scholarly article | Q13442814 |
P2093 | author name string | Richard A Van Etten | |
Lyuba Varticovski | |||
Nari Harakawa | |||
Ryan P Million | |||
Sergei Roumiantsev | |||
P2860 | cites work | The Grb2 binding site is required for the induction of chronic myeloid leukemia-like disease in mice by the Bcr/Abl tyrosine kinase | Q22254573 |
Bcr-Abl oncoproteins bind directly to activators of the Ras signalling pathway | Q24324144 | ||
Chronic myelocytic leukemia with eosinophilia, t(9;12)(q34;p13), and ETV6-ABL gene rearrangement: case report and review of the literature | Q28198326 | ||
Cloning of p97/Gab2, the major SHP2-binding protein in hematopoietic cells, reveals a novel pathway for cytokine-induced gene activation | Q28609054 | ||
Critical role for Gab2 in transformation by BCR/ABL | Q28610046 | ||
Specific motifs recognized by the SH2 domains of Csk, 3BP2, fps/fes, GRB-2, HCP, SHC, Syk, and Vav | Q29615971 | ||
Autoinhibition of Bcr-Abl through its SH3 domain | Q30164601 | ||
Mutational analysis of the regulatory function of the c-Abl Src homology 3 domain | Q30167708 | ||
Chronic myelogenous leukemia blast cell proliferation is inhibited by peptides that disrupt Grb2-SoS complexes | Q30167948 | ||
Identification of an atypical Grb2 carboxyl-terminal SH3 domain binding site in Gab docking proteins reveals Grb2-dependent and -independent recruitment of Gab1 to receptor tyrosine kinases | Q30168876 | ||
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 | Q30175351 | ||
bcr-abl oncogene renders myeloid cell line factor independent: potential autocrine mechanism in chronic myeloid leukemia. | Q53524893 | ||
Il-3-dependent mouse clones that express B-220 surface antigen, contain Ig genes in germ-line configuration, and generate B lymphocytes in vivo. | Q54447711 | ||
Creation of deletion, insertion and substitution mutations using a single pair of primers and PCR | Q71575792 | ||
Retroviral vectors for production of interleukin-12 in the bone marrow to induce a graft-versus-leukemia effect | Q71871199 | ||
Cutting edge: gab2 mediates an inhibitory phosphatidylinositol 3'-kinase pathway in T cell antigen receptor signaling | Q73086137 | ||
BCR/ABL-negative chronic myeloid leukemia with ETV6/ABL fusion | Q73870300 | ||
Efficient and rapid induction of a chronic myelogenous leukemia-like myeloproliferative disease in mice receiving P210 bcr/abl-transduced bone marrow | Q77531813 | ||
Signal transduction pathways involved in BCR-ABL transformation | Q30176519 | ||
Mutant forms of growth factor-binding protein-2 reverse BCR-ABL-induced transformation | Q30192925 | ||
Introduction of a loss-of-function point mutation from the SH3 region of the Caenorhabditis elegans sem-5 gene activates the transforming ability of c-abl in vivo and abolishes binding of proline-rich ligands in vitro. | Q30193411 | ||
BCR-ABL-induced oncogenesis is mediated by direct interaction with the SH2 domain of the GRB-2 adaptor protein | Q30194769 | ||
Molecular cytogenetic and clinical findings in ETV6/ABL1-positive leukemia | Q31913748 | ||
Transplantable myeloproliferative disease induced in mice by an interleukin 6 retrovirus | Q33354120 | ||
Socs-1 inhibits TEL-JAK2-mediated transformation of hematopoietic cells through inhibition of JAK2 kinase activity and induction of proteasome-mediated degradation | Q33559005 | ||
Transformation of an interleukin 3-dependent hematopoietic cell line by the chronic myelogenous leukemia-specific P210bcr/abl protein | Q33682660 | ||
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 | Q33885920 | ||
Oncogenic v-Abl tyrosine kinase can inhibit or stimulate growth, depending on the cell context | Q33938463 | ||
The NH(2)-terminal coiled-coil domain and tyrosine 177 play important roles in induction of a myeloproliferative disease in mice by Bcr-Abl | Q33967112 | ||
