FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2980225087> ?p ?o ?g. }

• W2980225087 abstract "Abstract B-cell chronic lymphocytic leukemia (B-CLL) is the most common leukemia in adults and is characterized by the accumulation of mature B lymphocytes in the G0/G1 phase of the cell cycle, expressing B-cell related (i.e. CD19, surface immunoglobulins) and unrelated molecules (CD5 and CD23). The signal transduction pathways underlying the abnormalities of these leukemic cells are poorly understood and no data are available on deregulated cell signalling in B-CLL. Since Lyn activation plays a pivotal role in the signaling cascade triggered by BCR engagement, we investigated whether this kinase may be involved in CLL pathogenesis. In this study, we investigated freshly isolated and purified malignant B cells obtained from 40 CLL patients and we observed that the Src-kinase Lyn, the switch molecule coupling B-cell-receptor to downstream signaling, displays anomalous properties. Western blot and confocal analyses demonstrated that Lyn is overexpressed at the protein level in leukemic cells as compared to normal B-lymphocytes with a substantial aliquot of the kinase anomalously present in the cytosol of leukemic cells. While in normal B lymphocytes Lyn activation is triggered by B-cell-receptor engagement with anti-IgM antibodies, in freshly isolated leukemic cells this kinase is constitutively active and accounts for high basal protein tyrosine-phosphorylation and low responsiveness to IgM-ligation. To address the question of whether the upregulation of Lyn protein and activity plays a role in the defective apoptosis of leukemic cells, we investigated the relationship between Lyn and the cell survival of malignant lymphocytes in the presence of either dexamethazone and cyclosporin A, which are known to induce apoptosis of human lymphocytes, or PP2 and SU6656, which are selective inhibitors of Lyn. When leukemic cells were cultured in the presence of cyclosporin A or dexamethazone, a marked increase in apoptosis was observed as compared to cells cultured in medium alone, and this effect correlated with a great decrease in both basal activity and protein level of Lyn. The exposure of the leukemic cells to PP2 and SU6656 caused both the inhibition of the overexpressed Lyn activity and marked cell apoptosis. These findings suggest a direct correlation between high basal Lyn activity and defects in the induction of apoptosis in leukemic cells. They also support a critical role for Lyn in B-CLL pathogenesis and identify this tyrosine kinase as a potential therapeutic target for drugs capable of inducing apoptosis in B-CLL leukemic cells." @default.
• W2980225087 created "2019-10-18" @default.
• W2980225087 creator A5000434082 @default.
• W2980225087 creator A5002636444 @default.
• W2980225087 creator A5013236194 @default.
• W2980225087 creator A5042203481 @default.
• W2980225087 creator A5052547325 @default.
• W2980225087 creator A5058504277 @default.
• W2980225087 creator A5067581342 @default.
• W2980225087 creator A5078427766 @default.
• W2980225087 creator A5087722204 @default.
• W2980225087 date "2004-11-16" @default.
• W2980225087 modified "2023-10-16" @default.
• W2980225087 title "Leukemic B Cells from Patients with Chronic Lymphocytic Leukemia Show Anomalous Lyn Tyrosine Kinase which Contributes to Defective Apoptosis." @default.
• W2980225087 doi "https://doi.org/10.1182/blood.v104.11.1917.1917" @default.
• W2980225087 hasPublicationYear "2004" @default.
• W2980225087 type Work @default.
• W2980225087 sameAs 2980225087 @default.
• W2980225087 citedByCount "0" @default.
• W2980225087 crossrefType "journal-article" @default.
• W2980225087 hasAuthorship W2980225087A5000434082 @default.
• W2980225087 hasAuthorship W2980225087A5002636444 @default.
• W2980225087 hasAuthorship W2980225087A5013236194 @default.
• W2980225087 hasAuthorship W2980225087A5042203481 @default.
• W2980225087 hasAuthorship W2980225087A5052547325 @default.
• W2980225087 hasAuthorship W2980225087A5058504277 @default.
• W2980225087 hasAuthorship W2980225087A5067581342 @default.
• W2980225087 hasAuthorship W2980225087A5078427766 @default.
• W2980225087 hasAuthorship W2980225087A5087722204 @default.
• W2980225087 hasConcept C108636557 @default.
• W2980225087 hasConcept C157695867 @default.
• W2980225087 hasConcept C159654299 @default.
• W2980225087 hasConcept C170493617 @default.
• W2980225087 hasConcept C175818844 @default.
• W2980225087 hasConcept C184235292 @default.
• W2980225087 hasConcept C190283241 @default.
• W2980225087 hasConcept C203014093 @default.
• W2980225087 hasConcept C2777938653 @default.
• W2980225087 hasConcept C2778453870 @default.
• W2980225087 hasConcept C2778461978 @default.
• W2980225087 hasConcept C2778957590 @default.
• W2980225087 hasConcept C35174551 @default.
• W2980225087 hasConcept C42362537 @default.
• W2980225087 hasConcept C43907098 @default.
• W2980225087 hasConcept C502942594 @default.
• W2980225087 hasConcept C55493867 @default.
• W2980225087 hasConcept C62478195 @default.
• W2980225087 hasConcept C86803240 @default.
• W2980225087 hasConcept C95444343 @default.
• W2980225087 hasConceptScore W2980225087C108636557 @default.
• W2980225087 hasConceptScore W2980225087C157695867 @default.
• W2980225087 hasConceptScore W2980225087C159654299 @default.
• W2980225087 hasConceptScore W2980225087C170493617 @default.
• W2980225087 hasConceptScore W2980225087C175818844 @default.
• W2980225087 hasConceptScore W2980225087C184235292 @default.
• W2980225087 hasConceptScore W2980225087C190283241 @default.
• W2980225087 hasConceptScore W2980225087C203014093 @default.
• W2980225087 hasConceptScore W2980225087C2777938653 @default.
• W2980225087 hasConceptScore W2980225087C2778453870 @default.
• W2980225087 hasConceptScore W2980225087C2778461978 @default.
• W2980225087 hasConceptScore W2980225087C2778957590 @default.
• W2980225087 hasConceptScore W2980225087C35174551 @default.
• W2980225087 hasConceptScore W2980225087C42362537 @default.
• W2980225087 hasConceptScore W2980225087C43907098 @default.
• W2980225087 hasConceptScore W2980225087C502942594 @default.
• W2980225087 hasConceptScore W2980225087C55493867 @default.
• W2980225087 hasConceptScore W2980225087C62478195 @default.
• W2980225087 hasConceptScore W2980225087C86803240 @default.
• W2980225087 hasConceptScore W2980225087C95444343 @default.
• W2980225087 hasLocation W29802250871 @default.
• W2980225087 hasOpenAccess W2980225087 @default.
• W2980225087 hasPrimaryLocation W29802250871 @default.
• W2980225087 hasRelatedWork W1481677180 @default.
• W2980225087 hasRelatedWork W2005556418 @default.
• W2980225087 hasRelatedWork W2021494482 @default.
• W2980225087 hasRelatedWork W2100751415 @default.
• W2980225087 hasRelatedWork W2134495747 @default.
• W2980225087 hasRelatedWork W2135781988 @default.
• W2980225087 hasRelatedWork W2572838557 @default.
• W2980225087 hasRelatedWork W2601929339 @default.
• W2980225087 hasRelatedWork W2980225087 @default.
• W2980225087 hasRelatedWork W96390394 @default.
• W2980225087 isParatext "false" @default.
• W2980225087 isRetracted "false" @default.
• W2980225087 magId "2980225087" @default.
• W2980225087 workType "article" @default.