Anti-CSNK2A1 monoclonal antibody

A bovine bacterial artificial chromosome (BAC) library was screened for the prescence of six genes (IL2RA, VIM, THBD, PLC-II, CSNK2A1 and TOP1) previously assigned to human chromosomes 10 or 20 (HSA10 or HSA20). Four of the genes were found represented in the bovine BAC library by at least one clone. The identified BAC clones were used as probes in single-color fluorescence in-situ hybridization (FISH) to determine the chromosomal band location of each gene. As predicted by the human/bovine comparative map and comparative chromosome painting analysis, the four genes mapped to bovine chromosome 13 (BTA13). Dual-color FISH was then used to integrate these four type I markers into the existing BTA13 genome map. These FISH results anchor the BTA13 genome map from bands 14-23, and confirm the presence of a conserved HSA10 homologous synteny group on BTA13 centromeric to a HSA20 homologous segment.

Postmenopausal osteoporosis (PMOP), as well as its associated increased risk for fragility fracture, is one of the most disabling consequences of aging in women. This present study aimed to identify candidate genes that involve pathogenesis of PMOP and the therapeutic mechanism of Liuweidihuang (LWDH) pills on PMOP. We integrated microarray datasets of PMOP derived from the Gene Expression Omnibus (GEO) to screen differentially expressed genes (DEGs) between PMOP and normal controls as well as patients with PMOP and patients after treatment of LWDH pills. GO and KEGG enrichment analysis for DEGs were performed. The shared DEGs, associated with both the pathogenesis of PMOP and the therapeutic mechanism of LWDH, were further analyzed by protein-protein interaction (PPI) network. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to verify the DEGs obtained by our integrated analysis. Compared with normal controls, 1732 DEGs in PMOP were obtained with p<0.05. According to the qRT-PCR results, expression of ATF2, FBXW7, RDX, and RBBP4 was consistent with that in our integrated analysis, generally. GO and KEGG enrichment analysis showed that those DEGs were significantly enriched in regulation of transcription, DNA-dependent, cytoplasm, protein binding, and MAPK signaling pathway. A total of 58 shared DEGs in PMOP versus normal control and in patients with PMOP versus patients after LWDH treatment were identified, which had opposite expression trend in these two comparisons. In the PPI network, CSNK2A1, ATF2, and FBXW7 were three hub proteins. Three genes including ATF2, FBXW7, and RDX were speculated to be therapeutic targets of LWDH for PMOP based on BATMAN-TCM database. We speculated that three genes of ATF2, FBXW7, and RDX may play crucial roles in both pathogenesis of PMOP and therapeutic mechanism of LWDH on PMOP. Our results may provide clues for the molecular pathogenesis of PMOP and offer new possibilities for treatment of PMOP.