Models of chronic myeloid leukemia | Q34214855 | ||
The novel activation of ABL by fusion to an ets-related gene, TEL. | Q34314786 | ||
Fusion of PDGF receptor beta to a novel ets-like gene, tel, in chronic myelomonocytic leukemia with t(5;12) chromosomal translocation | Q34340175 | ||
In vitro transformation of immature hematopoietic cells by the P210 BCR/ABL oncogene product of the Philadelphia chromosome | Q34347155 | ||
Genetic requirement for Ras in the transformation of fibroblasts and hematopoietic cells by the Bcr-Abl oncogene | Q36364351 | ||
The P190, P210, and P230 forms of the BCR/ABL oncogene induce a similar chronic myeloid leukemia-like syndrome in mice but have different lymphoid leukemogenic activity | Q36368162 | ||
Structural and signaling requirements for BCR-ABL-mediated transformation and inhibition of apoptosis | Q36555271 | ||
SH1 domain autophosphorylation of P210 BCR/ABL is required for transformation but not growth factor independence | Q36676458 | ||
The BCR-ABL oncogene transforms Rat-1 cells and cooperates with v-myc | Q36768150 | ||
Alternative forms of the BCR-ABL oncogene have quantitatively different potencies for stimulation of immature lymphoid cells | Q36776463 | ||
The noncatalytic src homology region 2 segment of abl tyrosine kinase binds to tyrosine-phosphorylated cellular proteins with high affinity | Q37378589 | ||
Oligomerization of the ABL tyrosine kinase by the Ets protein TEL in human leukemia | Q38354873 | ||
Transient response to imatinib mesylate (STI571) in a patient with the ETV6-ABL t(9;12) translocation | Q40645637 | ||
A coiled-coil oligomerization domain of Bcr is essential for the transforming function of Bcr-Abl oncoproteins | Q40657033 | ||
TEL-JAK2 constitutively activates the extracellular signal-regulated kinase (ERK), stress-activated protein/Jun kinase (SAPK/JNK), and p38 signaling pathways | Q40714424 | ||
Activation of c-Abl kinase activity and transformation by a chemical inducer of dimerization | Q40810145 | ||
Bcr-Abl has a greater intrinsic capacity than v-Abl to induce the neoplastic expansion of myeloid cells | Q40827710 | ||
The src homology 2 domain of Bcr/Abl is required for efficient induction of chronic myeloid leukemia-like disease in mice but not for lymphoid leukemogenesis or activation of phosphatidylinositol 3-kinase | Q40835186 | ||
The docking molecule gab2 is induced by lymphocyte activation and is involved in signaling by interleukin-2 and interleukin-15 but not other common gamma chain-using cytokines | Q40874856 | ||
CGP 57148, a tyrosine kinase inhibitor, inhibits the growth of cells expressing BCR-ABL, TEL-ABL, and TEL-PDGFR fusion proteins | Q41073724 | ||
p210BCR/ABL, p190BCR/ABL, and TEL/ABL activate similar signal transduction pathways in hematopoietic cell lines | Q41166915 | ||
Alternative signals to RAS for hematopoietic transformation by the BCR-ABL oncogene | Q41294331 | ||
kat: a high-efficiency retroviral transduction system for primary human T lymphocytes | Q41497070 | ||
Genetic analysis of protein tyrosine phosphatases | Q41732769 | ||
Tyrosine kinase activity and transformation potency of bcr-abl oncogene products. | Q41740883 | ||
Cell cycle-dependent activation of Ras. | Q42806454 | ||
PI 3-kinase activation in BCR/abl-transformed hematopoietic cells does not require interaction of p85 SH2 domains with p210 BCR/abl | Q42809591 | ||
Bcr-Abl efficiently induces a myeloproliferative disease and production of excess interleukin-3 and granulocyte-macrophage colony-stimulating factor in mice: a novel model for chronic myelogenous leukemia | Q42824835 | ||
The coiled-coil domain and Tyr177 of bcr are required to induce a murine chronic myelogenous leukemia-like disease by bcr/abl. | Q43945195 | ||
