The Experts below are selected from a list of 139533 Experts worldwide ranked by ideXlab platform
Richard Marais - One of the best experts on this subject based on the ideXlab platform.
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oncogenic braf induces melanoma cell invasion by downregulating the cgmp specific phosphodiesterase pde5a
Cancer Cell, 2011Co-Authors: Imanol Arozarena, Berta Sanchezlaorden, Leisl M Packer, Cristina Hidalgocarcedo, Robert Hayward, Amaya Viros, Erik Sahai, Richard MaraisAbstract:Summary We show that in melanoma cells oncogenic BRAF, acting through MEK and the transcription factor BRN2, downregulates the cGMP-specific phosphodiesterase PDE5A. Although PDE5A Downregulation causes a small decrease in proliferation, its major impact is to stimulate a dramatic increase in melanoma cell invasion. This is because PDE5A Downregulation leads to an increase in cGMP, which induces an increase in cytosolic Ca 2+ , stimulating increased contractility and inducing invasion. PDE5A Downregulation also this leads to an increase in short-term and long-term colonization of the lungs by melanoma cells. We do not observe this pathway in NRAS mutant melanoma or BRAF mutant colorectal cells. Thus, we show that in melanoma cells oncogenic BRAF induces invasion through Downregulation of PDE5A.
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oncogenic braf induces melanoma cell invasion by downregulating the cgmp specific phosphodiesterase pde5a
Faculty of Health; Institute of Health and Biomedical Innovation, 2011Co-Authors: Imanol Arozarena, Berta Sanchezlaorden, Leisl M Packer, Cristina Hidalgocarcedo, Robert Hayward, Amaya Viros, Erik Sahai, Richard MaraisAbstract:*This article is free to read on the publisher's website* We show that in melanoma cells oncogenic BRAF, acting through MEK and the transcription factor BRN2, downregulates the cGMP-specific phosphodiesterase PDE5A. Although PDE5A Downregulation causes a small decrease in proliferation, its major impact is to stimulate a dramatic increase in melanoma cell invasion. This is because PDE5A Downregulation leads to an increase in cGMP, which induces an increase in cytosolic Ca2+, stimulating increased contractility and inducing invasion. PDE5A Downregulation also this leads to an increase in short-term and long-term colonization of the lungs by melanoma cells. We do not observe this pathway in NRAS mutant melanoma or BRAF mutant colorectal cells. Thus, we show that in melanoma cells oncogenic BRAF induces invasion through Downregulation of PDE5A.
Giyoung Kim - One of the best experts on this subject based on the ideXlab platform.
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melittin induces bcl 2 and caspase 3 dependent apoptosis through Downregulation of akt phosphorylation in human leukemic u937 cells
Toxicon, 2008Co-Authors: Dongoh Moon, Yung Hyun Choi, Sungyong Park, Nam Deuk Kim, Chan Lee, Giyoung KimAbstract:Melittin (MEL), a major polypeptide in bee venom (BV), is known to inhibit proliferation and induce apoptosis in cancer cells. However, the molecular mechanisms involved in MEL-induced apoptosis have not been fully elucidated, especially in human leukemic cells. In the present study, we report that MEL induces apoptosis in leukemic U937 cells through downregulating Akt signal pathways. Furthermore, MEL-induced apoptosis was accompanied by Downregulation of Bcl-2 and activation of caspase-3. The induction of apoptosis also was accompanied by the Downregulation of the inhibitor of apoptosis protein (IAP) family proteins. Treatment of U937 cells with the caspase-3 inhibitor, z-DEVD-fmk, was capable of significantly restoring cell viability in MEL-treated cells. Additionally, the caspase-3 mediated apoptotic response was significantly attenuated in Bcl-2-overexpressing U937 cells treated with MEL. These results indicate that Downregulation of Bcl-2 plays a major role in activation of caspase-3 following MEL exposure. MEL also triggered Downregulation of Akt. LY294002 (an inhibitor of Akt) significantly decreased cell viability and increased the proportion of cells with sub-G1 phase DNA content. The results indicated that key regulators in MEL-induced apoptosis in human leukemic U937 cells include Bcl-2 and caspase-3, which are controlled through the Akt signaling pathway.
