(Cell Reports 41, 111623; November 8, 2022)
As this paper was originally published, Figure 5C included a sample that was inadvertently shown twice. Because this paper was published in 2022, the paper itself cannot be updated, but the revised Figure 5C can be seen below. The authors apologize for any confusion that may have occurred due to the original figure. Dr. Atfi can be reached at azeddine.atfi@gmail.com in addition to the correspondence provided above.
Over the past several decades, researchers have identified the genes and proteins in plants that initiate the cellular self-destruct sequence. During that time, they also found shared elements of this “resistome” at work in mammalian.
Plant nucleotide-binding leucine-rich repeat (NLR) immune receptors detect pathogen effectors and activate immunity. Coiled-coil NLRs (CNLs) form resistosomes as Ca2+-permeable channels in the plasma membrane (PM). However, the mechanism by which resistosomes activate cell death remains unclear.
The ring, which resembles a wreath or a necklace, the author said, is a combination of proteins that bind to a cell membrane and six channels that orient themselves to run through the membrane. The team made this discovery working with Arabidopsis and Nicotiana bethamaian, popular plant model systems, and a high resolution total internal reflection fluorescence microscope.
The authors show that the CNL SUPPRESSOR OF mkk1 mkk2 2 (SUMM2), unlike canonical CNLs that use a MADA motif to penetrate the PM, tethers to the PM through N-myristoylation, a common feature among many CNLs.
PM targeting via N-myristoylation is essential for SUMM2-induced cell death. Upon activation, SUMM2 promotes the association of the lipase-like proteins ENHANCED DISEASE SUSCEPTIBILITY 1 (EDS1) and PHYTOALEXIN DEFICIENT 4 (PAD4) with the helper NLR-ACTIVATED DISEASE RESISTANCE 1-LIKE 1 (ADR1-L1).
Active SUMM2 induces the clustering of multiple ADR1-L1 resistosomes into a ring-like assembly colocalized with the EDS1–PAD4 complex, and the EDS1–PAD4–ADR1 module is essential for SUMM2-activated cell death.
The finding invites new questions about what exactly the rings do and how they do it. The team’s current hypothesis is that the rings enable communication with nearby cells, sending inflammation signals that can help initiate cell death in a targeted way. ScienceMission sciencenewshighlights.
Efficient energy harvesting for applications such as radioisotope thermoelectric generators and heat-recovery systems require novel thermoelectric materials with exceptional performance. This work demonstrates thermoelectric capabilities of n-type MoS2/MoSe2 heterojunctions fabricated by scalable radiofrequency sputtering. These heterostructures demonstrated an outstanding experimental Seebeck coefficient of ~ − 1.1 mV K−1 (ΔT = 40 K), arising from thermally activated carriers with a low activation energy of 32 meV, and estimated thermoelectric figure-of-merit (ZT) values of ~ 1.0. Furthermore, computational calculations within framework of Density Functional Theory corroborate experimental findings allowing to elucidate a crucial role of atomic-scale in determining anisotropic thermoelectric properties.
Aneurysmal subarachnoid hemorrhage is a critical condition with high case-fatality and lasting impacts on survivors. Acute events that are the direct result of aneurysm rupture, such as acute ischemia, elevated intracranial pressure, cerebral edema, seizures, and hydrocephalus, lead to early brain injury. A delayed cascade of processes, including a prominent systemic inflammatory response, may lead to secondary brain injury and delayed cerebral ischemia, which often further impairs recovery. Systemic complications, including cardiac and pulmonary dysfunction, fever, and electrolyte imbalances, arise in the interplay between early and secondary brain injury and challenge the clinical course.
What determines how long people live, and how much of their lifespan is influenced by genetics?
For many years, scientists believed the genetic contribution to human lifespan was relatively modest compared with other biological traits. Earlier estimates placed the heritability of lifespan at around 20 to 25 percent, and some more recent large studies suggested it might be even lower, in some cases below 10 percent.
A new study from the Weizmann Institute of Science now challenges that view. The research, published in the journal Science, reports that genetic differences may account for roughly half of the variation in human lifespan. This estimate is more than double many previous calculations. The work was led by Ben Shenhar in the laboratory of Prof. Uri Alon of the Weizmann Institute’s Molecular Cell Biology Department.
(Cell Reports 45, 116734; January 27, 2026)
When this paper was published on December 18, 2025, Figure S2 inadvertently omitted panel C. The article has since been updated online with the correct, complete figure. For readers’ convenience, both the original and corrected figures can be seen below. The authors apologize for the error.
Clinically available KRAS inhibitors mainly target G12C, which is rare in PDAC and often acquires resistance. Oncogenic KRAS inactivates RB1 via CDK4/6, while RB1 mutation is rare. Thus, CDK4/6 inhibition offers an indirect strategy to counter KRAS-driven malignancy without direct KRAS targeting.
Virtually all pancreatic ductal adenocarcinomas (PDACs) are initiated by activating mutations in the oncogene KRAS, which occur in multiple distinct allelic forms. Although considerable efforts have led to the development of inhibitors targeting specific mutant KRAS proteins, the only agents currently approved for clinical use selectively target the KRASG12C variant. However, KRASG12C mutations are exceedingly rare in pancreatic cancer.
Furthermore, in patients with KRASG12C-mutant pancreatic cancer, treatment with KRASG12C inhibitors has shown only modest clinical benefit, comparable to that of conventional chemotherapeutic regimens, and even in cases with an initial objective response, acquired resistance almost invariably emerges within a limited time frame.
People with autism may be up to six times more likely to develop Parkinson’s disease in later life. New research offers a potential explanation based on the role of transporter molecules that recycle unused dopamine in the brain.
Dopamine is a neurotransmitter crucial for managing movement and executive functions, and for reinforcing behavior. It’s well known that Parkinson’s is characterized by a drop in dopamine levels, while disruptions in the transport of the chemical have also been linked to autism.
With that context, researchers led by a team from the University of Missouri in the US took a novel approach using a technology known as a DaT SPECT scan, which is typically used to diagnose Parkinson’s in much older people.
