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.
about
TEL is a sequence-specific transcriptional repressorActivation of FIP1L1-PDGFRalpha requires disruption of the juxtamembrane domain of PDGFRalpha and is FIP1L1-independentOncogenic targeting of an activated tyrosine kinase to the Golgi apparatus in a glioblastomaNative interface of the SAM domain polymer of TEL.Polymerization of the SAM domain of TEL in leukemogenesis and transcriptional repressionActivation of tyrosine kinases by mutation of the gatekeeper threonineYolk sac angiogenic defect and intra-embryonic apoptosis in mice lacking the Ets-related factor TELZNF198-FGFR1 transforms Ba/F3 cells to growth factor independence and results in high level tyrosine phosphorylation of STATS 1 and 5Phosphatidylinositol 3-kinase p85{alpha} subunit-dependent interaction with BCR/ABL-related fusion tyrosine kinases: molecular mechanisms and biological consequences.Signal transduction and cellular functions of the TEL/ARG oncoprotein.Genetic complementation of cytokine signaling identifies central role of kinases in hematopoietic cell proliferation.A current review of targeted therapeutics for ovarian cancer.STAT signaling in the pathogenesis and treatment of cancerTransformation of hematopoietic cell lines to growth-factor independence and induction of a fatal myelo- and lymphoproliferative disease in mice by retrovirally transduced TEL/JAK2 fusion genes.A single amino acid substitution in a WW-like domain of diverse members of the PDGF receptor subfamily of tyrosine kinases causes constitutive receptor activation.The ETV6-NTRK3 gene fusion encodes a chimeric protein tyrosine kinase that transforms NIH3T3 cells.Fatal myeloproliferation, induced in mice by TEL/PDGFbetaR expression, depends on PDGFbetaR tyrosines 579/581Signaling in leukemia: which messenger to kill?Cdk10, a Cdc2-related kinase, associates with the Ets2 transcription factor and modulates its transactivation activity.Both TEL and AML-1 contribute repression domains to the t(12;21) fusion protein.Stimulation of platelet-derived growth factor receptor beta (PDGFRbeta) activates ADAM17 and promotes metalloproteinase-dependent cross-talk between the PDGFRbeta and epidermal growth factor receptor (EGFR) signaling pathways.Proteins of the ETS family with transcriptional repressor activity.Expression of a homodimeric type I cytokine receptor is required for JAK2V617F-mediated transformation.Signal transduction and transforming properties of the TEL-TRKC fusions associated with t(12;15)(p13;q25) in congenital fibrosarcoma and acute myelogenous leukemia.Cellular signalling pathways: new targets in leukaemia therapy.Class III receptor tyrosine kinases: role in leukaemogenesis.Receptor tyrosine kinase mutations in myeloid neoplasms.Congenital mesoblastic nephroma t(12;15) is associated with ETV6-NTRK3 gene fusion: cytogenetic and molecular relationship to congenital (infantile) fibrosarcomaTHOC5 spliceosome protein: a target for leukaemogenic tyrosine kinases that affects inositol lipid turnover.PDGF induced microRNA alterations in cancer cells.The TEL/ETV6 gene is required specifically for hematopoiesis in the bone marrowBicc1 Polymerization Regulates the Localization and Silencing of Bound mRNA.The t(1;12)(q21;p13) translocation of human acute myeloblastic leukemia results in a TEL-ARNT fusion.Myeloproliferative disease induced by TEL-PDGFRB displays dynamic range sensitivity to Stat5 gene dosage.Evidence