K. Kuida

Publications51
h-index25
Citations8,179
Highly Influential Citations258
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Decreased apoptosis in the brain and premature lethality in CPP32-deficient mice
PROGRAMMED cell death (apoptosis) is a prominent feature of the development of the immune and nervous systems1,2. The identification of the Caenorhabditis elegans cell death gene, ced-3, as a… Expand
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The Birc1e cytosolic pattern-recognition receptor contributes to the detection and control of Legionella pneumophila infection
Baculovirus inhibitor of apoptosis repeat-containing 1 (Birc1) proteins have homology to several germline-encoded receptors of the innate immune system. However, their function in immune surveillance… Expand
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Reduced Apoptosis and Cytochrome c–Mediated Caspase Activation in Mice Lacking Caspase 9
Caspases are essential components of the mammalian cell death machinery. Here we test the hypothesis that Caspase 9 (Casp9) is a critical upstream activator of caspases through gene targeting in… Expand
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Activation of the STAT signaling pathway can cause expression of caspase 1 and apoptosis.
Protein tyrosine kinases activate the STAT (signal transducer and activator of transcription) signaling pathway, which can play essential roles in cell differentiation, cell cycle control, and… Expand
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Inhibition of autophagy prevents hippocampal pyramidal neuron death after hypoxic-ischemic injury.
Neonatal hypoxic/ischemic (H/I) brain injury causes neurological impairment, including cognitive and motor dysfunction as well as seizures. However, the molecular mechanisms regulating neuron death… Expand
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Apoptosis initiated by Bcl-2-regulated caspase activation independently of the cytochrome c/Apaf-1/caspase-9 apoptosome
Apoptosis is an evolutionarily conserved cell suicide process executed by cysteine proteases (caspases) and regulated by the opposing factions of the Bcl-2 protein family. Mammalian caspase-9 and its… Expand
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Caspase Inhibition Extends the Commitment to Neuronal Death Beyond Cytochrome c Release to the Point of Mitochondrial Depolarization
Nerve growth factor (NGF) deprivation induces a Bax-dependent, caspase-dependent programmed cell death in sympathetic neurons. We examined whether the release of cytochrome c was accompanied by the… Expand
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Caspase-2 is not required for thymocyte or neuronal apoptosis even though cleavage of caspase-2 is dependent on both Apaf-1 and caspase-9
We have generated rat monoclonal antibodies that specifically recognise caspase-2 from many species, including mouse, rat and humans. Using these antibodies, we have investigated caspase-2… Expand
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Transforming growth factor beta-dependent sequential activation of Smad, Bim, and caspase-9 mediates physiological apoptosis in gastric epithelial cells.
Transforming growth factor beta (TGF-beta) has been implicated in the maintenance of homeostasis in various organs, including the gastric epithelium. In particular, TGF-beta-induced signaling was… Expand
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Caspase knockouts: matters of life and death
Apoptosis, the seemingly counter-intuitive act of physiological cell suicide, is accomplished by an evolutionarily conserved death program that is centered on the activation of a group of… Expand
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