Transformation of hematopoietic cells by BCR/ABL requires activation of a PI-3k/Akt-dependent pathway.
about
Akt and mTOR in B Cell Activation and DifferentiationUV induces phosphorylation of protein kinase B (Akt) at Ser-473 and Thr-308 in mouse epidermal C1 41 cells through hydrogen peroxideActivation of protein kinase B beta and gamma isoforms by insulin in vivo and by 3-phosphoinositide-dependent protein kinase-1 in vitro: comparison with protein kinase B alphaThe PI3K-PDK1 connection: more than just a road to PKBTLS/FUS, a pro-oncogene involved in multiple chromosomal translocations, is a novel regulator of BCR/ABL-mediated leukemogenesis.Role for the adaptor protein Grb10 in the activation of AktMolecular cloning of Ian4: a BCR/ABL-induced gene that encodes an outer membrane mitochondrial protein with GTP-binding activitySwitching Akt: from survival signaling to deadly responseRegulation of G1 progression by the PTEN tumor suppressor protein is linked to inhibition of the phosphatidylinositol 3-kinase/Akt pathwayDepletion of Pleckstrin homology domain leucine-rich repeat protein phosphatases 1 and 2 by Bcr-Abl promotes chronic myelogenous leukemia cell proliferation through continuous phosphorylation of Akt isoformsKinase-independent mechanisms of resistance of leukemia stem cells to tyrosine kinase inhibitorsNuclear export of proteins and drug resistance in cancerA potent and highly specific FN3 monobody inhibitor of the Abl SH2 domainNovel targeted therapies for Bcr-Abl positive acute leukemias: beyond STI571.Transformation of myeloid leukemia cells to cytokine independence by Bcr-Abl is suppressed by kinase-defective HckTC21 mediates transformation and cell survival via activation of phosphatidylinositol 3-kinase/Akt and NF-kappaB signaling pathwayThe interaction of the Bcr-Abl tyrosine kinase with the Src kinase Hck is mediated by multiple binding domainsThe PIM kinases in hematological cancersModulation of Akt and ERK1/2 pathways by resveratrol in chronic myelogenous leukemia (CML) cells results in the downregulation of Hsp70Inhibition of class II phosphoinositide 3-kinase gamma expression by p185(Bcr-Abl) contributes to impaired chemotaxis and aberrant homing of leukemic cellsIdentification of drug combinations containing imatinib for treatment of BCR-ABL+ leukemiasIcaritin shows potent anti-leukemia activity on chronic myeloid leukemia in vitro and in vivo by regulating MAPK/ERK/JNK and JAK2/STAT3 /AKT signalingsSrc family kinases phosphorylate the Bcr-Abl SH3-SH2 region and modulate Bcr-Abl transforming activity.Phosphatidylinositol 3-kinase p85{alpha} subunit-dependent interaction with BCR/ABL-related fusion tyrosine kinases: molecular mechanisms and biological consequences.The Src family kinase Hck couples BCR/ABL to STAT5 activation in myeloid leukemia cells.Progressive changes in the leukemogenic signaling in BCR/ABL-transformed cells.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 malignancySignal transducer and activator of transcription (STAT)5 activation by BCR/ABL is dependent on intact Src homology (SH)3 and SH2 domains of BCR/ABL and is required for leukemogenesisc-Myb and its target Bmi1 are required for p190BCR/ABL leukemogenesis in mouse and human cellsRequirement of c-Myb for p210(BCR/ABL)-dependent transformation of hematopoietic progenitors and leukemogenesisChanges in the proteome associated with the action of Bcr-Abl tyrosine kinase are not related to transcriptional regulation.Suppression of apoptosis induced by growth factor withdrawal by an oncogenic form of c-Cbl.Tumor suppression by phospholipase C-beta3 via SHP-1-mediated dephosphorylation of Stat5.A BCR-ABL mutant lacking direct binding sites for the GRB2, CBL and CRKL adapter proteins fails to induce leukemia in miceA non-Smad mechanism of fibroblast activation by transforming growth factor-beta via c-Abl and Egr-1: selective modulation by imatinib mesylate.Targeting the phosphoinositide 3-kinase pathway in hematologic malignanciesBeneficial effects of mood stabilizers lithium, valproate and lamotrigine in experimental stroke models.Combination of the ABL kinase inhibitor imatinib with the Janus kinase 2 inhibitor TG101348 for targeting residual BCR-ABL-positive cells.The PTEN/MMAC1 tumor suppressor phosphatase functions as a negative regulator of the phosphoinositide 3-kinase/Akt pathway.AKT2 is a downstream target of metabotropic glutamate receptor 1 (Grm1).