for a role of NF-kappaB in the survival of hematopoietic cells mediated by interleukin 3 and the oncogenic TEL/platelet-derived growth factor receptor beta fusion proteinGenetic alterations activating kinase and cytokine receptor signaling in high-risk acute lymphoblastic leukemia.Potentiation of antileukemic therapies by the dual PI3K/PDK-1 inhibitor, BAG956: effects on BCR-ABL- and mutant FLT3-expressing cells.Structure of the Ets-1 pointed domain and mitogen-activated protein kinase phosphorylation site.High-throughput sequence analysis of the tyrosine kinome in acute myeloid leukemia.Engineering a BCR-ABL-activated caspase for the selective elimination of leukemic cells
P2860
Q22010632-7B89E09F-8D7B-41A9-A360-DE039A4538A1Q24545984-66DCFB7C-02B3-41CC-BEED-331F31F5E137Q24599766-5DF90771-F32A-4222-B568-D9F6B046C184Q24801634-4BD6896B-BB78-4904-AEDC-59978126FA0BQ27633822-68561734-0EC4-4151-A72C-3BC3CCB1A0E9Q27652166-C93A9747-2FAD-426D-973C-04147491F162Q28592571-2072D901-5388-4107-87F4-449EB161B511Q28609080-1100887C-C397-4E71-AE54-E703F53FB63EQ30160146-B220E010-6BAB-45B7-84B7-60E38D27E57CQ30160307-A1FBE7BA-E3FB-4BC9-B2C4-2C88CF3395B4Q31029794-AC863399-4CEF-4B48-A449-CF2C4807DC47Q33580998-F9CAE0E4-3353-4C22-86A1-021AE983E380Q33712802-357399FD-8264-4DAC-A979-3017A1C5D15AQ33889476-08537790-AF9E-48EC-9567-931D620000B0Q33890119-6F636ADE-A41A-41BF-BE23-29668435302DQ33892265-C0AABF1A-A7AB-4603-A7EA-7DA3FC681FA9Q33939204-06E0E75C-6D23-4C5C-AA38-3EBC1B78DFF2Q33939607-0CAAF9E7-5E5F-4A2C-B55B-584B19662CE3Q33943441-3ADC5E49-6076-492E-AB50-6F912E68241AQ33959609-34D0E756-FC4E-4B56-A315-2EDD8AE75DCDQ34042804-8C341332-616F-4E1A-A858-254CE9AEAF9DQ34139422-A426992D-FF26-4773-B9BA-F9B9EFE5F820Q34245259-A3D8EBC9-96DD-45C5-91C1-CC3588F37190Q34486039-BA58F245-1B48-4577-9207-59E065B8C011Q34527660-BA1D839A-7748-4D32-A26C-A8F7D06731C9Q34557003-DC188500-8296-40E5-B706-CADAE9DD0F90Q34655403-ECEBA1F6-8D0E-490A-8FE7-F93557D7B9C0Q34754714-5FB1BAA0-E320-423E-BE18-AD4487D7513CQ34765282-8B1C0A48-8253-4326-B4CC-3E17B0EA9DBDQ35017837-ABAF4594-C1F0-4BFE-A9DA-80CBF8070992Q35206654-63FA9B0A-DE88-4EC5-BBA3-9ED1D14BB362Q35718106-8C02071A-EF87-4C29-85CF-2D16562F03EFQ35801750-7CBC23B9-B72A-4C8B-B334-D713568B00D6Q35804404-819870DA-DEF2-4CE1-BABE-41B4C29C2CFFQ36167190-9A713054-586B-4AA3-8EBF-AF9C25D19D5DQ36174146-057B1958-53EE-4B47-8B77-80DF656A2E53Q36508937-3F85126D-F06E-419A-ACD1-3354EDEB08DBQ36518727-E6DB80CC-5477-49CF-B7AE-14C205FC3787Q36591388-D0FF22DA-4992-447D-A9A8-EF59F24CEA77Q36598253-66FCEC76-9D0B-4C75-97F4-D93F173CFD18
P2860
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.
description
article científic
@ca
article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
@tr
scientific article published on December 1996
@en
vedecký článok
@sk
vetenskaplig artikel
@sv
videnskabelig artikel
@da
vědecký článek
@cs
name
The TEL/platelet-derived growt ...... -dependent signaling pathways.
@en
The TEL/platelet-derived growth factor beta receptor
@nl
type
label
The TEL/platelet-derived growt ...... -dependent signaling pathways.
@en
The TEL/platelet-derived growth factor beta receptor
@nl
prefLabel
The TEL/platelet-derived growt ...... -dependent signaling pathways.
@en
The TEL/platelet-derived growth factor beta receptor
@nl
P2093
P2860
P356
P1476
The TEL/platelet-derived growt ...... -dependent signaling pathways.
@en
P2093
D G Gilliland
G F Barker
M H Tomasson
P2860
P304
14845-14850
P356
10.1073/PNAS.93.25.14845
P407
P577
1996-12-01T00:00:00Z