M3K13 ELISA Kit

c-Myc (Myc) is one of the most frequently dysregulated oncogenic transcription factors in human cancer. By functionally screening a microRNA (miR) library, we identified miR-206 as being a synthetic lethal in Myc over-expressing human cancer cells. miR-206 inhibited MAP3K13, which resulted in Myc protein de-stabilization, and an inhibition of anchorage-independent growth and in vivo tumorigenesis by Myc over-expressing human cancer cells. Eliminating MAP3K13 by shRNA recapitulated the effects caused by miR-206, thus supporting the idea that miR-206's effect on Myc was mediated through MAP3K13. Conversely, enforced expression of MAP3K13 stabilized Myc by promoting its N-terminal phosphorylation and enhancing its transcriptional activity. Gene expression analyses of breast cancers expressing high levels of Myc indicated that low miR-206 expression and high MAP3K13 expression correlated with poor patient survival. The critical link between miR-206 and MAP3K13 in the development of Myc over-expressing human cancers suggests potential points of therapeutic intervention for this molecular sub-category.

Dehong humped cattle (DHH) is an indigenous zebu breed from southwestern China that possesses characteristics of heat tolerance and strong disease resistance and adapts well to the local tropical and subtropical climatic conditions. However, information on selection signatures of DHH is scarce. Herein, we compared the genomes of DHH and each of Diqing and Zhaotong cattle breeds using the population differentiation index (F-ST), cross-population extended haplotype homozygosity (XP-EHH) and cross-population composite likelihood ratio (XP-CLR) methods to explore the genomic signatures of heat tolerance and disease resistance in DHH. Several pathways and genes carried selection signatures, including thermal sweating (calcium signaling pathway), heat shock (HSF1) and oxidative stress response (PLCB1, PLCB4), coat color (RAB31), feed intake (ATP8A1, SHC3) and reproduction (TP63, MAP3K13, PTPN4, PPP3CC, ADAMTSL1, SS18L1, OSBPL2, TOX, RREB1, GRK2). These identified pathways and genes may contribute to heat tolerance in DHH. Simultaneously, we also identified LIPH, TP63 and CBFA2T3 genes under positive selection that were associated with immunity.