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by
Nathan, Sarah Ruth, author.
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cellular energetics. Acute overload of mitochondrial calcium will induce cell death and is implicated in
by
Si, Yuan, author.
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functions and increased vulnerability to death. Great efforts have been spent to study the mechanisms
by
Kubiak, Jeffrey M., author.
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-mediated cell death. Finally, in Chapter 4, we outline future uses for our synthetic circuit to dissect the
by
Kim, Hanna, author.
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mitochondrial dynamics, autophagy, and cell death pathways, which can ultimately manifest as DA
by
Schultz, Laura Elizabeth, author.
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-dependent programmed cell death. Together these results suggest distinct requirements for Rbbp4 in neural
by
Uddin, Mohammad Burhan, author.
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), and resensitized SW48/TP53-Dox cells to anticancer drugs and induced apoptotic cell death and reduced
by
Host, Kurtis Matthew, author.
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death 1 (PD-1) receptor on T cells. PD-1:PD-L1 engagement blocks T cell receptor (TCR) signaling
by
Liu, Qi, author.
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tumor cell death and long-term memory immune responses.
by
Sivathanu, Vivek, author.
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death, and intracellular organelle damage. None of these downsides actually present themselves with f
by
Rushing, Amanda Williams, author.
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reactive oxygen species, and the prevention of oxidative stress-induced cell death. We also evaluated the
by
Guo, Rui, author.
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-culturing PRRSV-infected cells with uninfected cells rescued PRRSV-induced cell death. Mitochondrion was observed
by
Yu, Diankun, author.
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differently expressed genes (DEGs) in gene ontology (GO) terms of cell death, neuron projection development

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