In this paper, we propose a learning method for an agent to interact with other agents effectively. This method, MULA-C, improves efficiency of the learning, by clustering agents, and influences the learning experience of one agent to other agents which belong to the same cluster. Similarity among agents is evaluated by similarity among Q-values of agents. We give the detail explanation of learning method of MULA-C, and present the result of experiments which shows the effectiveness of MULA-C.

Mediator is a coregulatory complex that plays essential roles in multiple processes of transcription regulation. One of the human Mediator subunits, MED26, has a role in recruitment of the super elongation complex (SEC) to polyadenylated genes and little elongation complex (LEC) to non‐polyadenylated genes, including small nuclear RNAs (snRNAs) and replication‐dependent histone (RDH) genes. MED26‐containing Mediator plays a role in 3′ Pol II pausing at the proximal region of transcript end sites in RDH genes through recruitment of Cajal bodies (CBs) (...) to histone locus bodies (HLBs). This finding suggests that Mediator is involved in the association of CBs with HLBs to facilitate 3′ Pol II pausing and subsequent 3′‐end processing by supplying 3′‐end processing factors from CBs. Thus, we argue the possibility that Mediator is involved in the organization of nuclear bodies to orchestrate multiple processes of gene transcription. (shrink)

Chemotherapy is an important therapeutic approach for cancer treatment. However, drug resistance is an obstacle that often impairs the successful use of chemotherapies. Therefore, overcoming drug resistance would lead to better therapeutic outcomes for cancer patients. Recently, studies by our own and other groups have demonstrated that there is an intimate correlation between the loss of the F‐box and WD repeat domain‐containing 7 (FBW7) tumor suppressor and the incurring drug resistance. While loss of FBW7 sensitizes cancer cells to certain drugs, (...) FBW7‐/‐ cells are more resistant to other types of chemotherapies. FBW7 exerts its tumor suppressor function by promoting the degradation of various oncoproteins that regulate many cellular processes, including cell cycle progression, cellular metabolism, differentiation, and apoptosis. Since loss of the FBW7 tumor suppressor is linked to drug resistance, FBW7 may represent a novel therapeutic target to increase drug sensitivity of cancer cells to conventional chemotherapeutics. This paper thus focuses on the new functional aspects of FBW7 in drug resistance. (shrink)