Assignment1 of the feline Fas ligand gene (TNFSF6) to chromosome F1q12→q13 by fluorescence in situ hybridization
Assignment1 of the feline Fas ligand gene (TNFSF6) to chromosome F1q12→q13 by fluorescence in situ hybridization
复制标题
通过荧光原位杂交将猫 Fas 配体基因 (TNFSF6) 分配到染色体 F1q12→q13
DOI:
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发表时间:
2001
影响因子:
1.7
通讯作者:
H. Tsujimoto
中科院分区:
文献类型:
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作者:
Y. Fujino;T. Mizuno;K. Masuda;K. Ohno;H. Satoh;H. Tsujimoto
Fas ligand (FasL) is a member of the tumor necrosis factor family cytokines and induces apoptosis by binding to its receptor, Fas. FasL is predominantly expressed on natural killer (NK) cells and activated T lymphocytes, and also constitutively expressed in immune-privileged sites such as the eye and testis (Nagata, 1997). In human, FasL-mediated cell death has a crucial role in the regulation of lymphocyte homeostasis, and the immune response to viruses and tumor cells; its deregulation is associated with the pathogenesis of various autoimmune diseases (Nagata, 1997) and immunodeficiency caused by virus infection (Geleziunas et al., 2001). Similarly, it is reported that various tumors expressing FasL constitutively are proposed to counterattack the cytotoxic lymphocytes and consequently evade specific immune surveillance (Strand et al., 1996). Further, an elevated level of the soluble-formed FasL which may cause systemic tissue damage has been observed in sera of the patients with large granular lymphocytic leukemia and NK cell lymphoma (Tanaka et al., 1996). Analysis of the FasL gene in immune-mediated diseases, immunodeficiency and malignant tumors will provide a clue to the etiology and molecular pathogenesis, and may have prognostic and therapeutic implications. In cats, apoptosis has been shown to be associated with the pathogenesis of immune-mediated diseases (Center, 1999), viral diseases (Ohno et al., 1993; Rojko et al., 1996) and malignant tumors (Anilkumar et al., 1994). In order to provide basic cytogenetic information on the FasL gene in the cat, we regionally assigned the feline FasL gene (TNFSF6) to chromosome F1q12→q13 by fluorescence in situ hybridization. Interestingly, monosomy and deletion of feline chromosome F1 were observed in feline leukemia virus-positive and negative lymphomas (Gulino, 1992), and a large marker chromosome F1 was detected in a cat with fibrosarcoma (Mayr et al., 1996). Therefore the present data will help to investigate molecular pathogenesis of apoptosis-related diseases in cats and also to understand comparative cytogenetics. Since the human FASL was mapped on 1q23 (Takahashi et al., 1994), the feline FasL is the first gene locus proving conservation of synteny between the feline chromosome F1 and the long arm of human chromosome 1 (O’Brien et al., 1997).
影响因子:
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作者:
Gulino,SE
通讯作者:
Gulino,SE
DOI:
10.1007/978-3-642-79850-4_2
发表时间:
1996
期刊:
Progress in molecular and subcellular biology.
影响因子:
--
作者:
Rojko,JL;Hartke,JR;Cheney,CM;Phipps,AJ;Neil,JC
通讯作者:
Neil,JC