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Cell Growth and Development

Direct Interaction of Jak1 and v-Abl Is Required for v-Abl-Induced Activation of STATs and Proliferation

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Pages 6795-6804 | Received 04 Feb 1998, Accepted 23 Jul 1998, Published online: 28 Mar 2023

REFERENCES

  • Burfoot, M. S., N. C. Rogers, D. Watling, J. M. Smith, S. Pons, G. Paonessaw, S. Pellegrini, M. F. White, and I. M. Kerr 1997. Janus kinase-dependent activation of insulin receptor substrate 1 in response to interleukin-4, oncostatin M, and the interferons. J. Biol. Chem. 272: 24183–24190.
  • Campbell, G., C. L. Yu, R. Jove, and C. Carter-Su 1997. Constitutive activation of JAK1 in Src-transformed cells. J. Biol. Chem. 272: 2591–2594.
  • Cao, X., A. Tay, G. R. Guy, and Y. H. Tan 1996. Activation and association of Stat3 with Src in v-Src-transformed cell lines. Mol. Cell. Biol. 16: 1595–1603.
  • Carlesso, N., D. A. Frank, and J. D. Griffin 1996. Tyrosyl phosphorylation and DNA binding activity of signal transducers and activators of transcription (STAT) proteins in hematopoietic cell lines transformed by Bcr/Abl. J. Exp. Med. 183: 811–820.
  • Chai, S. K., G. L. Nichols, and P. Rothman 1997. Constitutive activation of JAKs and STATs in BCR-Abl-expressing cell lines and peripheral blood cells derived form leukemic patients. J. Immunol. 159: 4720–4728.
  • Chaturvedi, P., S. Sharma, and E. P. Reddy 1997. Abrogation of interleukin-3 dependence of myeloid cells by the v-src oncogene requires SH2 and SH3 domains which specify activation of STATs. Mol. Cell. Biol. 17: 3295–3304.
  • Chen, S.-C., D. Redenius, J. C. Young, and R. C. Schwartz 1993. Synergy of IL-7 and v-Ha-ras in the in vitro neoplastic progression of murine pre-B cells. Oncogene 8: 2119–2125.
  • Cleveland, J. L., M. Dean, N. Rosenberg, J. Y. J. Wang, and U. R. Rapp 1989. Tyrosine kinase oncogenes abrogate interleukin-3 dependence of murine myeloid cells through signaling pathways involving c-myc: conditional regulation of c-myc transcription by temperature-sensitive v-abl. Mol. Cell. Biol. 9: 5685–5695.
  • Danial, N. N., A. Pernis, and P. B. Rothman 1995. Jak-STAT signaling induced by the v-Abl oncogene. Science 269: 1875–1877.
  • Danial, N. N., and P. B. Rothman. Unpublished results.
  • de Rooij, J., and J. L. Bos 1997. Minimal Ras-binding domain of Raf1 can be used as an activation-specific probe for Ras. Oncogene 14: 623–625.
  • Dorsch, M., P.-D. Fan, N. N. Danial, P. B. Rothman, and S. P. Goff 1997. The thrombopoietin receptor can mediate proliferation without activation of the Jak-STAT pathway. J. Exp. Med. 186: 1947–1955.
  • Downward, J. 1997. Role of phosphoinositide-3-OH kinase in Ras signaling. Adv. Second Messenger Phosphoprotein Res. 31: 1–10.
  • Ellis, C., M. Moran, F. McCormick, and T. Pawson 1990. Phosphorylation of GAP and GAP-associated proteins by transforming and mitogenic tyrosine kinases. Nature 343: 377–381.
  • Ernst, T. J., K. E. Slattery, and J. D. Griffin 1994. p210Bcr/Abl and p160v-Abl induce an increase in the tyrosine phosphorylation of p93c-Fes. J. Biol. Chem. 269: 5764–5769.
  • Fainstein, E., M. Einat, E. Gokkel, C. Marcelle, C. M. Croce, R. P. Gale, and E. Canaani 1989. Nucleotide sequence analysis of human ABL and BCR-ABL cDNAs. Oncogene 4: 1477–1481.
  • Feller, S. M., B. Knudsen, and H. Hanafusa 1994. c-Abl kinase regulates the protein binding activity of c-Crk. EMBO J. 13: 2341–2351.
  • Frangioni, J. V., and B. G. Neel 1993. Solubilization and purification of enzymatically active glutathione S-transferase (pGEX) fusion proteins. Anal. Biochem. 210: 179–187.
  • Garcia, R., and R. Jove 1998. Activation of STAT transcription factors in oncogenic tyrosine kinase signaling. J. Biomed. Sci. 5: 79–85.
