Cell death mechanisms and regulation

PANoptosis, a combination of inflammatory cell death mechanisms, induced 1 by Ophiobolin A in breast cancer cell lines

This study shows that ophiobolin A induces PANoptosis in breast cancer cells through RIPK1-dependent mechanisms, leading to lytic and pro-inflammatory cell death.

Loofah, a newly characterized adhesion protein, suppresses cell death in long-lived Drosophila hindgut enterocytes

The paper identifies Loofah, an adhesion protein, as a suppressor of cell death in long-lived Drosophila hindgut enterocytes by maintaining FasIII membrane localization.

Early-peaking caspase-7 activity at the plasma membrane drives apoptotic phosphatidylserine exposure

This study identifies caspase-7 as responsible for early-peaking caspase activity at the plasma membrane during apoptosis, which drives phosphatidylserine exposure and efferocytosis.

Omics analysis reveals striking effects of progesterone receptor on mitochondria and mitochondria-mediated apoptosis independent of caspases in Breast Cancer cells

This study uses omics analysis to show that PR agonist R5020 induces anti-proliferative and proapoptotic effects in breast cancer cells through mitochondrial pathways independent of caspases.

Differential regulation of BAX and BAK apoptotic activity revealed by a novel small molecule

This study identifies a small molecule that differentially regulates BAX and BAK apoptotic activity by modulating their interaction with VDAC2, revealing therapeutic potential for overcoming drug resistance in leukemia.

Regeneration following tissue necrosis is mediated by non-apoptotic caspase activity

The paper investigates necrosis-induced regeneration in Drosophila, showing non-apoptotic caspase activity drives reparative proliferation independent of known mechanisms.

RIPK3-dependent sequential recruitment of MLKL and RIPK1 drives PANoptotic cell death and chemokine production

This study identifies a RIPK3-dependent PANoptosome assembly mechanism that integrates pyroptotic, apoptotic, and necroptotic pathways, driving immunogenic cell death and chemokine production.

Chemical Tools Based on the Tetrapeptide Sequence of IL-18 Reveals Shared Specificities between Inflammatory and Apoptotic Initiator Caspases

The paper develops a new peptide-based inhibitor targeting caspase-8 and reveals shared specificities between inflammatory and apoptotic caspases.

RIPK1 is essential for Herpes Simplex Virus-triggered ZBP1-dependent necroptosis in human cells

This study shows that RIPK1 is essential for ZBP1-dependent necroptosis in human cells but not in mice, highlighting a species-specific mechanism.

Inactivation of necroptosis-promoting protein MLKL creates a therapeutic vulnerability in colorectal cancer cells.

This study shows that inhibiting MLKL in colorectal cancer cells enhances their sensitivity to homoharringtonine, a drug that blocks autophagy, by disrupting VPS37A-dependent autophagy and triggering parthanatos.

Quantification of SARM1 activity in human peripheral blood mononuclear cells

This study quantifies SARM1 activity in human PBMCs using agonists and inhibitors, showing dose-dependent cAPDR increases and potential for clinical readouts.

Raver1 links Ripk1 RNA splicing to caspase-8-mediated pyroptotic cell death, inflammation, and pathogen resistance

This study identifies Raver1 as a regulator of Ripk1 RNA splicing, which affects caspase-8-mediated pyroptosis, inflammation, and resistance to Yersinia infection.

IAP antagonists potentiate TNFα-triggered apoptosis but selectively eliminate senescent tumor cells independently of TNFα

This study shows IAP antagonists induce apoptosis in senescent tumor cells both with and without TNF, suggesting they can eliminate TIS cells and sensitize non-senescent cells through TNF.

Lactoferrin-Derived Peptide Chimera Induces Caspase-independent Cell Death in Multiple Myeloma

This study shows lactoferrin-derived peptide chimera induces caspase-independent cell death in multiple myeloma cells by promoting nuclear translocation of apoptosis-inducing factor and endonuclease G.

