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Results: 1-7 |
Results: 7
Cooperation of BCR-ABL and AML1/MDS1/EVI1 in blocking myeloid differentiation and rapid induction of an acute myelogenous leukemia
Authors: Cuenco, GM Ren, RB
Citation: Gm. Cuenco et Rb. Ren, Cooperation of BCR-ABL and AML1/MDS1/EVI1 in blocking myeloid differentiation and rapid induction of an acute myelogenous leukemia, ONCOGENE, 20(57), 2001, pp. 8236-8248
The NH2-terminal coiled-coil domain and tyrosine 177 play important roles in induction of a myeloproliferative disease in mice by Bcr-Abl
Authors: Zhang, ZW Subrahmanyam, R Wong, R Gross, AW Ren, RB
Citation: Zw. Zhang et al., The NH2-terminal coiled-coil domain and tyrosine 177 play important roles in induction of a myeloproliferative disease in mice by Bcr-Abl, MOL CELL B, 21(3), 2001, pp. 840-853
The SH2 domain of Bcr-Abl is not required to induce a murine myeloproliferative disease; however, SH2 signaling influences disease latency and phenotype
Authors: Zhang, XW Wong, R Hao, SX Pear, WS Ren, RB
Citation: Xw. Zhang et al., The SH2 domain of Bcr-Abl is not required to induce a murine myeloproliferative disease; however, SH2 signaling influences disease latency and phenotype, BLOOD, 97(1), 2001, pp. 277-287
Bcr-Abl has a greater intrinsic capacity than v-Abl to induce the neoplastic expansion of myeloid cells
Authors: Gross, AW Ren, RB
Citation: Aw. Gross et Rb. Ren, Bcr-Abl has a greater intrinsic capacity than v-Abl to induce the neoplastic expansion of myeloid cells, ONCOGENE, 19(54), 2000, pp. 6286-6296
Expression of interferon consensus sequence binding protein (ICSBP) is downregulated in Bcr-Abl-induced murine chronic myelogenous leukemia-like disease, and forced coexpression of ICSBP inhibits Bcr-Abl-induced myeloproliferative disorder
Authors: Hao, SX Ren, RB
Citation: Sx. Hao et Rb. Ren, Expression of interferon consensus sequence binding protein (ICSBP) is downregulated in Bcr-Abl-induced murine chronic myelogenous leukemia-like disease, and forced coexpression of ICSBP inhibits Bcr-Abl-induced myeloproliferative disorder, MOL CELL B, 20(4), 2000, pp. 1149-1161
Polarized distribution of Bcr-Abl in migrating myeloid cells and co-localization of Bcr-Abl and its target proteins
Authors: Skourides, PA Perera, SA Ren, RB
Citation: Pa. Skourides et al., Polarized distribution of Bcr-Abl in migrating myeloid cells and co-localization of Bcr-Abl and its target proteins, ONCOGENE, 18(5), 1999, pp. 1165-1176
Bcr-Abl with an SH3 deletion retains the ability to induce a myeloproliferative disease in mice, yet c-Abl activated by an SH3 deletion induces only lymphoid malignancy
Authors: Gross, AW Zhang, XW Ren, RB
Citation: Aw. Gross et al., Bcr-Abl with an SH3 deletion retains the ability to induce a myeloproliferative disease in mice, yet c-Abl activated by an SH3 deletion induces only lymphoid malignancy, MOL CELL B, 19(10), 1999, pp. 6918-6928
Risultati: 1-7 |