  • Hanratty, W. P., and C. R. Dearolf 1993. The Drosophila tumorous-lethal hematopoietic oncogene is a dominant mutation in the hopscotch locus. J. Gen. Genet. 238: 33–37.
  • Harrison, D. A., R. Binari, T. S. Nahreini, M. Gilman, and N. Perrimon 1995. Activation of a Drosophila Janus kinase (JAK) causes hematopoietic neoplasia and developmental defects. EMBO J. 14: 2857–2865.
  • Hevezi, P., K. Alin, and S. P. Goff 1993. Transforming activity and tissue tropism of hybrid retroviral genomes containing portions of the v-Abl and v-src oncogenes. Oncogene 8: 2413–2423.
  • Huebner, R. C., A. Engelman, L. Schiff, and N. Rosenberg 1988. Abelson virus sequences important in lymphoid transformation B cell development. In: Klineman, N., O. N. Witte, and M. Howard257–270Raven Press, New York, N.Y.
  • Ilaria, R. L.Jr., and R. A. Van Etten 1996. P120 and P190BCR/ABL induce the tyrosine phosphorylation and DNA binding activity of multiple specific STAT family members. J. Biol. Chem. 271: 31704–31710.
  • Jackson, P., and D. Baltimore 1989. N-terminal mutations activate the leukemogenic potential of the myristoylated form of c-abl. EMBO J. 8: 449–456.
  • Kipreos, E. T., and J. Y. J. Wang 1992. Cell cycle-regulated binding of c-Abl tyrosine kinase to DNA. Science 256: 382–385.
  • Kipreos, E. T., and J. Y. J. Wang 1990. Differential phosphorylation of c-Abl tyrosine kinase in cell cycle determined by cdc2 kinase and phosphatase activity. Science 248: 217–220.
  • Krishnan, K., R. Pine, and J. J. Krolewski 1997. Kinase-deficient forms of Jak 1 and Tyk 2 inhibit interferon α signaling in a dominant manner. Eur. J. Biochem. 247: 298–305.
  • Lacronique, V., A. Boureux, V. Della Valle, H. Poirel, C. T. Quang, M. Mauchauffe, C. Berthou, M. Lessard, R. Berger, J. Ghysdael, and O. A. Bernard 1997. A TEL-JAK2 fusion protein with constitutive kinase activity in human leukemia. Science 278: 1309–1312.
  • Leonard, W. J., and J. J. O’Shea 1998. JAKS and STATS: biological implications. Annu. Rev. Immunol. 16: 293–322.
  • Mathey-Prevot, B., G. Nabel, R. Palacios, and D. Baltimore 1986. Abelson virus abrogation of interleukin-3 dependence in a lymphoid cell line. Mol. Cell. Biol. 6: 4133–4135.
  • Mayer, B. J., P. K. Jackson, R. A. Van Etten, and D. Baltimore 1992. Point mutations in the abl SH2 domain coordinately impair phosphotyrosine binding in vitro and transforming activity in vivo. Mol. Cell. Biol. 12: 609–618.
  • McWhirther, J. R., and J. Y. J. Wang 1991. Activation of tyrosine kinase and microfilament-binding functions of c-Abl by bcr sequences in bcr/abl fusion proteins. Mol. Cell. Biol. 11: 1553–1565.
  • Miao, Y.-J., and J. Y. J. Wang 1996. Binding of A/T-rich DNA by three high mobility group-like domains in c-Abl tyrosine kinase. J. Biol. Chem. 271: 22823–22830.
  • Murtach, K., G. Skladany, J. Hoag, and N. Rosenberg 1986. Abelson murine leukemia virus variants with increased oncogenic potential. J. Virol. 60: 599–606.
  • O’Shea, J. J. 1997. Jaks, STATs, cytokine signal transduction, and immunoregulation: are we there yet? Immunity 7: 1–11.
  • Owen-Lynch, P. J., A. K. Y. Wong, and A. D. Whetton 1995. v-Abl-mediated apoptosis suppression is associated with SHC phosphorylation without concomitant mitogen-activated protein kinase activation. J. Biol. Chem. 270: 5956–5962.
  • Parmar, K., and N. Rosenberg 1996. Ras complements the carboxyl terminus of v-Abl protein in lymphoid transformation. J. Virol. 70: 1009–1015.
  • Peeters, P., S. D. Raynaud, J. Cools, I. Wlodarska, J. Grosgeorge, P. Philip, F. Monpoux, L. V. Rompaey, M. Baens, H. Van den Berghe, and P. Marynen 1997. Fusion of TEL, the ETS-variant gene 6 (ETV6), to the receptor-associated kinase Jak2 as a result of t(9;12) in a lymphoid and t(9;15;12) in a myeloid leukemia. Blood 90: 2535–2540.
