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Articles by J Liao
Total Records ( 3 ) for J Liao
  H Wang , A Zhao , L Chen , X Zhong , J Liao , M Gao , M Cai , D. H Lee , J Li , D Chowdhury , Y. g Yang , G. P Pfeifer , Y Yen and X. Xu
 

Human Rap1-interacting protein 1 (RIF1) contributes to the ataxia telangiectasia, mutated-mediated DNA damage response against the dexterous effect of DNA lesions and plays a critical role in the S-phase checkpoint. However, the molecular mechanisms by which human RIF1 conquers DNA aberrations remain largely unknown. We here showed that inhibition of RIF1 expression by small interfering RNA led to defective homologous recombination-mediated DNA double-strand break repair and sensitized cancer cells to camptothecin or staurosporine treatment. RIF1 underwent caspase-dependent cleavage upon apoptosis. We further found that RIF1 was highly expressed in human breast tumors, and its expression status was positively correlated with differentiation degrees of invasive ductal carcinoma of the breast. Our results suggest that RIF1 encodes an anti-apoptotic factor required for DNA repair and is a potential target for cancer treatment.

  J Liao , Q Qi , X Zhu , Y Cao and T. Li
 

IP multimedia subsystem (IMS) is over IP network architecture, but mobile IP cannot directly support session mobility controlled by session initiation protocol-based signaling. The long signaling delay for session reestablishment in application layer always results in session interruptions during the handoff. Therefore, handoff poses a challenge for quality of service (QoS) maintenance in IMS that targets to offer real-time multimedia applications over wireless mobile networks. The existing approaches to solve this problem depend on the advance resource reservation and the optimization of handoff control. Unfortunately, big cost of the advance resource reservation in neighboring domains is a major problem that leads to a serious signaling load and a waste of wireless bandwidth. To solve this issue, we present an enhanced IMS handoff mechanism (EHM) based on user mobility prediction to save network resources by avoiding multiple useless advance reservations. In addition, to support the heterogeneous access networks in IMS domain, EHM evolves a network selective scheme to utilize the network resources more efficiently. The architecture of EHM and the advance QoS negotiation signaling are also presented. We model the cost, the handoff delay and the session blocking probability for EHM and the previous work. Analytical and simulation results show that EHM can enhance the handoff performance, such as reducing resource reservation cost greatly, decreasing session reestablishment delay and making good use of multiple access network resources.

  B. C Betz , K. L Jordan Williams , C Wang , S. G Kang , J Liao , M. R Logan , C. H Kim and E. J. Taparowsky
 

Batf belongs to the activator protein 1 superfamily of basic leucine zipper transcription factors that includes Fos, Jun, and Atf proteins. Batf is expressed in mouse T and B lymphocytes, although the importance of Batf to the function of these lineages has not been fully investigated. We generated mice (BatfZ/Z) in which Batf protein is not produced. BatfZ/Z mice contain normal numbers of B cells but show reduced numbers of peripheral CD4+ T cells. Analysis of CD4+ T helper (Th) cell subsets in BatfZ/Z mice demonstrated that Batf is required for the development of functional Th type 17 (Th17), Th2, and follicular Th (Tfh) cells. In response to antigen immunization, germinal centers were absent in BatfZ/Z mice and the maturation of Ig-secreting B cells was impaired. Although adoptive transfer experiments confirmed that this B cell phenotype can be driven by defects in the BatfZ/Z CD4+ T cell compartment, stimulation of BatfZ/Z B cells in vitro, or by a T cell–independent antigen in vivo, resulted in proliferation but not class-switch recombination. We conclude that loss of Batf disrupts multiple components of the lymphocyte communication network that are required for a robust immune response.

 
 
 
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