Archives

  • 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • 2020-02
  • 2020-03
  • 2020-04
  • 2020-05
  • 2020-06
  • 2020-07
  • 2020-08
  • 2020-09
  • 2020-10
  • 2020-11
  • 2020-12
  • 2021-01
  • 2021-02
  • 2021-03
  • 2021-04
  • 2021-05
  • 2021-06
  • 2021-07
  • 2021-08
  • 2021-09
  • 2021-10
  • 2021-11
  • 2021-12
  • 2022-01
  • 2022-02
  • 2022-03
  • 2022-04
  • 2022-05
  • 2022-06
  • 2022-07
  • 2022-08
  • 2022-09
  • 2022-10
  • 2022-11
  • 2022-12
  • 2023-01
  • 2023-02
  • 2023-03
  • 2023-04
  • 2023-05
  • 2023-06
  • 2023-07
  • 2023-08
  • 2023-09
  • 2023-10
  • 2023-11
  • 2023-12
  • 2024-01
  • 2024-02
  • 2024-03
  • br Site of expression FASTK is expressed in

    2021-09-18


    Site of expression FASTK is expressed in various parts of human body including heart, skeletal muscle, brain, placenta, lung, liver, kidney pancreas (Ota et al., 2004) and many other organs (Fig. 1). It has been reported that FASTK is highly expressed in pancreatic tumors, where it is involved in cell proliferation, adhesion, and motility (Bauer et al., 2009, Simarro et al., 2010b). Under normal condition, FASTK prominently localized in nucleus and mitochondria but least in cytoplasm (Fig. 2). FASTK also over-expressed in the cutaneous T cell lymphoma mycosis fungoides (van Doorn et al., 2009). Depletion of TIA1 and T cell intracellular Ag-1 related protein (TIAR; a closely related homologue) helps to promote the expression of transcripts encoding proteins (Piecyk et al., 2000, Dixon et al., 2003, Lopez de Silanes et al., 2005). In HeLa cells, knockdown of TIA1/TIAR leads to increased cell proliferation, as well as able to alter Cyanine 5-dUTP and anchorage-independent growth (Reyes et al., 2009). Overexpression of FASTK reduces the expression of TIA1/TIAR and thus promotes the cell survival and proliferation.
    Conclusions
    Conflict of interests
    Acknowledgments SS is grateful to the University Grants Commission, Government of India, New Delhi for the award of DS Kothari Postdoctoral fellowship [BSR/BL/13-14/0483]. SBS thanks Department of Biotechnology, New Delhi for the award of DBT-Research Associate. VK thanks Department of Science and Technology for the award of DST-Fast track Fellowship [SB/YS/LS-161/2014]. FA and MIH thank to the Department of Science and Technology (EMR/2015/002372) financial support.
    INTRODUCTION Rheumatoid arthritis (RA) is an immune-mediated disease, which characteristically presents as a gradually symmetrical polyarthritis. The pathology of the disease process produces an inflammatory response of the synovial membrane secondary to hyperplasia of synovial cells, production of excess synovial fluid, and the development of pannus in the synovium. This often leads to the destruction of articular cartilage and ankylosis of the joints. The cause of this chronic inflammation is not yet clear. However, one of the basic, major hypotheses is that of inadequate apoptosis. Recent studies noted that the pseudo-tumoral expansion of fibroblast-like synoviocytes (FLS), which invade and destroy the joint structure, was closely associated with imbalanced cell proliferation and apoptosis. Expression abnormalities of apoptosis-related genes and the impairment of cell apoptosis are two essential factors of RA. Numerous molecules and receptors have been defined in the regulation of cell apoptosis; however, the Fas-Fas ligand death receptor pathway is significantly involved in the pathogenesis of RA. Various types of innate and adaptive immune cells have been shown to coordinately contribute to the pathophysiology of RA, and lymphocyte infiltration is increased significantly in synovial joints. Within the immune system, CD4 + T cells are important players in the normal development of numerous cellular and humoral immune responses. CD4 + T cells participate in all stages of immune responses as an important effector of T lymphocytes. RA is characterized by severe chronic synovitis with an abundance of CD4 + T cells and macrophages in the inflamed synovial tissue. Thus, CD4+ T cells play a central role by expressing multiple immune regulatory molecules that are involved in RA pathogenesis. Quantitative and/or qualitative (functional) deficiencies of CD4 + T cell subsets have been suggested to contribute to the development of RA. In this study, we evaluated the Fas/FasL-mediated pathway and related protein expression on CD4+ T cells in peripheral blood of RA patients before and after treatment with Xingfeng Capsule (XFC) compared with leflunomide (LEF), which has recently become a first-line drug in the treatment of RA.
    METHODS