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Enhancing venetoclax activity in acute myeloid leukemia by co-targeting MCL1

Leukemia, 2018-02, Vol.32 (2), p.303-312

2018

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RIPK1- and RIPK3-induced cell death mode is determined by target availability

Cell death and differentiation, 2014-10, Vol.21 (10), p.1600-1612

2014

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TNF can activate RIPK3 and cause programmed necrosis in the absence of RIPK1

Cell death & disease, 2013-01, Vol.4 (1), p.e465-e465

2013

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Necroptosis induced by RIPK3 requires MLKL but not Drp1

Cell death & disease, 2014-02, Vol.5 (2), p.e1086-e1086

2014

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In mouse embryonic fibroblasts, neither caspase-8 nor cellular FLICE-inhibitory protein (FLIP) is necessary for TNF to activate NF-κB, but caspase-8 is required for TNF to cause cell death, and induction of FLIP by NF-κB is required to prevent it

Cell death and differentiation, 2012-05, Vol.19 (5), p.808-815

2012

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In mouse embryonic fibroblasts, neither caspase-8 nor cellular FLICE-inhibitory protein (FLIP) is necessary for TNF to activate NF-[kappa]B, but caspase-8 is required for TNF to cause cell death, and induction of FLIP by NF-[kappa]B is required to prevent it

Cell death and differentiation, 2012-05, Vol.19 (5), p.808

2012

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Phosphorylation of hnRNP K by cyclin-dependent kinase 2 controls cytosolic accumulation of TDP-43

Human molecular genetics, 2015-03, Vol.24 (6), p.1655-1669

2015

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TDP-43 mutations causing amyotrophic lateral sclerosis are associated with altered expression of RNA-binding protein hnRNP K and affect the Nrf2 antioxidant pathway

Human molecular genetics, 2017-05, Vol.26 (9), p.1732-1746

2017

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Mitochondrial apoptosis is dispensable for NLRP3 inflammasome activation but non-apoptotic caspase-8 is required for inflammasome priming

EMBO reports, 2014-09, Vol.15 (9), p.982-990

2014

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The MCL1 inhibitor S63845 is tolerable and effective in diverse cancer models

Nature (London), 2016-10, Vol.538 (7626), p.477-482

2016

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CREB-binding protein (CBP) regulates β-adrenoceptor (β-AR)-mediated apoptosis

Cell death and differentiation, 2013-07, Vol.20 (7), p.941-952

2013

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In TNF-stimulated cells, RIPK1 promotes cell survival by stabilizing TRAF2 and cIAP1, which limits induction of non-canonical NF-κB and activation of caspase-8

The Journal of biological chemistry, 2016-01, Vol.291 (5), p.2547-2547

2016

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Altered B-lymphopoiesis in mice with deregulated thrombopoietin signaling

Scientific reports, 2017-11, Vol.7 (1), p.14953-10, Article 14953

2017

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Proinflammatory microenvironment promotes lymphoma progression in mice with high megakaryocyte and TPO levels

Blood advances, 2023-04, Vol.7 (8), p.1560-1571

2023

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In TNF-stimulated Cells, RIPK1 Promotes Cell Survival by Stabilizing TRAF2 and cIAP1, which Limits Induction of Non-canonical NF-κB and Activation of Caspase-8

The Journal of biological chemistry, 2011-04, Vol.286 (15), p.13282-13291

2011

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Clinical MDR1 inhibitors enhance Smac-mimetic bioavailability to kill murine LSCs and improve survival in AML models

Blood advances, 2020-10, Vol.4 (20), p.5062-5077

2020

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CREB-binding protein (CBP) regulates [beta]-adrenoceptor ([beta]-AR)-mediated apoptosis

Cell death and differentiation, 2013-07, Vol.20 (7), p.941

2013

Volltextzugriff (PDF)

Mitochondrial apoptosis is dispensable for NLRP 3 inflammasome activation but non‐apoptotic caspase‐8 is required for inflammasome priming

EMBO reports, 2014-09, Vol.15 (9), p.982-990

2014

Volltextzugriff (PDF)

In TNF-stimulated cells, RIPK1 promotes cell survival by stabilizing TRAF2 and cIAP1, which limits induction of non-canonical NF-kappaB and activation of caspase-8

The Journal of biological chemistry, 2011-04, Vol.286 (15), p.13282-13291

2011

Volltextzugriff (PDF)

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Enhancing venetoclax activity in acute myeloid leukemia by co-targeting MCL1

RIPK1- and RIPK3-induced cell death mode is determined by target availability

TNF can activate RIPK3 and cause programmed necrosis in the absence of RIPK1

Necroptosis induced by RIPK3 requires MLKL but not Drp1

In mouse embryonic fibroblasts, neither caspase-8 nor cellular FLICE-inhibitory protein (FLIP) is necessary for TNF to activate NF-κB, but caspase-8 is required for TNF to cause cell death, and induction of FLIP by NF-κB is required to prevent it

In mouse embryonic fibroblasts, neither caspase-8 nor cellular FLICE-inhibitory protein (FLIP) is necessary for TNF to activate NF-[kappa]B, but caspase-8 is required for TNF to cause cell death, and induction of FLIP by NF-[kappa]B is required to prevent it

Phosphorylation of hnRNP K by cyclin-dependent kinase 2 controls cytosolic accumulation of TDP-43

TDP-43 mutations causing amyotrophic lateral sclerosis are associated with altered expression of RNA-binding protein hnRNP K and affect the Nrf2 antioxidant pathway

Mitochondrial apoptosis is dispensable for NLRP3 inflammasome activation but non-apoptotic caspase-8 is required for inflammasome priming

The MCL1 inhibitor S63845 is tolerable and effective in diverse cancer models

Intact TP-53 function is essential for sustaining durable responses to BH3-mimetic drugs in leukemias

CREB-binding protein (CBP) regulates β-adrenoceptor (β-AR)-mediated apoptosis

In TNF-stimulated cells, RIPK1 promotes cell survival by stabilizing TRAF2 and cIAP1, which limits induction of non-canonical NF-κB and activation of caspase-8

Altered B-lymphopoiesis in mice with deregulated thrombopoietin signaling

Proinflammatory microenvironment promotes lymphoma progression in mice with high megakaryocyte and TPO levels

In TNF-stimulated Cells, RIPK1 Promotes Cell Survival by Stabilizing TRAF2 and cIAP1, which Limits Induction of Non-canonical NF-κB and Activation of Caspase-8

Clinical MDR1 inhibitors enhance Smac-mimetic bioavailability to kill murine LSCs and improve survival in AML models

CREB-binding protein (CBP) regulates [beta]-adrenoceptor ([beta]-AR)-mediated apoptosis

Mitochondrial apoptosis is dispensable for NLRP 3 inflammasome activation but non‐apoptotic caspase‐8 is required for inflammasome priming

In TNF-stimulated cells, RIPK1 promotes cell survival by stabilizing TRAF2 and cIAP1, which limits induction of non-canonical NF-kappaB and activation of caspase-8

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