Structural Basis for the Assembly of Amyloid Fibrils by the Master Cell-Signaling Regulator Human Receptor-Interacting Protein Kinase 1

This study determines the high-resolution structure of human RIPK1 homomeric amyloid fibrils, revealing structural differences from RIPK3 fibrils that inform necroptosis mechanisms.

Unraveling the molecular mechanism underlying the anticancer activity of CISD2/NAF-144-67

This study identifies how NAF-144-67 targets CISD2/NAF-1 in cancer cells, disrupts its dimeric structure, and enhances anticancer activity through dimeric forms.

Microsporidian Nosema bombycis secretes serine protease inhibitor to suppress host cell apoptosis via caspase BmICE

This paper identifies NbSPN14, a serine protease inhibitor secreted by Nosema bombycis, which inhibits host cell apoptosis by interacting with BmICE, providing insights into pathogen-host interactions.

An activation-based high throughput screen identifies caspase-10 inhibitors

This study identifies caspase-10 inhibitors using an activation-based high-throughput screen, revealing inhibitors that preferentially target the zymogen form of caspase-10.

Evidence for a RIPK1-independent survival mechanism for CASPASE-8 in αβ T cells

This study identifies a CASPASE8-dependent survival mechanism in CD8 T cells independent of RIPK1-mediated necroptosis suppression.

Developmental delay ensures global tissue size robustness upon local induction of apoptosis

The study shows that tissue size remains robust during mild apoptosis induction through a global growth delay rather than local proliferation, using Drosophila wing discs.

SARM1 Activation Promotes Axonal Degeneration Via a Two-Step Liquid-to-Solid Phase Transition

This study reveals a two-step liquid-to-solid phase transition mechanism by which SARM1 activation leads to axonal degeneration, with implications for therapeutic development.

LIN-35 and the DREAM complex promote temperature stress induced increases in germline apoptosis and cytoplasmic streaming in C. elegans

The paper investigates how moderate temperature stress affects germline apoptosis and cytoplasmic streaming in C. elegans, identifying LIN-35 and the DREAM complex as key regulators.

An Ionic Sensor acts in Parallel to dSarm to Promote Neurodegeneration

The paper identifies dWnk as an ionic/osmotic sensor that promotes neurodegeneration alongside dSarm in Drosophila, converging on Axundead for axon death.

Membrane Tension Drives Opening of NINJ1 Lesions in Dying Cells

This study shows membrane tension drives NINJ1 filament opening, causing cell lysis, and explains why NINJ2 fails to form lesions.

TRAIL induces caspase-dependent cleavage of specific components of the clathrin-mediated endocytosis machinery

This study shows TRAIL induces caspase-dependent cleavage of AP2 and CHC, with AP2 cleavage requiring caspase-8 and CHC cleavage requiring both caspase-8 and caspase-3.

NINJ1 is activated by calcium-driven plasma membrane lipid scrambling during lytic cell death

The paper identifies calcium-driven lipid scrambling as the mechanism activating NINJ1-mediated plasma membrane rupture during lytic cell death.

RBP4 functions as an antagonistic ligand of orphan DR6

This study identifies RBP4 as an antagonistic ligand of DR6, showing it prevents DR6-driven neurodegeneration by promoting dimerization and blocking prodegenerative interactions.

A lipid signature of BAK-driven apoptotic pore formation

The paper identifies a lipid signature associated with BAK-driven apoptotic pore formation and shows cholesterol inhibits pore formation by preventing BAK clustering.

Computational Analysis of Zn2+ Mediated Non-Competitive Inhibition to Caspase-3

This study uses computational methods to analyze Zn2+-mediated non-competitive inhibition of caspase-3, revealing atomic-level insights into its mechanism and potential therapeutic applications.

Caspase-Activated DNase Localizes to Cancer Causing Translocation Breakpoints During Cell Differentiation

The paper identifies CAD-bound genes involved in both muscle cell differentiation and cancer-causing translocations, showing CAD-induced breaks are physiologic in differentiation and linked to oncogenic gene regulation.