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key regulators in bee venom induced apoptosis are bcl 2 and caspase 3 in human leukemic u937 cells through Downregulation of erk and akt
International Immunopharmacology, 2006Co-Authors: Dongoh Moon, Yung Hyun Choi, Sungyong Park, Moonsoo Heo, Kicheon Kim, Cheol Park, Giyoung KimAbstract:Bee venom (BV) has been known to inhibit proliferation and induce apoptosis in cancer cells. However, the molecular mechanisms involved in BV-induced apoptosis are still uncharacterized in human leukemic cells. In the present study, we report that BV induces apoptosis in leukemic U937 cells through Downregulation of ERK and Akt signal pathway. Furthermore, BV-induced apoptosis was accompanied by Downregulation of Bcl-2, activation of caspase-3 and a subsequent poly(ADP-ribose)polymerase (PARP) cleavages. The induction of apoptosis also was accompanied by the Downregulation of the inhibitor of apoptosis protein (IAP) family proteins. Caspase-3 inhibitor, z-DEVD-fmk, was significantly capable of restoring cell viability and BV-induced apoptosis through caspase-3 activation was significantly attenuated in Bcl-2-overexpressing cells. These results indicate that Downregulation of Bcl-2 plays a major role in the initiation as an activator of a caspase-3 involved with BV-induced apoptosis. BV also triggered the activation of p38 MAPK and JNK, and Downregulation of ERK and Akt. PD98059 (an inhibitor of ERK) or LY294002 (an inhibitor of Akt), but not an inhibitor of p38 MAPK and JNK, significantly decreased cell viability and increased lactate dehydrogenase (LDH) release. The results indicated that key regulators in BV-induced apoptosis are Bcl-2 and caspase-3 in human leukemic U937 cells through Downregulation of the ERK and Akt signal pathway.
Imanol Arozarena - One of the best experts on this subject based on the ideXlab platform.
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oncogenic braf induces melanoma cell invasion by downregulating the cgmp specific phosphodiesterase pde5a
Cancer Cell, 2011Co-Authors: Imanol Arozarena, Berta Sanchezlaorden, Leisl M Packer, Cristina Hidalgocarcedo, Robert Hayward, Amaya Viros, Erik Sahai, Richard MaraisAbstract:Summary We show that in melanoma cells oncogenic BRAF, acting through MEK and the transcription factor BRN2, downregulates the cGMP-specific phosphodiesterase PDE5A. Although PDE5A Downregulation causes a small decrease in proliferation, its major impact is to stimulate a dramatic increase in melanoma cell invasion. This is because PDE5A Downregulation leads to an increase in cGMP, which induces an increase in cytosolic Ca 2+ , stimulating increased contractility and inducing invasion. PDE5A Downregulation also this leads to an increase in short-term and long-term colonization of the lungs by melanoma cells. We do not observe this pathway in NRAS mutant melanoma or BRAF mutant colorectal cells. Thus, we show that in melanoma cells oncogenic BRAF induces invasion through Downregulation of PDE5A.
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oncogenic braf induces melanoma cell invasion by downregulating the cgmp specific phosphodiesterase pde5a
Faculty of Health; Institute of Health and Biomedical Innovation, 2011Co-Authors: Imanol Arozarena, Berta Sanchezlaorden, Leisl M Packer, Cristina Hidalgocarcedo, Robert Hayward, Amaya Viros, Erik Sahai, Richard MaraisAbstract:*This article is free to read on the publisher's website* We show that in melanoma cells oncogenic BRAF, acting through MEK and the transcription factor BRN2, downregulates the cGMP-specific phosphodiesterase PDE5A. Although PDE5A Downregulation causes a small decrease in proliferation, its major impact is to stimulate a dramatic increase in melanoma cell invasion. This is because PDE5A Downregulation leads to an increase in cGMP, which induces an increase in cytosolic Ca2+, stimulating increased contractility and inducing invasion. PDE5A Downregulation also this leads to an increase in short-term and long-term colonization of the lungs by melanoma cells. We do not observe this pathway in NRAS mutant melanoma or BRAF mutant colorectal cells. Thus, we show that in melanoma cells oncogenic BRAF induces invasion through Downregulation of PDE5A.
Dongoh Moon - One of the best experts on this subject based on the ideXlab platform.
