Potential role of Bcr-Abl in the activation of JAK1 kinase

Clinical Cancer Research

Volumn 3, Issue 2, 1997, Pages 145-149

  Henderson, Ying C ^a,c   Guo, Xiang Yang David ^a,c   Greenberger, Joel ^b   Deisseroth, Albert B ^c,d  

^a UNIVERSITY OF TEXAS   (United States)

^b UNIVERSITY OF PITTSBURGH MEDICAL CENTER   (United States)

^c YALE CANCER CENTER   (United States)

^d YALE UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

BCR ABL PROTEIN; GAMMA INTERFERON RECEPTOR; JAK1 KINASE; PROTEIN TYROSINE KINASE; UNCLASSIFIED DRUG;

ARTICLE; CONTROLLED STUDY; ENZYME ACTIVATION; GENETIC TRANSFECTION; HUMAN; HUMAN CELL; LEUKEMIA CELL; MOUSE; NONHUMAN; PRIORITY JOURNAL;

CELLS, CULTURED; DNA-BINDING PROTEINS; ENZYME ACTIVATION; FUSION PROTEINS, BCR-ABL; HUMANS; JANUS KINASE 1; K562 CELLS; PHOSPHORYLATION; PROTEIN-TYROSINE KINASES; STAT1 TRANSCRIPTION FACTOR; TRANS-ACTIVATORS; TRANSFECTION;

EID: 0031038109     PISSN: 10780432     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Article

References (31)

