C-Jun N-Terminal Kinases - Explore the Science & Experts | ideXlab

Scan Science and Technology

Contact Leading Edge Experts & Companies

C-Jun N-Terminal Kinases

The Experts below are selected from a list of 96 Experts worldwide ranked by ideXlab platform

Dai Ayusawa – 1st expert on this subject based on the ideXlab platform

  • Cardiolipin activates MAP Kinases during premature senescence in normal human fibroblasts
    Biogerontology, 2007
    Co-Authors: Palaniyappan Arivazhagan, Dai Ayusawa

    Abstract:

    Lipids are major structural components of cellular membranes and regulate various signaling pathways as a mediator of the signals or a source of new signals. Our earlier studies show that cardiolipin very sensitively induces premature senescence in normal human fibroblasts. To understand a molecular basis for the action of cardiolipin, we tested whether the mitogen-activated protein (MAP) kinase cascades have a role in the above phenomenon. As expected, cardiolipin activated phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2), C-Jun N-Terminal Kinases (JNK), and p38 map kinase (p38) of the MAP kinase family as in replicatively senesced cells. These results suggest that cardiolipin uses signaling pathways similar to those in replicative senescence to lead to premature senescence.

Maria Angelica Selim – 2nd expert on this subject based on the ideXlab platform

  • The role of the C-Jun N-Terminal Kinase signaling pathway in skin cancer
    American Journal of Cancer Research, 2012
    Co-Authors: Jennifer Y. Zhang, Maria Angelica Selim

    Abstract:

    The C-Jun N-Terminal Kinases (JNK), along with Erk and p38, constitute the principle members of the mitogen-activated protein kinase (MAPK) family. JNK functions primarily through AP1 family transcription factors to regulate a plethora of cellular processes, including cell proliferation, differentiation, survival and migration. It also cross-talks and integrates with other signaling pathways in a cell context-specific and cell type-specific manner. The current views of JNK function in various skin cancers and the need of developing JNK subunit-specific inhibitors for cancer type-specific applications have been summarized in this review.

  • Review Article The role of the C-Jun N-Terminal Kinase signaling pathway in skin cancer
    , 2012
    Co-Authors: Jennifer Y. Zhang, Maria Angelica Selim

    Abstract:

    The C-Jun N-Terminal Kinases (JNK), along with Erk and p38, constitute the principle members of the mitogen-activated protein kinase (MAPK) family. JNK functions primarily through AP1 family transcription factors to regulate a plethora of cellular processes, including cell proliferation, differentiation, survival and migration. It also cross-talks and integrates with other signaling pathways in a cell context-specific and cell type-specific manner. The current views of JNK function in various skin cancers and the need of developing JNK subunit-specific inhibitors for cancer type-specific applications have been summarized in this review.

Palaniyappan Arivazhagan – 3rd expert on this subject based on the ideXlab platform

  • Cardiolipin activates MAP Kinases during premature senescence in normal human fibroblasts
    Biogerontology, 2007
    Co-Authors: Palaniyappan Arivazhagan, Dai Ayusawa

    Abstract:

    Lipids are major structural components of cellular membranes and regulate various signaling pathways as a mediator of the signals or a source of new signals. Our earlier studies show that cardiolipin very sensitively induces premature senescence in normal human fibroblasts. To understand a molecular basis for the action of cardiolipin, we tested whether the mitogen-activated protein (MAP) kinase cascades have a role in the above phenomenon. As expected, cardiolipin activated phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2), C-Jun N-Terminal Kinases (JNK), and p38 map kinase (p38) of the MAP kinase family as in replicatively senesced cells. These results suggest that cardiolipin uses signaling pathways similar to those in replicative senescence to lead to premature senescence.