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melittin induces bcl 2 and caspase 3 dependent apoptosis through Downregulation of akt phosphorylation in human leukemic u937 cells
Toxicon, 2008Co-Authors: Dongoh Moon, Yung Hyun Choi, Sungyong Park, Nam Deuk Kim, Chan Lee, Giyoung KimAbstract:Melittin (MEL), a major polypeptide in bee venom (BV), is known to inhibit proliferation and induce apoptosis in cancer cells. However, the molecular mechanisms involved in MEL-induced apoptosis have not been fully elucidated, especially in human leukemic cells. In the present study, we report that MEL induces apoptosis in leukemic U937 cells through downregulating Akt signal pathways. Furthermore, MEL-induced apoptosis was accompanied by Downregulation of Bcl-2 and activation of caspase-3. The induction of apoptosis also was accompanied by the Downregulation of the inhibitor of apoptosis protein (IAP) family proteins. Treatment of U937 cells with the caspase-3 inhibitor, z-DEVD-fmk, was capable of significantly restoring cell viability in MEL-treated cells. Additionally, the caspase-3 mediated apoptotic response was significantly attenuated in Bcl-2-overexpressing U937 cells treated with MEL. These results indicate that Downregulation of Bcl-2 plays a major role in activation of caspase-3 following MEL exposure. MEL also triggered Downregulation of Akt. LY294002 (an inhibitor of Akt) significantly decreased cell viability and increased the proportion of cells with sub-G1 phase DNA content. The results indicated that key regulators in MEL-induced apoptosis in human leukemic U937 cells include Bcl-2 and caspase-3, which are controlled through the Akt signaling pathway.
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key regulators in bee venom induced apoptosis are bcl 2 and caspase 3 in human leukemic u937 cells through Downregulation of erk and akt
International Immunopharmacology, 2006Co-Authors: Dongoh Moon, Yung Hyun Choi, Sungyong Park, Moonsoo Heo, Kicheon Kim, Cheol Park, Giyoung KimAbstract:Bee venom (BV) has been known to inhibit proliferation and induce apoptosis in cancer cells. However, the molecular mechanisms involved in BV-induced apoptosis are still uncharacterized in human leukemic cells. In the present study, we report that BV induces apoptosis in leukemic U937 cells through Downregulation of ERK and Akt signal pathway. Furthermore, BV-induced apoptosis was accompanied by Downregulation of Bcl-2, activation of caspase-3 and a subsequent poly(ADP-ribose)polymerase (PARP) cleavages. The induction of apoptosis also was accompanied by the Downregulation of the inhibitor of apoptosis protein (IAP) family proteins. Caspase-3 inhibitor, z-DEVD-fmk, was significantly capable of restoring cell viability and BV-induced apoptosis through caspase-3 activation was significantly attenuated in Bcl-2-overexpressing cells. These results indicate that Downregulation of Bcl-2 plays a major role in the initiation as an activator of a caspase-3 involved with BV-induced apoptosis. BV also triggered the activation of p38 MAPK and JNK, and Downregulation of ERK and Akt. PD98059 (an inhibitor of ERK) or LY294002 (an inhibitor of Akt), but not an inhibitor of p38 MAPK and JNK, significantly decreased cell viability and increased lactate dehydrogenase (LDH) release. The results indicated that key regulators in BV-induced apoptosis are Bcl-2 and caspase-3 in human leukemic U937 cells through Downregulation of the ERK and Akt signal pathway.
Yung Hyun Choi - One of the best experts on this subject based on the ideXlab platform.
