RIPK1 protein, human

Known as: Receptor-Interacting Serine/Threonine Kinase 1, receptor (TNFRSF)-interacting serine-threonine kinase 1, human, RIP Protein Kinase 
Receptor-interacting serine/threonine-protein kinase 1 (671 aa, ~76 kDa) is encoded by the human RIPK1 gene. This protein plays a role in signaling… (More)
National Institutes of Health

Papers overview

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Review
2017
Review
2017
Necroptosis is a form of regulated cell death, which is induced by ligand binding to TNF family death domain receptors, pattern… (More)
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Highly Cited
2014
Highly Cited
2014
Necroptosis has emerged as an important pathway of programmed cell death in embryonic development, tissue homeostasis, immunity… (More)
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Highly Cited
2014
Highly Cited
2014
Upon ligand binding, RIPK1 is recruited to tumor necrosis factor receptor superfamily (TNFRSF) and Toll-like receptor (TLR… (More)
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Highly Cited
2014
Highly Cited
2014
Receptor-interacting protein kinase (RIPK)-1 is involved in RIPK3-dependent and -independent signaling pathways leading to cell… (More)
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Highly Cited
2010
Highly Cited
2010
Polycomb proteins play essential roles in stem cell renewal and human disease. Recent studies of HOX genes and X inactivation… (More)
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Highly Cited
2009
Highly Cited
2009
Smac mimetics induce apoptosis synergistically with TNF-alpha by triggering the formation of a caspase-8-activating complex… (More)
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Highly Cited
2004
Highly Cited
2004
Angiogenesis inhibitors are receiving increased attention as cancer therapeutics, but little is known of the cellular effects of… (More)
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Highly Cited
1997
Highly Cited
1997
AMPA glutamate receptors mediate the majority of rapid excitatory synaptic transmission in the central nervous system1,2 and play… (More)
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Highly Cited
1996
Highly Cited
1996
Through its type 1 receptor (TNFR1), the cytokine TNF elicits an unusually wide range of biological responses, including… (More)
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Highly Cited
1996
Highly Cited
1996
The death domain of tumor necrosis factor (TNF) receptor-1 (TNFR1) triggers distinct signaling pathways leading to apoptosis and… (More)
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