Stat4- and Stat6-deficient mice as models for manipulating T helper cell responses

被引：20

作者：

Grusby, MJ

机构：

[1] Harvard School of Public Health, Department of Cancer Biology, Boston

来源：

BIOCHEMICAL SOCIETY TRANSACTIONS | 1997年 / 25卷 / 02期

关键词：

D O I：

10.1042/bst0250359

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

[No abstract available]

引用

页码：359 / 360

页数：2

共 23 条

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[5] AN INTERLEUKIN-4-INDUCED TRANSCRIPTION FACTOR - IL-4 STAT
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[J]. SCIENCE, 1994, 265 (5179) : 1701 - 1706
[6] DEVELOPMENT OF TH1 CD4+ T-CELLS THROUGH IL-12 PRODUCED BY LISTERIA-INDUCED MACROPHAGES
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[J]. SCIENCE, 1993, 260 (5107) : 547 - 549
[7] INTERLEUKIN-12 SIGNALING IN T-HELPER TYPE-1 (TH1) CELLS INVOLVES TYROSINE PHOSPHORYLATION OF SIGNAL TRANSDUCER AND ACTIVATOR OF TRANSCRIPTION (STAT)3 AND STAT4
JACOBSON, NG
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MURPHY, KM
[J]. JOURNAL OF EXPERIMENTAL MEDICINE, 1995, 181 (05) : 1755 - 1762
[8] Stat6 is required for mediating responses to IL-4 and for the development of Th2 cells
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[9] Impaired IL-12 responses and enhanced development of Th2 cells in Stat4-deficient mice
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[J]. NATURE, 1996, 382 (6587) : 174 - 177
[10] AN IL-4 RECEPTOR REGION CONTAINING AN INSULIN-RECEPTOR MOTIF IS IMPORTANT FOR IL4-MEDIATED IRS-1 PHOSPHORYLATION AND CELL-GROWTH
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[J]. CELL, 1994, 76 (05) : 811 - 820

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