PRIAM: Privacy Preserving Identity and Access Management Scheme in Cloud

( Jinbo Xiong ),( Zhiqiang Yao ),( Jianfeng Ma ),( Ximeng Liu ),( Qi Li ),( Jun Ma ) 한국인터넷정보학회 2014 KSII Transactions on Internet and Information Syst Vol.8 No.1

Each cloud service has numerous owners and tenants, so it is necessary to construct a privacy preserving identity management and access control mechanism for cloud computing. On one hand, cloud service providers (CSP) depend on tenant`s identity information to enforce appropriate access control so that cloud resources are only accessed by the authorized tenants who are willing to pay. On the other hand, tenants wish to protect their personalized service access patterns, identity privacy information and accessing newfangled cloud services by on-demand ways within the scope of their permissions. There are many identity authentication and access control schemes to address these challenges to some degree, however, there are still some limitations. In this paper, we propose a new comprehensive approach, called Privacy pReserving Identity and Access Management scheme, referred to as PRIAM, which is able to satisfy all the desirable security requirements in cloud computing. The main contributions of the proposed PRIAM scheme are threefold. First, it leverages blind signature and hash chain to protect tenant`s identity privacy and implement secure mutual authentication. Second, it employs the service-level agreements to provide flexible and on-demand access control for both tenants and cloud services. Third, it makes use of the BAN logic to formally verify the correctness of the proposed protocols. As a result, our proposed PRIAM scheme is suitable to cloud computing thanks to its simplicity, correctness, low overhead, and efficiency.

Nuclear Factor-Kappa B Regulation of Osteoclastogenesis and Osteoblastogenesis

Brendan F. Boyce,Jinbo Li,Zhenqiang Yao,Lianping Xing 대한내분비학회 2023 Endocrinology and metabolism Vol.38 No.5

Maintenance of skeletal integrity requires the coordinated activity of multinucleated bone-resorbing osteoclasts and bone-forming osteoblasts. Osteoclasts form resorption lacunae on bone surfaces in response to cytokines by fusion of precursor cells. Osteoblasts are derived from mesenchymal precursors and lay down new bone in resorption lacunae during bone remodeling. Nuclear factorkappa B (NF-κB) signaling regulates osteoclast and osteoblast formation and is activated in osteoclast precursors in response to the essential osteoclastogenic cytokine, receptor activator of NF-κB ligand (RANKL), which can also control osteoblast formation through RANK-RANKL reverse signaling in osteoblast precursors. RANKL and some pro-inflammatory cytokines, including tumor necrosis factor (TNF), activate NF-κB signaling to positively regulate osteoclast formation and functions. However, these cytokines also limit osteoclast and osteoblast formation through NF-κB signaling molecules, including TNF receptor-associated factors (TRAFs). TRAF6 mediates RANKL-induced osteoclast formation through canonical NF-κB signaling. In contrast, TRAF3 limits RANKL- and TNF-induced osteoclast formation, and it restricts transforming growth factor β (TGFβ)-induced inhibition of osteoblast formation in young and adult mice. During aging, neutrophils expressing TGFβ and C-C chemokine receptor type 5 (CCR5) increase in bone marrow of mice in response to increased NF-κB-induced CC motif chemokine ligand 5 (CCL5) expression by mesenchymal progenitor cells and injection of these neutrophils into young mice decreased bone mass. TGFβ causes degradation of TRAF3, resulting in decreased glycogen synthase kinase-3β/β-catenin-mediated osteoblast formation and age-related osteoporosis in mice. The CCR5 inhibitor, maraviroc, prevented accumulation of TGFβ+/CCR5+ neutrophils in bone marrow and increased bone mass by inhibiting bone resorption and increasing bone formation in aged mice. This paper updates current understanding of how NF-κB signaling is involved in the positive and negative regulation of cytokine-mediated osteoclast and osteoblast formation and activation with a focus on the role of TRAF3 signaling, which can be targeted therapeutically to enhance bone mass.

NF-κB-Mediated Regulation of Osteoclastogenesis

Brendan F. Boyce,Yan Xiu,Jinbo Li,Lianping Xing,Zhenqiang Yao 대한내분비학회 2015 Endocrinology and metabolism Vol.30 No.1

Osteoclasts are multinucleated cells formed mainly on bone surfaces in response to cytokines by fusion of bone marrow-derived myeloid lineage precursors that circulate in the blood. Major advances in understanding of the molecular mechanisms regulating osteoclast formation and functions have been made in the past 20 years since the discovery that their formation requires nuclear factor-kappa B (NF-κB) signaling and that this is activated in response to the essential osteoclastogenic cytokine, receptor activator of NF-κB ligand (RANKL), which also controls osteoclast activation to resorb (degrade) bone. These studies have revealed that RANKL and some pro-inflammatory cytokines, including tumor necrosis factor, activate NF-κB and downstream signaling, including c-Fos and nuclear factor of activated T-cells, cytoplasmic 1 (NFATc1), and inhibition of repressors of NFATc1 signaling, to positively regulate osteoclast formation and functions. However, these cytokines also activate NF-κB signaling that can limit osteoclast formation through the NF-κB signaling proteins, TRAF3 and p100, and the suppressors of c-Fos/NFATc1 signaling, IRF8, and RBP-J. This paper reviews current understanding of how NF-κB signaling is involved in the positive and negative regulation of cytokine-mediated osteoclast formation and activation.

Different divergence events for three pairs of PEBPs in Gossypium as implied by evolutionary analysis

Youjun Lu,Wei Chen,Lanjie Zhao,Jinbo Yao,Yan Li,Weijun Yang,Ziyang Liu,Yongshan Zhang,Jie Sun 한국유전학회 2019 Genes & Genomics Vol.41 No.4

Introduction The phosphatidylethanolamine-binding protein (PEBP) gene family plays a crucial role in seed germination, reproductive transformation, and other important developmental processes in plants, but its distribution in Gossypium genomes or species, evolutionary properties, and the fates of multiple duplicated genes remain unclear. Objectives The primary objectives of this study were to elucidate the distribution and characteristics of PEBP genes in Gossypium, as well as the evolutionary pattern of duplication and deletion, and functional differentiation of PEBPs in plants. Methods Using the PEBP protein sequences in Arabidopsis thaliana as queries, blast alignment was carried out for the identification of PEBP genes in four sequenced cotton species. Using the primers designed according to the PEBP genome sequences, PEBP genes were cloned from 15 representative genomes of Gossypium genus, and the gene structure, CDS sequence, protein sequence and properties were predicted and phylogenetic analysis was performed. Taking PEBP proteins of grape as reference, grouping of orthologous gene, analysis of phylogeny and divergence of PEBPs in nine species were conducted to reconstruct the evolutionary pattern of PEBP genes in plants. Results We identified and cloned 160 PEBPs from 15 cotton species, and the phylogenetic analysis showed that the genes could be classified into the following three subfamilies: MFT-like, FT-like and TFL1-like. There were eight single orthologous group (OG) members in each diploid and 16 double OG members in each tetraploid. An analysis of the expression and selective pressure indicated that expression divergence and strong purification selection within the same OG presented in the PEBP gene family. Conclusion An evolutionary pattern of duplication and deletion of the PEBP family in the evolutionary history of Gossypium was suggested, and three pairs of genes resulted from different whole-genome duplication events.