The Experts below are selected from a list of 55413 Experts worldwide ranked by ideXlab platform

Juan L. Iovanna - One of the best experts on this subject based on the ideXlab platform.

  • Tumor necrosis factor α triggers Antiapoptotic mechanisms in rat pancreatic cells through pancreatitis-associated protein I activation
    Gastroenterology, 2000
    Co-Authors: David Malka, Sophie Vasseur, Jean-charles Dagorn, Patrick Verrando, Nelson Dusetti, Hans Bödeker, Emilia M. Ortiz, Juan L. Iovanna
    Abstract:

    Abstract Background & Aims: Tumor necrosis factor (TNF)-α contributes to the development of acute pancreatitis. Because TNF-α is involved in the control of apoptosis, we studied its interaction with the pancreatic apoptotic pathway. Methods: Pancreatic acinar AR4-2J cells were used. Apoptosis was monitored by morphologic and biochemical criteria. Results: TNF-α induced apoptosis in AR4-2J cells. Induction was strongly enhanced in cells treated with actinomycin D, suggesting that TNF-α activated concomitantly an Antiapoptotic mechanism through newly synthesized proteins. This mechanism involved activation of nuclear factor–κB (NF-κB) and mitogen-activated protein (MAP) kinases because their inhibition worsened TNF-α–induced apoptosis. The Antiapoptotic pancreatitis-associated protein (PAP) I is a candidate for mediating TNF-α activity. Its expression is induced by TNF-α, and cells overexpressing PAP I show significantly less apoptosis on exposure to TNF-α. We examined whether TNF-α induction of PAP I expression was mediated by NF-κB or MAP kinases by using specific inhibitors of both pathways. Inhibition of NF-κB had no effect. However, inhibitors of MEK1 eliminated PAP I induction. Conclusions: TNF-α induces concomitantly proapoptotic and Antiapoptotic mechanisms in pancreatic AR4-2J cells. Antiapoptotic mechanisms are mediated by NF-κB and MAP kinases, and PAP I is one of the effectors of apoptosis inhibition. GASTROENTEROLOGY 2000;119:816-828

  • Tumor necrosis factor α triggers Antiapoptotic mechanisms in rat pancreatic cells through pancreatitis-associated protein I activation
    Gastroenterology, 2000
    Co-Authors: David Malka, Sophie Vasseur, Jean-charles Dagorn, Patrick Verrando, Nelson Dusetti, Hans Bödeker, Emilia M. Ortiz, Juan L. Iovanna
    Abstract:

    Tumor necrosis factor (TNF)-alpha contributes to the development of acute pancreatitis. Because TNF-alpha is involved in the control of apoptosis, we studied its interaction with the pancreatic apoptotic pathway. Pancreatic acinar AR4-2J cells were used. Apoptosis was monitored by morphologic and biochemical criteria. TNF-alpha induced apoptosis in AR4-2J cells. Induction was strongly enhanced in cells treated with actinomycin D, suggesting that TNF-alpha activated concomitantly an Antiapoptotic mechanism through newly synthesized proteins. This mechanism involved activation of nuclear factor-kappaB (NF-kappaB) and mitogen-activated protein (MAP) kinases because their inhibition worsened TNF-alpha-induced apoptosis. The Antiapoptotic pancreatitis-associated protein (PAP) I is a candidate for mediating TNF-alpha activity. Its expression is induced by TNF-alpha, and cells overexpressing PAP I show significantly less apoptosis on exposure to TNF-alpha. We examined whether TNF-alpha induction of PAP I expression was mediated by NF-kappaB or MAP kinases by using specific inhibitors of both pathways. Inhibition of NF-kappaB had no effect. However, inhibitors of MEK1 eliminated PAP I induction. TNF-alpha induces concomitantly proapoptotic and Antiapoptotic mechanisms in pancreatic AR4-2J cells. Antiapoptotic mechanisms are mediated by NF-kappaB and MAP kinases, and PAP I is one of the effectors of apoptosis inhibition.