P2860
Q21131224-E5224AEE-F9F7-441E-A8B4-C145350F3523Q23911187-DAECB193-7D4F-4E6C-AF68-7183D159AE64Q24530736-B19C8FC6-A527-4460-8907-24CC97853350Q24531972-148A1101-D212-4607-B5C4-4B6B9B6A8B92Q24533281-3F5EA140-F4DE-4A4C-9D75-96C83B632BC4Q24537512-DB3E785F-DE0C-4C85-ABFA-11625F797D93Q24613207-FAAB09DE-70D6-4796-A611-5938AAE3C82CQ24632379-42E99C9B-F699-4331-AD4A-ABAE4D5DB50CQ24653458-34924168-52DA-4393-955D-F92D9BA4FB11Q24658292-8BED8B59-82AF-4DFF-874F-7282DB0A258FQ26849792-1A72D8A2-E655-4B26-BBA6-2FF087E00B47Q27012444-4C5C49E2-609F-4506-9CCA-2558745B3C32Q27660385-368BA293-6217-417E-BA0F-D4F97A61F2F3Q27824789-97F68D66-98A1-41BF-A541-A6F745316938Q28138004-1C9A52EC-0E4F-4534-9FEB-BF100DA27FFAQ28202079-5DE1E4FE-61E5-42EA-9F64-A78B6A0DD167Q28210453-9C97C579-A714-41F4-9BF9-ABD1801C6CBDQ28258028-6A392812-4030-4E2D-94ED-C291E322BBB1Q28472533-660F3150-23D4-4C83-85B1-BC056E264796Q28512494-4F7C5727-1A02-4347-8ED6-2938539A30A1Q28540799-B6885182-0D11-44F9-BC79-DABDA3C378BDQ28741022-E277A9E8-43B8-4FE1-BE1B-D2057E5F2F37Q30159676-2BA65979-F19D-44E4-AA3F-D8C54BAC29A7Q30160146-0525BB1A-A42F-41A4-ABD2-0BA9B3F0986EQ30165112-763FECBB-82B4-4C40-B854-6859D3BB6CE3Q30168802-BFF937BE-3868-42CD-8C37-0F08F42ED279Q30175351-E9D70E17-CADD-439B-9A57-97F3825D0556Q30175784-9858C3EF-57BD-471A-8F87-CB24B17FCDDCQ30424785-31176B6D-E6EF-45DB-B57D-AB17D60E85E7Q30439716-B57B3BB5-0AE5-416A-8BF5-9A4A1A182A1AQ30875394-13EE5935-EC80-4AF7-A23D-4CF3CECF110CQ31672728-B36D7AF6-F276-405D-B0EF-0CA833523FC9Q33289385-1DCC16AD-19B1-4265-97F0-A2EFBC4A6011Q33510153-939827C2-66BE-4957-8AFF-678FD3D3AF5AQ33551475-A1076FFB-0C87-408C-9737-1C96FEE45F11Q33558141-ACFB94B4-CB26-46D4-B2E4-F655A54FE9D9Q33566724-FBBE04F2-E6EE-48AD-BBBC-190CFCEE2753Q33576089-1570C73F-300C-47F4-879D-E30EB0A19B5FQ33599964-D241D3DB-B597-4359-82CD-37147FA0E20DQ33605016-DCA9DB0B-922D-42E6-9256-55A72A85AC60
P2860
Transformation of hematopoietic cells by BCR/ABL requires activation of a PI-3k/Akt-dependent pathway.
description
1997 nî lūn-bûn
@nan
1997 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած
@hyw
1997 թվականի հոտեմբերին հրատարակված գիտական հոդված
@hy
1997年の論文
@ja
1997年論文
@yue
1997年論文
@zh-hant
1997年論文
@zh-hk
1997年論文
@zh-mo
1997年論文
@zh-tw
1997年论文
@wuu
name
Transformation of hematopoieti ...... a PI-3k/Akt-dependent pathway.
@ast
Transformation of hematopoieti ...... a PI-3k/Akt-dependent pathway.
@en
Transformation of hematopoieti ...... a PI-3k/Akt-dependent pathway.
@nl
type
label
Transformation of hematopoieti ...... a PI-3k/Akt-dependent pathway.
@ast
Transformation of hematopoieti ...... a PI-3k/Akt-dependent pathway.
@en
Transformation of hematopoieti ...... a PI-3k/Akt-dependent pathway.
@nl
prefLabel
Transformation of hematopoieti ...... a PI-3k/Akt-dependent pathway.
@ast
Transformation of hematopoieti ...... a PI-3k/Akt-dependent pathway.
@en
Transformation of hematopoieti ...... a PI-3k/Akt-dependent pathway.
@nl
P2093
P2860
P356
P1433
P1476
Transformation of hematopoieti ...... a PI-3k/Akt-dependent pathway
@en
P2093
A Bellacosa
B Calabretta
D Perrotti
M Majewski
M Nieborowska-Skorska
P N Tsichlis
R Martinez
P2860
P304
P356
10.1093/EMBOJ/16.20.6151
P407
P577
1997-10-01T00:00:00Z