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maritoclax enhances trail induced apoptosis via chop mediated upregulation of dr5 and mir 708 mediated Downregulation of cflip
Molecules, 2018Co-Authors: Miyeon Jeon, Seon Min Woo, Seung Un Seo, Kyoung-jin Min, Yung Hyun Choi, Sanghyun Kim, Dongeun Kim, Taejin Lee, Shin Kim, Jongwook ParkAbstract:Maritoclax, an active constituent isolated from marine bacteria, has been known to induce Mcl-1 Downregulation through proteasomal degradation. In this study, we investigated the sensitizing effect of maritoclax on tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis in human renal carcinoma cells. We found that combined treatment with maritoclax and TRAIL markedly induced apoptosis in renal carcinoma (Caki, ACHN and A498), lung cancer (A549) and hepatocellular carcinoma (SK-Hep1) cells. The upregulation of death receptor 5 (DR5) and Downregulation of cellular FLICE-inhibitory protein (cFLIP) were involved in maritoclax plus TRAIL-induced apoptosis. Maritoclax-induced DR5 upregulation was regulated by induction of C/EBP homologous protein (CHOP) expression. Interestingly, maritoclax induced cFLIP Downregulation through the increased expression of miR-708. Ectopic expression of cFLIP prevented combined maritoclax and TRAIL-induced apoptosis. Taken together, maritoclax sensitized TRAIL-induced apoptosis through CHOP-mediated DR5 upregulation and miR-708-mediated cFLIP Downregulation.
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melittin induces bcl 2 and caspase 3 dependent apoptosis through Downregulation of akt phosphorylation in human leukemic u937 cells
Toxicon, 2008Co-Authors: Dongoh Moon, Yung Hyun Choi, Sungyong Park, Nam Deuk Kim, Chan Lee, Giyoung KimAbstract:Melittin (MEL), a major polypeptide in bee venom (BV), is known to inhibit proliferation and induce apoptosis in cancer cells. However, the molecular mechanisms involved in MEL-induced apoptosis have not been fully elucidated, especially in human leukemic cells. In the present study, we report that MEL induces apoptosis in leukemic U937 cells through downregulating Akt signal pathways. Furthermore, MEL-induced apoptosis was accompanied by Downregulation of Bcl-2 and activation of caspase-3. The induction of apoptosis also was accompanied by the Downregulation of the inhibitor of apoptosis protein (IAP) family proteins. Treatment of U937 cells with the caspase-3 inhibitor, z-DEVD-fmk, was capable of significantly restoring cell viability in MEL-treated cells. Additionally, the caspase-3 mediated apoptotic response was significantly attenuated in Bcl-2-overexpressing U937 cells treated with MEL. These results indicate that Downregulation of Bcl-2 plays a major role in activation of caspase-3 following MEL exposure. MEL also triggered Downregulation of Akt. LY294002 (an inhibitor of Akt) significantly decreased cell viability and increased the proportion of cells with sub-G1 phase DNA content. The results indicated that key regulators in MEL-induced apoptosis in human leukemic U937 cells include Bcl-2 and caspase-3, which are controlled through the Akt signaling pathway.
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key regulators in bee venom induced apoptosis are bcl 2 and caspase 3 in human leukemic u937 cells through Downregulation of erk and akt
International Immunopharmacology, 2006Co-Authors: Dongoh Moon, Yung Hyun Choi, Sungyong Park, Moonsoo Heo, Kicheon Kim, Cheol Park, Giyoung KimAbstract:Bee venom (BV) has been known to inhibit proliferation and induce apoptosis in cancer cells. However, the molecular mechanisms involved in BV-induced apoptosis are still uncharacterized in human leukemic cells. In the present study, we report that BV induces apoptosis in leukemic U937 cells through Downregulation of ERK and Akt signal pathway. Furthermore, BV-induced apoptosis was accompanied by Downregulation of Bcl-2, activation of caspase-3 and a subsequent poly(ADP-ribose)polymerase (PARP) cleavages. The induction of apoptosis also was accompanied by the Downregulation of the inhibitor of apoptosis protein (IAP) family proteins. Caspase-3 inhibitor, z-DEVD-fmk, was significantly capable of restoring cell viability and BV-induced apoptosis through caspase-3 activation was significantly attenuated in Bcl-2-overexpressing cells. These results indicate that Downregulation of Bcl-2 plays a major role in the initiation as an activator of a caspase-3 involved with BV-induced apoptosis. BV also triggered the activation of p38 MAPK and JNK, and Downregulation of ERK and Akt. PD98059 (an inhibitor of ERK) or LY294002 (an inhibitor of Akt), but not an inhibitor of p38 MAPK and JNK, significantly decreased cell viability and increased lactate dehydrogenase (LDH) release. The results indicated that key regulators in BV-induced apoptosis are Bcl-2 and caspase-3 in human leukemic U937 cells through Downregulation of the ERK and Akt signal pathway.