David Malka - One of the best experts on this subject based on the ideXlab platform.

  • Tumor necrosis factor α triggers Antiapoptotic mechanisms in rat pancreatic cells through pancreatitis-associated protein I activation
    Gastroenterology, 2000
    Co-Authors: David Malka, Sophie Vasseur, Jean-charles Dagorn, Patrick Verrando, Nelson Dusetti, Hans Bödeker, Emilia M. Ortiz, Juan L. Iovanna
    Abstract:

    Abstract Background & Aims: Tumor necrosis factor (TNF)-α contributes to the development of acute pancreatitis. Because TNF-α is involved in the control of apoptosis, we studied its interaction with the pancreatic apoptotic pathway. Methods: Pancreatic acinar AR4-2J cells were used. Apoptosis was monitored by morphologic and biochemical criteria. Results: TNF-α induced apoptosis in AR4-2J cells. Induction was strongly enhanced in cells treated with actinomycin D, suggesting that TNF-α activated concomitantly an Antiapoptotic mechanism through newly synthesized proteins. This mechanism involved activation of nuclear factor–κB (NF-κB) and mitogen-activated protein (MAP) kinases because their inhibition worsened TNF-α–induced apoptosis. The Antiapoptotic pancreatitis-associated protein (PAP) I is a candidate for mediating TNF-α activity. Its expression is induced by TNF-α, and cells overexpressing PAP I show significantly less apoptosis on exposure to TNF-α. We examined whether TNF-α induction of PAP I expression was mediated by NF-κB or MAP kinases by using specific inhibitors of both pathways. Inhibition of NF-κB had no effect. However, inhibitors of MEK1 eliminated PAP I induction. Conclusions: TNF-α induces concomitantly proapoptotic and Antiapoptotic mechanisms in pancreatic AR4-2J cells. Antiapoptotic mechanisms are mediated by NF-κB and MAP kinases, and PAP I is one of the effectors of apoptosis inhibition. GASTROENTEROLOGY 2000;119:816-828

  • Tumor necrosis factor α triggers Antiapoptotic mechanisms in rat pancreatic cells through pancreatitis-associated protein I activation
    Gastroenterology, 2000
    Co-Authors: David Malka, Sophie Vasseur, Jean-charles Dagorn, Patrick Verrando, Nelson Dusetti, Hans Bödeker, Emilia M. Ortiz, Juan L. Iovanna
    Abstract:

    Tumor necrosis factor (TNF)-alpha contributes to the development of acute pancreatitis. Because TNF-alpha is involved in the control of apoptosis, we studied its interaction with the pancreatic apoptotic pathway. Pancreatic acinar AR4-2J cells were used. Apoptosis was monitored by morphologic and biochemical criteria. TNF-alpha induced apoptosis in AR4-2J cells. Induction was strongly enhanced in cells treated with actinomycin D, suggesting that TNF-alpha activated concomitantly an Antiapoptotic mechanism through newly synthesized proteins. This mechanism involved activation of nuclear factor-kappaB (NF-kappaB) and mitogen-activated protein (MAP) kinases because their inhibition worsened TNF-alpha-induced apoptosis. The Antiapoptotic pancreatitis-associated protein (PAP) I is a candidate for mediating TNF-alpha activity. Its expression is induced by TNF-alpha, and cells overexpressing PAP I show significantly less apoptosis on exposure to TNF-alpha. We examined whether TNF-alpha induction of PAP I expression was mediated by NF-kappaB or MAP kinases by using specific inhibitors of both pathways. Inhibition of NF-kappaB had no effect. However, inhibitors of MEK1 eliminated PAP I induction. TNF-alpha induces concomitantly proapoptotic and Antiapoptotic mechanisms in pancreatic AR4-2J cells. Antiapoptotic mechanisms are mediated by NF-kappaB and MAP kinases, and PAP I is one of the effectors of apoptosis inhibition.

