Stem cell factor, the JAK-STAT pathway and signal transduction

被引：41

作者：

Linnekin, D ^{[1
]}

Mou, S ^{[1
]}

Deberry, CS ^{[1
]}

Weiler, SR ^{[1
]}

Keller, JR ^{[1
]}

Ruscetti, FW ^{[1
]}

Longo, DL ^{[1
]}

机构：

[1] NCI, Lab Leukocyte Biol, Div Basic Sci, Frederick Canc Res & Dev Ctr, Frederick, MD 21701 USA

来源：

LEUKEMIA & LYMPHOMA | 1997年 / 27卷 / 5-6期

关键词：

cytokines; growth factors; signal transduction; hematopoiesis;

D O I：

10.3109/10428199709058310

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Recent work has demonstrated the importance of Janus family kinases (JAKs) and signal transducers and activators of transcription (STATs) in the stimulus-response coupling of receptors lacking intrinsic tyrosine kinase activity. In particular, the JAK-STAT pathway appears critical in signal transduction by interferon as well as numerous hematopoietic growth factors interacting with members of the hemapoietin receptor superfamily. Although ligands that interact with receptor tyrosine kinases (RTK), such as epidermal growth factor (EGF), platelet-derived growth factor (PDGF) and colony stimulating factor-1 (CSF-1), have been shown to induce increases in phosphorylation of both JAKs and STATs, little is known about activation of this pathway by stem cell factor (SCF). This review will summarize what is known about the JAK/STAT pathway in relation to SCF signal transduction.

引用

页码：439 / 444

页数：6

共 39 条

[1] MOLECULAR-CLONING OF MAST-CELL GROWTH-FACTOR, A HEMATOPOIETIN THAT IS ACTIVE IN BOTH MEMBRANE-BOUND AND SOLUBLE FORMS [J].

ANDERSON, DM ;

LYMAN, SD ;

BAIRD, A ;

WIGNALL, JM ;

EISENMAN, J ;

RAUCH, C ;

MARCH, CJ ;

BOSWELL, HS ;

GIMPEL, SD ;

COSMAN, D ;

WILLIAMS, DE .

CELL, 1990, 63 (01) :235-243

[2] MYC BUT NOT FOS RESCUE OF PDGF SIGNALING BLOCK CAUSED BY KINASE INACTIVE SRC [J].

BARONE, MV ;

COURTNEIDGE, S .

NATURE, 1995, 378 (6556) :509-512

[3]

BRIZZI MF, 1994, J BIOL CHEM, V269, P31680

[4] JAK-STAT PATHWAYS AND TRANSCRIPTIONAL ACTIVATION IN RESPONSE TO IFNS AND OTHER EXTRACELLULAR SIGNALING PROTEINS [J].

DARNELL, JE ;

KERR, IM ;

STARK, GR .

SCIENCE, 1994, 264 (5164) :1415-1421

[5] STAT activation by epidermal growth factor (EGF) and amphiregulin - Requirement for the EGF receptor kinase but not for tyrosine phosphorylation sites or JAK1 [J].

David, M ;

Wong, L ;

Flavell, R ;

Thompson, SA ;

Wells, A ;

Larner, AC ;

Johnson, GR .

JOURNAL OF BIOLOGICAL CHEMISTRY, 1996, 271 (16) :9185-9188

[6] SIGNAL-TRANSDUCTION - BEATING A PATH TO MYC [J].

EISENMAN, RN ;

COOPER, JA .

NATURE, 1995, 378 (6556) :438-439

[7] TRANSCRIPTION FACTOR P91 INTERACTS WITH THE EPIDERMAL GROWTH-FACTOR RECEPTOR AND MEDIATES ACTIVATION OF THE C-FOS GENE PROMOTER [J].

FU, XY ;

ZHANG, JJ .

CELL, 1993, 74 (06) :1135-1145

[8]

GALLI SJ, 1994, ADV IMMUNOL, V55, P1

[9]

Gotoh A, 1996, BLOOD, V88, P138

[10] THE HEMATOPOIETIC GROWTH FACTOR-KL IS ENCODED BY THE SI-LOCUS AND IS THE LIGAND OF THE C-KIT RECEPTOR, THE GENE-PRODUCT OF THE W-LOCUS [J].

HUANG, E ;

NOCKA, K ;

BEIER, DR ;

CHU, TY ;

BUCK, J ;

LAHM, HW ;

WELLNER, D ;

LEDER, P ;

BESMER, P .

CELL, 1990, 63 (01) :225-233

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