Mouse Anti Human Creatine Kinase Hybridoma [DL-BSU]

Back-round: We encountered 2 patients with increased activities of the creatine kinase (CK)-BB isoenzyme in their sera. Here we examined the relation among CK-BB activity, expression of CKB mRNA in peripheral blood, and hypermethylation of the CKB. Methods: The 2 patients and other 26 patients with hematologic malignancies, and some cancer cell lines were subjected to measurement of serum CK activity, CK isoenzyme analysis, CKB mRNA expression analysis by RT-PCR, and methylation analysis of the CKB promoter region. Results: CK-BB activity and proportion of leukemia blasts were correlated in the 2 patients. CKB mRNA was increased in peripheral blood during an increase in leukemia blast numbers. In contrast, none of the other 26 patients showed CK-BB activity or expression of CKB mRNA. In all of the patients with hematologic disorders, the analyzed region of CKB promoter was mostly unmethylated. However, some of cancer cell lines showed the methylated pattern. CKB mRNA was expressed at higher levels in cells with an unmethylated CKB promoter than in cells with a methylated promoter. Conclusions: Expression of CKB mRNA and CK-B sometimes occurred in blastic transformation of the hematopoietic system. A relation between CKB mRNA expression and methylation of the CKB promoter was suggested. (c) 2005 Elsevier B.V. All rights reserved.

Brain creatine kinase (CKB) has a central role in the regeneration of ATP in the brain. During postnatal development of rat brain cerebrum, the CKB protein level was very low at postnatal day 1 and week 1 but by week 4 had increased 6- to 7-fold and remained constant through week 10. Surprisingly, CKB mRNA levels were already maximal at postnatal day 1 and week 1, indicating that CKB protein expression does not simply reflect the levels of CKB mRNA and is likely regulated posttranscriptionally during early postnatal times. Interestingly, the majority of cytoplasmic CKB mRNA was found to be associated with polyribosomes both at postnatal day 3 and week 6. Therefore, low CKB protein levels at early postnatal times could either be due to (1) normal translation initiation of CKB mRNA followed by a subsequent arrest during elongation or termination and/or (2) normal translation of CKB mRNA followed by rapid degradation of CKB protein. However, CKB protein increased coincidently with ubiquitous mitochondrial CK protein, suggesting that a functional phosphocreatine energy shuttle is formed in the cerebrum during postnatal development. The apparent posttranscriptional regulation of CKB in early postnatal cerebrum contrasts with the transcriptional regulation controlling accumulation of CKB protein in postnatal developing cerebellum. Copyright (C) 2003 S. Karger AG, Basel.