Emilia M. Ortiz - One of the best experts on this subject based on the ideXlab platform.

  • Tumor necrosis factor α triggers Antiapoptotic mechanisms in rat pancreatic cells through pancreatitis-associated protein I activation
    Gastroenterology, 2000
    Co-Authors: David Malka, Sophie Vasseur, Jean-charles Dagorn, Patrick Verrando, Nelson Dusetti, Hans Bödeker, Emilia M. Ortiz, Juan L. Iovanna
    Abstract:

    Abstract Background & Aims: Tumor necrosis factor (TNF)-α contributes to the development of acute pancreatitis. Because TNF-α is involved in the control of apoptosis, we studied its interaction with the pancreatic apoptotic pathway. Methods: Pancreatic acinar AR4-2J cells were used. Apoptosis was monitored by morphologic and biochemical criteria. Results: TNF-α induced apoptosis in AR4-2J cells. Induction was strongly enhanced in cells treated with actinomycin D, suggesting that TNF-α activated concomitantly an Antiapoptotic mechanism through newly synthesized proteins. This mechanism involved activation of nuclear factor–κB (NF-κB) and mitogen-activated protein (MAP) kinases because their inhibition worsened TNF-α–induced apoptosis. The Antiapoptotic pancreatitis-associated protein (PAP) I is a candidate for mediating TNF-α activity. Its expression is induced by TNF-α, and cells overexpressing PAP I show significantly less apoptosis on exposure to TNF-α. We examined whether TNF-α induction of PAP I expression was mediated by NF-κB or MAP kinases by using specific inhibitors of both pathways. Inhibition of NF-κB had no effect. However, inhibitors of MEK1 eliminated PAP I induction. Conclusions: TNF-α induces concomitantly proapoptotic and Antiapoptotic mechanisms in pancreatic AR4-2J cells. Antiapoptotic mechanisms are mediated by NF-κB and MAP kinases, and PAP I is one of the effectors of apoptosis inhibition. GASTROENTEROLOGY 2000;119:816-828

  • Tumor necrosis factor α triggers Antiapoptotic mechanisms in rat pancreatic cells through pancreatitis-associated protein I activation
    Gastroenterology, 2000
    Co-Authors: David Malka, Sophie Vasseur, Jean-charles Dagorn, Patrick Verrando, Nelson Dusetti, Hans Bödeker, Emilia M. Ortiz, Juan L. Iovanna
    Abstract:

    Tumor necrosis factor (TNF)-alpha contributes to the development of acute pancreatitis. Because TNF-alpha is involved in the control of apoptosis, we studied its interaction with the pancreatic apoptotic pathway. Pancreatic acinar AR4-2J cells were used. Apoptosis was monitored by morphologic and biochemical criteria. TNF-alpha induced apoptosis in AR4-2J cells. Induction was strongly enhanced in cells treated with actinomycin D, suggesting that TNF-alpha activated concomitantly an Antiapoptotic mechanism through newly synthesized proteins. This mechanism involved activation of nuclear factor-kappaB (NF-kappaB) and mitogen-activated protein (MAP) kinases because their inhibition worsened TNF-alpha-induced apoptosis. The Antiapoptotic pancreatitis-associated protein (PAP) I is a candidate for mediating TNF-alpha activity. Its expression is induced by TNF-alpha, and cells overexpressing PAP I show significantly less apoptosis on exposure to TNF-alpha. We examined whether TNF-alpha induction of PAP I expression was mediated by NF-kappaB or MAP kinases by using specific inhibitors of both pathways. Inhibition of NF-kappaB had no effect. However, inhibitors of MEK1 eliminated PAP I induction. TNF-alpha induces concomitantly proapoptotic and Antiapoptotic mechanisms in pancreatic AR4-2J cells. Antiapoptotic mechanisms are mediated by NF-kappaB and MAP kinases, and PAP I is one of the effectors of apoptosis inhibition.