1. Rowley, J. D. A new consistent chromosomal abnormality in chronic myelogenous leukemia identified by quinacrine fluorescence and Giemsa staining. Nature (Lond.). 243: 290-293, 1973.
2. Gale, R. P., and Canaani, E. An 8-kilobase abl RNA transcript in chronic myelogenous leukemia. Proc. Natl. Acad. Sci. USA. 81: 5648-5652, 1984.
3. Ben-Neriah, Y., Daley, G. Q., Mes-Masson, A. M., Witte, O. N., and Baltimore, D. The chronic myelogenous leukemia-specific P210 protein is the product of the bcr/abl hybrid gene. Science (Washington DC), 233: 212-214, 1986.
4. Konopka, J. B., Watanabe, S. M., and Witte, O. N. An alteration of the human c-ABL protein in K562 leukemia cell unmasks associated tyrosine kinase activity. Cell, 37: 1035-1042, 1984.
5. Kloetzer, W., Kurzrock, R., Smith, L., Talpaz, M., Spiller, M., Gutterman, J., and Arlinghaus, R. The human cellular abl gene product in the chronic myelogenous leukemia cell line K562 has an associated tyrosine protein kinase activity. Virology, 140: 230-238, 1985.
6. McWhirter, J. R., Galasso, D. L., and Wang, J. Y. J. An actin-binding function contributes to transformation by the Bcr-Abl oncoprotein of Philadelpia chromosome-positive human leukemias. EMBO J., 12: 1533-1546, 1993.
7. Renshaw, M. W., McWhirter, J. R., and Wang, J. Y. J. The human leukemia oncogene Bcr-Abl abrogates the anchorage requirement but not the growth factor requirement for proliferation. Mol. Cell. Biol., 15: 1286-1293, 1995.
8. Ihle, J. N. Cytokine receptor signalling. Nature (Lond.), 377: 591-594, 1995.
9. Taniguchi, T. Cytokine signaling through nonreceptor protein tyrosine kinases. Science (Washington DC), 268: 251-255, 1995.
10. Wilks, A. F., Harpur, A. G., Kurban, R. R., Ralph, S. J., Zurcher, G., and Ziemiecki, A. Two novel protein-tyrosine kinases, each with a second phosphotransferase-related catalytic domain, define a new class of protein kinase. Mol. Cell. Biol, 11: 2057-2065, 1991.
11. Harpur, A. G., Andres, A-C., Ziemiecki, A., Aston, R. R., and Wilks, A. F. JAK2, a third member of the JAK family of protein tyrosine kinases. Oncogene, 7: 1347-1353, 1992.
12. Kawamura, M., McVicar, D.W., Johnston, J. A., Blake, T. B., Chen, Y-Q., Lal, B. K., Lloyd, A. R., Kelvin, D. J., Staples, J. E., Ortald, J. R., and O'Shea, J. J. Molecular cloning of L-JAK, a Janus family protein-tyrosine kinase expressed in natural killer cells and activated leukocytes. Proc. Natl. Acad. Sci. USA, 91: 6374-6378, 1994.
13. Firmbach-Kraft, I., Byers, M., Shows, T., Dalla-Favera, R., and Krolewski, J. J. Tyk2, prototype of a novel class of non-receptor tyrosine kinase genes. Oncogene, 5: 1329-1336, 1990.
14. Muller, M., Briscoe, J., Laxton, C., Guschin, D., Ziemiecki, A., Silvennoinen, O., Harpur, A. G., Barbieri, G., Witthugn, B. A., Schindler, C., Pellegrini, S., Wilks, A. F., Ihle, J. N., Stark, G. R., and Kerr, I. M. The protein tyrosine kinase JAK1 complements defects in interferon-α/β and -γ signal transduction. Nature (Lond.), 366: 129-135, 1993.
15. Watling, D., Guschin, D., Muller, M., Silvennoinen, O., Witthuhn, B. A., Quelle, F. W., Rogers, N. C., Schindler, C., Stark, G. R., Ihle, J. N., and Kerr, I. M. Complementation by the protein kinase JAK2 of a mutant cell line defective in the interferon-γ signal transduction pathway. Nature (Lond.), 366: 166-170, 1993.
16. Talpaz, M., Kantarjian, H. M., McCredie, K. B., Keating, M. J., Trujillo, J., and Gutterman, J. U. Clinical investigation of human α-interferon in chronic myelogenous leukemia. Blood, 69: 1280-1288, 1987.
17. Tum-1 JAK kinase causes leukemia-like hematopoietic defects. EMBO J., 14: 1412-1420, 1995.
18. Shuai, K., Ziemiecki, A., Wilks, A. F., Harpur, A.G., Sadowski, H. B., Gilman, M. Z., and Darnell, J. E. Polypeptide signalling to the nucleus through tyrosine phosphorylation of Jak and Stat proteins. Nature (Lond)., 366: 580-583, 1993.
19. Silvennoinen, O., Ihle, J. N., Schlessinger, J., and Levy, D.E. Interferon-induced nuclear signalling by Jak protein tyrosine kinases. Nature (Lond)., 366: 583-585, 1993.
20. Greenberg, J. S., Sakakeeny, M. A., Humphries, R. K., Eaves, C. J., and Eckner, R. J. Demonstration of permanent factor-dependent multi-potential (erythroid/neutrophil/basophil) hematopoietic progenitor cell lines. Proc. Natl. Acad. Sci. USA, 80: 2931-2935, 1983.
21. Migliaccio, G., Migliaccio, A. R., Keeider, B. L., Rovera, G., and Adamson, J. W. Selection of lineage-restricted cell lines immortalized at different stages of hematopoietic differentiation from the murine cell line 32D. J. Cell Biol., 109: 833-841, 1989.
22. Pendergast, A. M., Quilliam, L. A., Cripe, L. D., Bassing, G. H., Dai, Z., Li, N., Batzer, A., Rabun, K. M., Der, C. J., Schlessinger, L., and Gishizky, M. L. Bcr-abl-induced oncogenesis is mediated by direct interaction with SH2 domain of the Grb-2 adaptor protein. Cell, 75: 175-185, 1993.
23. + leukemia. Blood, 84: 1731-1736, 1994.
24. BCR/ABL. J. Biol. Chem., 270: 5039-5047, 1995.
25. Hu, P., Margolis, B., and Schlessinger, J. Vav: a potential link between tyrosine kinases and Ras-like GTPases in hematopoietic cell signaling. Bioassays, 15: 179-183, 1993.
26. BCR/ABL. EMBO J., 14: 257-265, 1995.
27. Muller, M., Laxton, C., Briscoe, J., Schindler, C., Improta, T., Darnell, J. E., Jr., Stark, G. R., and Kerr, I. M. Complementation of a mutant cell line: central role of the 91 kDa polypeptide of ISGF3 in the interferon-α or -γ signal transduction pathways. EMBO J., 12: 4221-4228, 1993.
28. Shuai, K., Horvath, C. M., Huang, L. H. T., Qureshi, S.A., Cowburn, D., and Darnell, J. E., Jr. Interferon activation of the transcription factor Stat91 involves dimerization through SH2-phosphotyrosyl peptide interactions. Cell, 76: 821-828, 1994.
29. Kumar, R., and Korutla, L. Induction of expression of interferon-stimulated gene factor-3 (ISGF-3) proteins by interferons. Exp. Cell Res., 216: 143-148, 1995.
30. Danial, N. N., Pernis, A., and Rothman, P. B. Jak-STAT signaling induced by the v-abl oncogene. Science (Washington DC), 269: 1875-1877, 1995.
31. Goff, S. P., Gilboa, E., Witte, O. N., and Baltimore, D. Structure of the Abelson murine leukemia virus genome and the homologous cellular gene: studies with cloned viral DNA. Cell, 22: 777-785, 1980.