Anti-Cdk2 (C-terminal) polyclonal antibody

Simple summary In this study, RNA-Seq data between liver tissues of Hanhyup chicken maintained in Korea and Kyrgyzstan was compared. We then investigated the candidate genes involved in response to environmental changes such as altitude, humidity, temperature etc. We found that 315 genes were differentially expressed genes (DEGs) in the Kyrgyz environment, out of which 174 and 141 were up- and down-regulated respectively. GO and KEGG pathway enriched between the two climatic conditions have been investigated. The identified candidate DEGs and enriched pathways may involve in the acclimatization of Hanhyup chicken to the Kyrgyz environment. Abstract RNA sequencing was used to profile the liver transcriptome of a Korean commercial chicken (Hanhyup) at two different environments (Korea and Kyrgyzstan) to investigate their role during acclimatization into different climatic conditions. Ten samples from each location were analyzed to identify candidate genes that respond to environmental changes such as altitude, humidity, temperature, etc. Sequencing reads were preprocessed, aligned with the reference genome, assembled and expressions were estimated through bioinformatics approaches. At a false discovery rate (FDR) <0.05 and fold change (FC) >= 2, we found 315 genes were DE. Out of 315 DE genes, 174 and 141 were up- and down-regulated respectively in the Kyrgyz environment. Gene ontology (GO) enrichment analysis showed that the differentially expressed genes (DEGs) were associated with energy metabolism such as pyruvate and lactate metabolic processes, and glycerol catabolic process. Similarly, KEGG pathway analysis indicated pyruvate metabolism, glycolysis/gluconeogenesis, biosynthesis, citrate cycles were differentially enriched in the Kyrgyz environment. DEGs like TSKU, VTG1, SGK, CDK2, etc. in such pathways are highly involved in the adaptation of organisms into diverse climatic conditions. Our investigation may serve as a resource for the chicken industry, especially in exporting Hanhyup chicken from Korea to other countries.

B-cell activating factor (BAFF) is a crucial survival factor for B cells, and excess BAFF contributes to development of autoimmune diseases. Recent studies have shown that rapamycin can prevent BAFF-induced B-cell proliferation and survival, but the underlying mechanism remains to be elucidated. Here we found that rapamycin inhibited human soluble BAFF (hsBAFF)-stimulated cell proliferation by inducing G(1)-cell cycle arrest, which was through downregulating the protein levels of CDK2, CDK4, CDK6, cyclin A, cyclin D1, and cyclin E. Rapamycin reduced hsBAFF-stimulated cell survival by downregulating the levels of anti-apoptotic proteins (Mcl-1, Bcl-2, Bcl-xL and survivin) and meanwhile upregulating the levels of pro-apoptotic proteins (BAK and BAX). The cytostatic and cytotoxic effects of rapamycin linked to its attenuation of hsBAFF-elevated intracellular free Ca2+ ([Ca2+](i)). In addition, rapamycin blocked hsBAFF-stimulated B-cell proliferation and survival by preventing hsBAFF from inactivating PTEN and activating the Akt-Erk1/2 pathway. Overexpression of wild type PTEN or ectopic expression of dominant negative Akt potentiated rapamycin's suppression of hsBAFF-induced Erk1/2 activation and proliferation/viability in Raji cells. Interestingly, PP242 (mTORC1/2 inhibitor) or Akt inhibitor X, like rapamycin (mTORC1 inhibitor), reduced the basal or hsBAFF-induced [Ca2+](i) elevations. Chelating [Ca2+](i) with BAPTA/AM, preventing [Ca2+](i) elevation using EGTA, 2-APB or verapamil, inhibiting CaMKII with KN93, or silencing CaMKII strengthened rapamycin's inhibitory effects. The results indicate that rapamycin inhibits BAFF-stimulated B-cell proliferation and survival by blunting mTORC1/2-mediated [Ca2+](i) elevations and suppressing Ca2+ -CaMKII-dependent PTEN/Akt-Erk1/2 signaling pathway. Our finding underscores that rapamycin may be exploited for prevention of excessive BAFF-induced aggressive B-cell malignancies and autoimmune diseases.