Hans Bödeker - One of the best experts on this subject based on the ideXlab platform.

  • Tumor necrosis factor α triggers Antiapoptotic mechanisms in rat pancreatic cells through pancreatitis-associated protein I activation
    Gastroenterology, 2000
    Co-Authors: David Malka, Sophie Vasseur, Jean-charles Dagorn, Patrick Verrando, Nelson Dusetti, Hans Bödeker, Emilia M. Ortiz, Juan L. Iovanna
    Abstract:

    Abstract Background & Aims: Tumor necrosis factor (TNF)-α contributes to the development of acute pancreatitis. Because TNF-α is involved in the control of apoptosis, we studied its interaction with the pancreatic apoptotic pathway. Methods: Pancreatic acinar AR4-2J cells were used. Apoptosis was monitored by morphologic and biochemical criteria. Results: TNF-α induced apoptosis in AR4-2J cells. Induction was strongly enhanced in cells treated with actinomycin D, suggesting that TNF-α activated concomitantly an Antiapoptotic mechanism through newly synthesized proteins. This mechanism involved activation of nuclear factor–κB (NF-κB) and mitogen-activated protein (MAP) kinases because their inhibition worsened TNF-α–induced apoptosis. The Antiapoptotic pancreatitis-associated protein (PAP) I is a candidate for mediating TNF-α activity. Its expression is induced by TNF-α, and cells overexpressing PAP I show significantly less apoptosis on exposure to TNF-α. We examined whether TNF-α induction of PAP I expression was mediated by NF-κB or MAP kinases by using specific inhibitors of both pathways. Inhibition of NF-κB had no effect. However, inhibitors of MEK1 eliminated PAP I induction. Conclusions: TNF-α induces concomitantly proapoptotic and Antiapoptotic mechanisms in pancreatic AR4-2J cells. Antiapoptotic mechanisms are mediated by NF-κB and MAP kinases, and PAP I is one of the effectors of apoptosis inhibition. GASTROENTEROLOGY 2000;119:816-828

  • Tumor necrosis factor α triggers Antiapoptotic mechanisms in rat pancreatic cells through pancreatitis-associated protein I activation
    Gastroenterology, 2000
    Co-Authors: David Malka, Sophie Vasseur, Jean-charles Dagorn, Patrick Verrando, Nelson Dusetti, Hans Bödeker, Emilia M. Ortiz, Juan L. Iovanna
    Abstract:

    Tumor necrosis factor (TNF)-alpha contributes to the development of acute pancreatitis. Because TNF-alpha is involved in the control of apoptosis, we studied its interaction with the pancreatic apoptotic pathway. Pancreatic acinar AR4-2J cells were used. Apoptosis was monitored by morphologic and biochemical criteria. TNF-alpha induced apoptosis in AR4-2J cells. Induction was strongly enhanced in cells treated with actinomycin D, suggesting that TNF-alpha activated concomitantly an Antiapoptotic mechanism through newly synthesized proteins. This mechanism involved activation of nuclear factor-kappaB (NF-kappaB) and mitogen-activated protein (MAP) kinases because their inhibition worsened TNF-alpha-induced apoptosis. The Antiapoptotic pancreatitis-associated protein (PAP) I is a candidate for mediating TNF-alpha activity. Its expression is induced by TNF-alpha, and cells overexpressing PAP I show significantly less apoptosis on exposure to TNF-alpha. We examined whether TNF-alpha induction of PAP I expression was mediated by NF-kappaB or MAP kinases by using specific inhibitors of both pathways. Inhibition of NF-kappaB had no effect. However, inhibitors of MEK1 eliminated PAP I induction. TNF-alpha induces concomitantly proapoptotic and Antiapoptotic mechanisms in pancreatic AR4-2J cells. Antiapoptotic mechanisms are mediated by NF-kappaB and MAP kinases, and PAP I is one of the effectors of apoptosis inhibition.

