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    • 5. 发明授权
    • T cell specific cDNA clone
    • T细胞特异性cDNA克隆
    • US4923799A
    • 1990-05-08
    • US100286
    • 1987-11-09
    • Tak W. Mak
    • Tak W. Mak
    • C07K14/725C07K14/82C12Q1/68G01N33/566
    • C12Q1/6881C07K14/7051C07K14/82G01N33/566C12Q2600/158
    • The invention provides a nucleic acid having a sequence which encodes a polypeptide that is at least part of a T cell antigen receptor. This encoded sequence is about 936 nucleotides in length and preferably is a human T cell antigen receptor. The nucleic acid sequence of one embodiment of the invention is shown in FIG. 3.The nucleic acid sequence may be used as a probe to determine whether an unknown cell, e.g., a tumor cell, is a T cell.Polypeptides encoded by the nucleic acid sequence include about 312 amino acids and are at least part of a T cell antigen receptor. They include at least one sequence which over 21 contiguous amino acids has greater than about 35% homology with mouse and human immunoglobin .lambda. light chains.Antibody to the polypeptide may be prepared and used to identify T cell antigen receptor and to determine whether an unknown cell, e.g., a tumor cell, is a T cell.
    • 本发明提供了具有编码至少部分T细胞抗原受体的多肽的序列的核酸。 该编码序列的长度约为936个核苷酸,优选为人T细胞抗原受体。 本发明的一个实施方案的核酸序列示于图1。 核酸序列可以用作探针以确定未知细胞,例如肿瘤细胞是否是T细胞。 由核酸序列编码的多肽包括约312个氨基酸,并且是T细胞抗原受体的至少一部分。 它们包括至少一个21个连续氨基酸与小鼠和人免疫球蛋白λ轻链具有大于约35%同源性的序列。 可以制备多肽的抗体并用于鉴定T细胞抗原受体并确定未知细胞,例如肿瘤细胞是否为T细胞。
    • 7. 发明授权
    • Mutant mouse lacking the expression of interferon regulatory factor 1
(IRF-1)
    • 缺乏干扰素调节因子1(IRF-1)表达的突变体小鼠
    • US5731490A
    • 1998-03-24
    • US392292
    • 1995-02-21
    • Tak W. MakTadatsugu Taniguchi
    • Tak W. MakTadatsugu Taniguchi
    • C07K14/47C12N15/85C12N15/00C12N5/10C12N15/87C12N15/90
    • C12N15/8509A01K67/0276C07K14/4702A01K2217/075A01K2227/105A01K2267/03
    • Interferon regulatory factor-1 (IRF-1) is implicated in the regulation of type I interferons (IFN) and cell growth. The invention is a mutant mouse lacking expression of the IRF-1 gene. Mice lacking IRF-1 did not differ from normal mice in size, behaviour, or reproductive ability. With fibroblasts derived from these mutant mice, it was shown that type I IFN induction is dramatically reduced when cells are induced by poly(I):poly(C). In contrast, no differences were found when cells are induced by New Castle Disease Virus (NDV), or induced by poly(I):poly(C) with prior treatment of IFN-.beta.. On the other hand, the induction levels of IFN-inducible genes such as MHC class I and 2'-5' oligoadenylate synthetase (2'5'OAS) were not affected. Collectively, these results illustrate an IRF-1 independent mechanism of gene induction for type I IFN and these IFN-inducible genes. The critical role of IRF-1 in the immune system has been documented for the first time by the observation that the number of TcR.alpha..beta..sup.+ CD4.sup.- CD8.sup.+ T cells were dramatically reduced in IRF-1 deficient mice. This phenotype may be ascribed to a thymocyte developmental defect between the double positive and single positive stages during CD8.sup.+ T cell ontogeny.
    • 干扰素调节因子-1(IRF-1)涉及I型干扰素(IFN)和细胞生长的调节。 本发明是缺少IRF-1基因表达的突变体小鼠。 缺乏IRF-1的小鼠与正常小鼠的大小,行为或生殖能力没有差异。 使用衍生自这些突变小鼠的成纤维细胞,显示当通过聚(I):聚(C)诱导细胞时,I型IFN诱导显着降低。 相比之下,当新城堡病毒(NDV)诱导细胞或由poly(I):poly(C))诱导IFN-β之前没有发现差异。 另一方面,IFN-诱导型基因如MHC I类和2'-5'寡腺苷酸合成酶(2'5'OAS)的诱导水平不受影响。 总而言之,这些结果说明了I型IFN和这些IFN诱导型基因的基因诱导的IRF-1独立机制。 IRF-1在免疫系统中的关键作用已经首次记录在IRF-1缺陷小鼠中,TcRαβ+ CD4-CD8 + T细胞数量急剧减少。 这种表型可能归因于CD8 + T细胞个体发育期间双阳性和单阳性阶段之间的胸腺细胞发育缺陷。