Tsukada S, Rawlings D J, Witte O N
Department of Microbiology and Molecular Genetics, University of California, Los Angeles 90024-1662.
Curr Opin Immunol. 1994 Aug;6(4):623-30. doi: 10.1016/0952-7915(94)90151-1.
The genetic defect associated with human X-linked agammaglobulinemia and murine X-linked immunodeficiency was recently shown to result from lack of function of a new cytoplasmic tyrosine kinase, called Bruton's tyrosine kinase (Btk). The phenotypes associated with these immunodeficiencies indicate that Btk plays a critical role in B-lymphocyte development. The distinctive protein structure of Btk and preliminary functional studies suggest that Btk may act in a novel manner in a variety of signaling pathways.
最近研究表明，与人类X连锁无丙种球蛋白血症和小鼠X连锁免疫缺陷相关的基因缺陷是由于一种名为布鲁顿酪氨酸激酶（Btk）的新型细胞质酪氨酸激酶功能缺失所致。与这些免疫缺陷相关的表型表明，Btk在B淋巴细胞发育中起关键作用。Btk独特的蛋白质结构和初步功能研究表明，Btk可能以一种新的方式作用于多种信号通路。