Nelson Dusetti - One of the best experts on this subject based on the ideXlab platform.

  • Tumor necrosis factor α triggers Antiapoptotic mechanisms in rat pancreatic cells through pancreatitis-associated protein I activation
    Gastroenterology, 2000
    Co-Authors: David Malka, Sophie Vasseur, Jean-charles Dagorn, Patrick Verrando, Nelson Dusetti, Hans Bödeker, Emilia M. Ortiz, Juan L. Iovanna
    Abstract:

    Abstract Background & Aims: Tumor necrosis factor (TNF)-α contributes to the development of acute pancreatitis. Because TNF-α is involved in the control of apoptosis, we studied its interaction with the pancreatic apoptotic pathway. Methods: Pancreatic acinar AR4-2J cells were used. Apoptosis was monitored by morphologic and biochemical criteria. Results: TNF-α induced apoptosis in AR4-2J cells. Induction was strongly enhanced in cells treated with actinomycin D, suggesting that TNF-α activated concomitantly an Antiapoptotic mechanism through newly synthesized proteins. This mechanism involved activation of nuclear factor–κB (NF-κB) and mitogen-activated protein (MAP) kinases because their inhibition worsened TNF-α–induced apoptosis. The Antiapoptotic pancreatitis-associated protein (PAP) I is a candidate for mediating TNF-α activity. Its expression is induced by TNF-α, and cells overexpressing PAP I show significantly less apoptosis on exposure to TNF-α. We examined whether TNF-α induction of PAP I expression was mediated by NF-κB or MAP kinases by using specific inhibitors of both pathways. Inhibition of NF-κB had no effect. However, inhibitors of MEK1 eliminated PAP I induction. Conclusions: TNF-α induces concomitantly proapoptotic and Antiapoptotic mechanisms in pancreatic AR4-2J cells. Antiapoptotic mechanisms are mediated by NF-κB and MAP kinases, and PAP I is one of the effectors of apoptosis inhibition. GASTROENTEROLOGY 2000;119:816-828

  • Tumor necrosis factor α triggers Antiapoptotic mechanisms in rat pancreatic cells through pancreatitis-associated protein I activation
    Gastroenterology, 2000
    Co-Authors: David Malka, Sophie Vasseur, Jean-charles Dagorn, Patrick Verrando, Nelson Dusetti, Hans Bödeker, Emilia M. Ortiz, Juan L. Iovanna
    Abstract:

    Tumor necrosis factor (TNF)-alpha contributes to the development of acute pancreatitis. Because TNF-alpha is involved in the control of apoptosis, we studied its interaction with the pancreatic apoptotic pathway. Pancreatic acinar AR4-2J cells were used. Apoptosis was monitored by morphologic and biochemical criteria. TNF-alpha induced apoptosis in AR4-2J cells. Induction was strongly enhanced in cells treated with actinomycin D, suggesting that TNF-alpha activated concomitantly an Antiapoptotic mechanism through newly synthesized proteins. This mechanism involved activation of nuclear factor-kappaB (NF-kappaB) and mitogen-activated protein (MAP) kinases because their inhibition worsened TNF-alpha-induced apoptosis. The Antiapoptotic pancreatitis-associated protein (PAP) I is a candidate for mediating TNF-alpha activity. Its expression is induced by TNF-alpha, and cells overexpressing PAP I show significantly less apoptosis on exposure to TNF-alpha. We examined whether TNF-alpha induction of PAP I expression was mediated by NF-kappaB or MAP kinases by using specific inhibitors of both pathways. Inhibition of NF-kappaB had no effect. However, inhibitors of MEK1 eliminated PAP I induction. TNF-alpha induces concomitantly proapoptotic and Antiapoptotic mechanisms in pancreatic AR4-2J cells. Antiapoptotic mechanisms are mediated by NF-kappaB and MAP kinases, and PAP I is one of the effectors of apoptosis inhibition.