Myeloproliferative disease induced by TEL-PDGFRB displays dynamic range sensitivity to Stat5 gene dosage

Blood

Volumn 109, Issue 9, 2007, Pages 3906-3914

  Cain, Jennifer A ^a   Xiang, Zhifu ^a   O'Neal, Julie ^a   Kreisel, Friederike ^b   Colson, Annalynn ^a   Luo, Hui ^a   Hennighausen, Lothar ^c   Tomasson, Michael H ^a,d  

^a USA   (United States)

^b WASHINGTON UNIVERSITY SCHOOL OF MEDICINE   (United States)

^c NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES   (United States)

^d Division of Oncology   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

HEMATOPOIETIC CELL KINASE; METHYLCELLULOSE; PEPTIDES AND PROTEINS; PLATELET DERIVED GROWTH FACTOR BETA RECEPTOR; PROTEIN FGR; PROTEIN TYROSINE KINASE; STAT1 PROTEIN; STAT5A PROTEIN; STAT5B PROTEIN; TRANSCRIPTION FACTOR ETV6; UNCLASSIFIED DRUG;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; BONE MARROW TRANSPLANTATION; CELL SUBPOPULATION; CONTROLLED STUDY; GENE DELETION; GENE DOSAGE; GENE TARGETING; GENETIC TRANSDUCTION; HEMATOPOIETIC STEM CELL; LIVER; MOUSE; MYELOPROLIFERATIVE DISORDER; NONHUMAN; ONCOGENE C MYC; PRIORITY JOURNAL; PROTEIN EXPRESSION; SURVIVAL TIME;

EID: 34247354963     PISSN: 00064971     EISSN: 00064971     Source Type: Journal    
DOI: 10.1182/blood-2006-07-036335     Document Type: Article

References (36)

