Severe defects in immunity and hematopoiesis caused by SHP-1 protein-tyrosine-phosphatase deficiency

被引：133

作者：

Shultz, LD

Rajan, TV

Greiner, DL

机构：

[1] UNIV CONNECTICUT, CTR HLTH, DEPT PATHOL, FARMINGTON, CT 06030 USA

[2] UNIV MASSACHUSETTS, SCH MED, DEPT MED, DIV DIABET, WORCESTER, MA 01605 USA

来源：

TRENDS IN BIOTECHNOLOGY | 1997年 / 15卷 / 08期

关键词：

D O I：

10.1016/S0167-7799(97)01060-3

中图分类号：

Q81 [生物工程学（生物技术）]; Q93 [微生物学];

学科分类号：

071005 ; 0836 ; 090102 ; 100705 ;

摘要：

Spontaneous mouse mutations that cause severe immunodeficiency or autoimmunity are invaluable tools with which to investigate the mammalian immune system. Mutations at the 'motheaten' locus result in severe immunological dysfunction due to disruption of the structural gene encoding Src-homology 2-domain phosphatase-1 (SHP-1), This natural model for a specific protein-tyrosine-phosphatase deficiency is being widely utilized to determine the role of SHP-1 in the negative regulation of multiple signaling pathways in a number of hematopoietic lineages.

引用

页码：302 / 307

页数：6

共 60 条

[31]

MEDLOCK ES, 1987, J IMMUNOL, V138, P3590

[32] Hematopoietic cell phosphatase, SHP-1, is constitutively associated with the SH2 domain-containing leukocyte protein, SLP-76, in B cells [J].