler et al., 2015). Interestingly, in some other studies low expression of CK1δ in cancer tissues has also been described (Fig. 8 and Table 5).

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    The mechanism by which p53 up-regulates CK1δ is not clear, and it may function at either the transcriptional level or the post-transcriptional level [28]. In agreement with CK1δ activity being reduced in p53 −/− lymphocytes [21], p53 and CK1δ might regulate each other with a positive relationship [28]. On the clinical side, spinal nerve injury decreased CK1ε mRNA (with 2.8-fold reduction) and protein levels in the spinal cord of the neuropathic pain-resistant N-type Ca2 + channel deficient mice, while CK1ε protein expression (but not messenger levels) was up-regulated in the dorsal root ganglion and spinal cord neurons in wild type mice [82].

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