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Michael S.-S. Su

Researcher at Vertex Pharmaceuticals

Publications -  25
Citations -  7751

Michael S.-S. Su is an academic researcher from Vertex Pharmaceuticals. The author has contributed to research in topics: Mitogen-activated protein kinase & MAP kinase kinase kinase. The author has an hindex of 21, co-authored 25 publications receiving 7538 citations.

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Reduced Apoptosis and Cytochrome c-Mediated Caspase Activation in Mice Lacking Caspase 9

TL;DR: Results indicate that Casp9 is a critical upstream activator of the caspase cascade in vivo, as indicated by the absence of Casp3-like cleavage and the restoration of cytochrome c-mediated cleavage after addition of in vitro-translated Casp 9.
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Altered cytokine export and apoptosis in mice deficient in interleukin-1 beta converting enzyme

TL;DR: Thymocytes from ICE-/- mice were sensitive to apoptosis induced by dexamethasone or ionizing radiation, but were resistant to apoptoses induced by Fas antibody, despite this defect in apoptosis.
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Activation of Interferon-γ Inducing Factor Mediated by Interleukin-1β Converting Enzyme

TL;DR: The interleukin-1 β converting enzyme (ICE) processes the inactive IL-1β precursor to the proinflammatory cytokine and cleave the precursor of interferon-γ inducing factor (IGIF) at the authentic processing site with high efficiency, thereby activating IGIF and facilitating its export.
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Interleukin-18 (ifngamma -inducing factor) induces il-8 and il-1beta via tnfalpha production from non-cd14+ human blood mononuclear cells

TL;DR: It is concluded that IL-18 possesses proinflammatory properties by direct stimulation of gene expression and synthesis of TNFalpha from CD3+/CD4+ and natural killer cells with subsequent production of IL-1beta and IL-8 from the CD14+ population.
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Extracellular signal-regulated kinase 2 is necessary for mesoderm differentiation

TL;DR: ERK2 plays an essential role in mesoderm differentiation during embryonic development, and treatment of mutant ES cells with the mitogen-activated protein kinase kinase inhibitor PD184352 decreased total ERK activity and expression of the mesodermal marker brachyury, suggesting that ERK1 can compensate for ERK2 in vitro.