  • Pendergast, A. M., J. A. Traugh, and O. N. Witte 1987. Normal cellular and transformation-associated abl proteins share common sites for protein kinase C phosphorylation. Mol. Cell. Biol. 7: 4280–4289.
  • Pendergast, A. M., L. A. Quilliam, L. D. Cripe, G. H. Bassing, Z. Dai, N. Li, A. Batzer, K. M. Rabun, C. J. Der, J. Schlessinger, and M. Gishizky 1993. BCR-ABL-induced oncogenesis is mediated by direct interaction with the SH2 domain of the Grb-2 adaptor protein. Cell 75: 175–185.
  • Prywes, R., J. G. Foulkes, N. Rosenberg, and D. Baltimore 1983. Sequences of the A-MuLV protein needed for fibroblast and lymphoid cell transformation. Cell 34: 569–579.
  • Prywes, R., J. Hoag, N. Rosenberg, and D. Baltimore 1985. Protein stabilization explains the gag requirement for transformation of lymphoid cells by Abelson murine leukemia virus. J. Virol. 54: 123–132.
  • Ren, R., Z.-S. Ye, and D. Baltimore 1994. Abl protein-tyrosine kinase selects the Crk adapter as a substrate using SH3-binding sites. Genes Dev. 8: 783–795.
  • Renshaw, M. W., E. T. Kipreos, M. R. Albrecht, and J. Y. J. Wang 1992. Oncogenic v-Abl tyrosine kinase can inhibit or stimulate growth depending on the cell context. EMBO J. 11: 3941–3951.
  • Renshaw, M. W., E. Lea-Chou, and J. Y. J. Wang 1995. Rac is required for v-Abl tyrosine kinase to activate mitogenesis. Curr. Biol. 6: 76–83.
  • Rosenberg, N. 1994. abl-mediated transformation, immunoglobulin gene rearrangements and arrest of B lymphocyte differentiation. Semin. Cancer Biol. 5: 95–102.
  • Rosenberg, N., and O. N. Witte 1980. Abelson murine leukemia virus mutants with alteration in the virus-specific p120 molecule. J. Virol. 33: 340–348.
  • Sawyers, C. L., W. Callahan, and O. N. Witte 1992. Dominant negative MYC blocks transformation by ABL oncogenes. Cell 70: 901–910.
  • Sawyers, C. L., J. McLaughlin, and O. N. Witte 1995. Genetic requirement for Ras in the transformation of fibroblasts and hematopoietic cells by the Bcr-Abl oncogene. J. Exp. Med. 181: 307–313.
  • Shi, Y., K. Alin, and S. P. Goff 1995. Abl-interactor-1, a novel SH3 protein binding to the carboxy-terminal portion of the Abl protein, suppresses v-Abl transforming activity. Genes Dev. 9: 2583–2597.
  • Shuai, K., J. Halpern, J. T. Hoeve, X. Rao, and C. L. Sawyers 1996. Constitutive activation of STAT5 by the BCR-ABL oncogene in chronic myelogenous leukemia. Oncogene 13: 247–254.
  • Van Beveren, C., J. Coffin, and S. Hughes 1985. Pages 852–866. RNA tumor viruses In: Weiss, R., N. Teich, H. Varmus, and J. Coffin2 Cold Spring Harbor Laboratory Press, Cold Spring Harbor, N.Y.
  • Van Etten, R. A., P. K. Jackson, D. Baltimore, M. C. Sanders, P. T. Matsudaira, and P. A. Janmey 1989. The COOH terminus of the c-Abl tyrosine kinase contains distinct F- and G-actin binding domains with bundling activity. J. Cell Biol. 124: 235–240.
  • Varticovski, L., G. Q. Daley, P. Jackson, D. Baltimore, and L. C. Cantley 1991. Activation of phosphatidylinositol 3-kinase in cells expressing abl oncogene variants. Mol. Cell. Biol. 11: 1107–1113.
  • Welch, P. J., and J. Y. J. Wang 1993. A C-terminal protein-binding domain in the retinoblastoma protein regulates nuclear c-Abl tyrosine kinase in the cell cycle. Cell 75: 779–790.
  • Winston, L. A., and T. Hunter 1996. Intracellular signalling: putting JAKs on the kinase MAP. Curr. Biol. 6: 668–671.
  • Yamanashi, Y., and D. Baltimore 1997. Identification of the Abl and rasGAP-associated 62 kDa protein as a docking protein, Dok. Cell 88: 205–211.
  • Young, J. C., M. L. Gishizky, and O. N. Witte 1991. Hyperexpression of interleukin-7 is not necessary or sufficient for transformation of a pre-B-lymphoid cell line. Mol. Cell. Biol. 11: 854–863.

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