The Tel-Abl (ETV6-Abl) tyrosine kinase, product of complex (9;12) translocations in human leukemia, induces distinct myeloproliferative disease in mice | Q44010415 | ||
Haemopoietic transformation by the TEL/ABL oncogene. | Q47720679 | ||
Interleukin 3 and granulocyte-macrophage colony-stimulating factor are not required for induction of chronic myeloid leukemia-like myeloproliferative disease in mice by BCR/ABL. | Q53401270 | ||
The SH2 domain of P210BCR/ABL is not required for the transformation of hematopoietic factor-dependent cells | Q53459784 | ||
P433 | issue | 11 | |
P407 | language of work or name | English | Q1860 |
P921 | main subject | cell biology | Q7141 |
P304 | page(s) | 4685-95 | |
P577 | publication date | 2004-06-01 | |
P1433 | published in | Molecular and Cellular Biology | Q3319478 |
P1476 | title | A direct binding site for Grb2 contributes to transformation and leukemogenesis by the Tel-Abl (ETV6-Abl) tyrosine kinase | |
P478 | volume | 24 |
Q42369243 | A Case of Chronic Myeloid Leukemia With Rare Variant ETV6/ABL1 Rearrangement. |
Q35856940 | A novel Stat3 binding motif in Gab2 mediates transformation of primary hematopoietic cells by the Stk/Ron receptor tyrosine kinase in response to Friend virus infection |
Q37674393 | ABL1 rearrangements in T-cell acute lymphoblastic leukemia |
Q40325416 | Activation of the NF-kappaB pathway by the leukemogenic TEL-Jak2 and TEL-Abl fusion proteins leads to the accumulation of antiapoptotic IAP proteins and involves IKKalpha. |
Q37768752 | Acute leukemias with ETV6/ABL1 (TEL/ABL) fusion: poor prognosis and prenatal origin. |
Q37331221 | Characterization of leukemias with ETV6-ABL1 fusion |
Q47572594 | ETV6-ABL1 fusion combined with monosomy 7 in childhood B-precursor acute lymphoblastic leukemia |
Q54597920 | FLT3 is fused to ETV6 in a myeloproliferative disorder with hypereosinophilia and a t(12;13)(p13;q12) translocation. |
Q21245511 | Function, regulation and pathological roles of the Gab/DOS docking proteins |
Q26823140 | GAB2--a scaffolding protein in cancer |
Q39998279 | Gab adapter proteins as therapeutic targets for hematologic disease |
Q33421439 | Germline mutations in ETV6 are associated with thrombocytopenia, red cell macrocytosis and predisposition to lymphoblastic leukemia. |
Q46048561 | Identification and characterization of activating ABL1 1b kinase mutations: impact on sensitivity to ATP-competitive and allosteric ABL1 inhibitors |
Q34565011 | Inhibition of Grb2 expression demonstrates an important role in BCR–ABL-mediated MAPK activation and transformation of primary human hematopoietic cells |
Q46375245 | Intrinsic differences between the catalytic properties of the oncogenic NUP214-ABL1 and BCR-ABL1 fusion protein kinases |
Q35071103 | Kinase domain mutants of Bcr-Abl exhibit altered transformation potency, kinase activity, and substrate utilization, irrespective of sensitivity to imatinib |
Q37369589 | Myeloproliferative neoplasm with ETV6-ABL1 fusion: a case report and literature review |
Q24322676 | Phosphorylation-dependent binding of 14-3-3 terminates signalling by the Gab2 docking protein |
Q46361900 | SHP2 is required for BCR-ABL1-induced hematologic neoplasia. |
Q36443429 | Structure, regulation, signaling, and targeting of abl kinases in cancer |
Q54397331 | TEL/AML1-positive patients lacking TEL exon 5 resemble canonical TEL/AML1 cases. |
Q40235633 | The Src tyrosine kinase Hck is required for Tel-Abl- but not for Tel-Jak2-induced cell transformation. |
Q42253878 | The role of RAS effectors in BCR/ABL induced chronic myelogenous leukemia |
Q38061546 | Variant of ETV6/ABL1 gene is associated with leukemia phenotype |
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