1. Golub TR, Barker GF, Lovett M, Gilliland DG. Fusion of PDGF receptor beta to a novel ets-like gene, tel, in chronic myelomonocytic leukemia with t(5;12) chromosomal translocation. Cell. 1994;77:307-316.
2. Carroll M, Tomasson MH, Barker GF, Golub TR, Gilliland DG. The TEL/platelet-derived growth factor beta receptor (PDGF beta R) fusion in chronic myelomonocytic leukemia is a transforming protein that self-associates and activates PDGF beta R kinase-dependent signaling pathways. Proc Natl Acad Sci U S A. 1996;93:14845-14850.
3. Jousset C, Carron C, Boureux A, et al. A domain of TEL conserved in a subset of ETS proteins defines a specific oligomerization interface essential to the mitogenic properties of the TEL-PDGFR beta oncoprotein. EMBO J. 1997;16:69-82.
4. Tran HH, Kim CA, Faham S, Siddall MC, Bowie JU. Native interface of the SAM domain polymer of TEL. BMC Struct Biol. 2002;2:5.
5. Bourgeade MF, Defachelles AS, Cayre YE. Myc is essential for transformation by TEL/platelet-derived growth factor receptor beta (PDGFRbeta). Blood. 1998;91:3333-3339.
6. Sternberg DW, Tomasson MH, Carroll M, et al. The TEL/PDGFbetaR fusion in chronic myelomonocytic leukemia signals through STAT5-dependent and STAT5-independent pathways. Blood. 2001;98:3390-3397.
7. Wilbanks AM, Mahajan S, Frank DA, Druker BJ, Gilliland DG, Carroll M. TEL/PDGFbetaR fusion protein activates STAT1 and STAT5: a common mechanism for transformation by tyrosine kinase fusion proteins. Exp Hematol. 2000;28:584-593.
8. Tomasson MH, Sternberg DW, Williams IR, et al. Fatal myeloproliferation, induced in mice by TEL/PDGFbetaR expression, depends on PDGFbetaR tyrosines 579/581. J Clin Invest. 2000;105:423-432.
9. Mori S, Ronnstrand L, Yokote K, et al. Identification of two juxtamembrane autophosphorylation sites in the PDGF beta-receptor; involvement in the interaction with Src family tyrosine kinases. EMBO J. 1993;12:2257-2264.
10. Valgeirsdottir S, Paukku K, Silvennoinen O, Heldin CH, Claesson-Welsh L. Activation of Stat5 by platelet-derived growth factor (PDGF) is dependent on phosphorylation sites in PDGF beta-receptor juxtamembrane and kinase insert domains. Oncogene. 1998;16:505-515.
11. Sachsenmaier C, Sadowski HB, Cooper JA. STAT activation by the PDGF receptor requires juxtamembrane phosphorylation sites but not Src tyrosine kinase activation. Oncogene. 1999;18:3583-3592.
12. Luo H, Li Q, O'Neal J, Kreisel F, Le Beau MM, Tomasson MH. c-Myc rapidly induces acute myeloid leukemia in mice without evidence of lymphoma-associated antiapoptotic mutations. Blood. 2005;106:2452-2461.
13. Meng F, Lowell CA. Lipopolysaccharide (LPS)-induced macrophage activation and signal transduction in the absence of Src-family kinases Hck, Fgr, and Lyn. J Exp Med. 1997;185:1661-1670.
14. Meraz MA, White JM, Sheehan KC, et al. Targeted disruption of the Stat1 gene in mice reveals unexpected physiologic specificity in the JAKSTAT signaling pathway. Cell. 1996;84:431-442.
15. Liu X, Robinson GW, Wagner KU, Garrett L, Wynshaw-Boris A, Hennighausen L. Stat5a is mandatory for adult mammary gland development and lactogenesis. Genes Dev. 1997;11:179-186.
16. Cui Y, Riedlinger G, Miyoshi K, et al. Inactivation of Stat5 in mouse mammary epithelium during pregnancy reveals distinct functions in cell proliferation, survival, and differentiation. Mol Cell Biol. 2004;24:8037-8047.
17. Udy GB, Towers RP, Snell RG, et al. Requirement of STAT5b for sexual dimorphism of body growth rates and liver gene expression. Proc Natl Acad Sci U S A. 1997;94:7239-7244.
18. Markel P, Shu P, Ebeling C, et al. Theoretical and empirical issues for marker-assisted breeding of congenic mouse strains. Nat Genet. 1997;17:280-284.
19. Traver D, Miyamoto T, Christensen J, Iwasaki-Arai J, Akashi K, Weissman IL. Fetal liver myelopoiesis occurs through distinct, prospectively isolatable progenitor subsets. Blood. 2001;98:627-635.
20. Hoelbl A, Kovacic B, Kerenyi MA, et al. Clarifying the role of Stat5 in lymphoid development and Abelson-induced transformation. Blood. 2006;107:4898-4906.
21. Yao Z, Cui Y, Watford WT, et al. Stat5a/b are essential for normal lymphoid development and differentiation. Proc Natl Acad Sci U S A. 2006;103:1000-1005.
22. Liu X, Robinson GW, Gouilleux F, Groner B, Hennighausen L. Cloning and expression of Stat5 and an additional homologue (Stat5b) involved in prolactin signal transduction in mouse mammary tissue. Proc Natl Acad Sci U S A. 1995;92:8831-8835.
23. Teglund S, McKay C, Schuetz E, et al. Stat5a and Stat5b proteins have essential and nonessential, or redundant, roles in cytokine responses. Cell. 1998;93:841-850.
24. Boucheron C, Dumon S, Santos SC, et al. A single amino acid in the DNA binding regions of STAT5A and STAT5B confers distinct DNA binding specificities. J Biol Chem. 1998;273:33936-33941.
25. Verdier F, Rabionet R, Gouilleux F, et al. A sequence of the CIS gene promoter interacts preferentially with two associated STAT5A dimers: a distinct biochemical difference between STAT5A and STAT5B. Mol Cell Biol. 1998;18:5852-5860.
26. Zhang S, Fukuda S, Lee Y, et al. Essential role of signal transducer and activator of transcription (Stat)5a but not Stat5b for Flt3-dependent signaling. J Exp Med. 2000;192:719-728.
27. Onishi M, Nosaka T, Misawa K, et al. Identification and characterization of a constitutively active STAT5 mutant that promotes cell proliferation. Mol Cell Biol. 1998;18:3871-3879.
28. Schwaller J, Parganas E, Wang D, et al. Stat5 is essential for the myelo- and lymphoproliferative disease induced by TEL/JAK2. Mol Cell. 2000;6:693-704.
29. Ye D, Wolff N, Li L, Zhang S, Ilaria RL Jr. STAT5 signaling is required for the efficient induction and maintenance of CML in mice. Blood. 2006;107:4917-4925.
30. Stephanou A, Latchman DS. Opposing actions of STAT-1 and STAT-3. Growth Factors. 2005;23:177-182.
31. Twamley-Stein GM, Pepperkok R, Ansorge W, Courtneidge SA. The Src family tyrosine kinases are required for platelet-derived growth factormediated signal transduction in NIH 3T3 cells. Proc Natl Acad Sci U S A. 1993;90:7696-7700.
32. Hu Y, Liu Y, Pelletier S, et al. Requirement of Src kinases Lyn, Hck and Fgr for BCR-ABL1-induced B-lymphoblastic leukemia but not chronic myeloid leukemia. Nat Genet. 2004;36:453-461.
33. Mermel CH, McLemore ML, Liu F, et al. Src family kinases are important negative regulators of GCSF-dependent granulopoiesis. Now available as Blood. 2006;108:2562-2568.
34. Benekli M, Baer MR, Baumann H, Wetzler M. Signal transducer and activator of transcription proteins in leukemias. Blood. 2003;101:2940-2954.
35. Frohling S, Scholl C, Gilliland DG, Levine RL. Genetics of myeloid malignancies: pathogenetic and clinical implications. J Clin Oncol. 2005;23:6285-6295.
36. Tefferi A, Gilliland DG. The JAK2V617F tyrosine kinase mutation in myeloproliferative disorders: status report and immediate implications for disease classification and diagnosis. Mayo Clin Proc. 2005;80:947-958.