cyclic-gmp and Thymus-Neoplasms

cyclic-gmp has been researched along with Thymus-Neoplasms* in 1 studies

Other Studies

1 other study(ies) available for cyclic-gmp and Thymus-Neoplasms

Article	Year
HA1004, an inhibitor of serine/threonine protein kinases, restores the sensitivity of thymic lymphomas to Ca2+-mediated apoptosis through a protein kinase A-independent mechanism. International immunopharmacology, 2002, Volume: 2, Issue:4 Our previous reports showed that thymic lymphomas arising in TCR transgenic mice are resistant to Ca2+-mediated apoptosis. Here we show that induction of apoptosis in thymic lymphomas involves a process that is cAMP-mediated and which depends on the activation of protein kinase A (PKA) despite the lower level of PKA type I in these lymphomas compared to thymocytes. Further, we show that treatment of the lymphomas with HA1004, a serine/threonine protein kinase inhibitor, restores their susceptibility to ionomycin-induced apoptosis. Results indicate that HA1004-induced restoration of sensitivity to ionomycin proceeds through a PKA-independent mechanism. Moreover, activation of PKA instead of its inhibition induces apoptosis of lymphoma cells. Topics: Animals; Apoptosis; Calcium; Cyclic AMP; Cyclic AMP-Dependent Protein Kinases; Cyclic GMP; Enzyme Activation; Enzyme Inhibitors; Isoquinolines; Lymphoma; Mice; Protein Serine-Threonine Kinases; Signal Transduction; Sulfonamides; Thymus Neoplasms; Tumor Cells, Cultured	2002

Article

Year

HA1004, an inhibitor of serine/threonine protein kinases, restores the sensitivity of thymic lymphomas to Ca2+-mediated apoptosis through a protein kinase A-independent mechanism.

International immunopharmacology, 2002, Volume: 2, Issue:4

Our previous reports showed that thymic lymphomas arising in TCR transgenic mice are resistant to Ca2+-mediated apoptosis. Here we show that induction of apoptosis in thymic lymphomas involves a process that is cAMP-mediated and which depends on the activation of protein kinase A (PKA) despite the lower level of PKA type I in these lymphomas compared to thymocytes. Further, we show that treatment of the lymphomas with HA1004, a serine/threonine protein kinase inhibitor, restores their susceptibility to ionomycin-induced apoptosis. Results indicate that HA1004-induced restoration of sensitivity to ionomycin proceeds through a PKA-independent mechanism. Moreover, activation of PKA instead of its inhibition induces apoptosis of lymphoma cells.

Topics: Animals; Apoptosis; Calcium; Cyclic AMP; Cyclic AMP-Dependent Protein Kinases; Cyclic GMP; Enzyme Activation; Enzyme Inhibitors; Isoquinolines; Lymphoma; Mice; Protein Serine-Threonine Kinases; Signal Transduction; Sulfonamides; Thymus Neoplasms; Tumor Cells, Cultured

2002