Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
Programmed cell death is regulated by the balance between activating and inhibitory signals. Here, we have identified RECS1 (responsive to centrifugal force and shear stress 1) [also known as TMBIM1 (transmembrane BAX inhibitor motif containing 1)] as a proapoptotic member of the TMBIM family. In contrast to other proteins of the TMBIM family, RECS1 expression induces cell death through the canonical mitochondrial apoptosis pathway. Unbiased screening indicated that RECS1 sensitizes cells to lysosomal perturbations. RECS1 localizes to lysosomes, where it regulates their acidification and calcium content, triggering lysosomal membrane permeabilization. Structural modeling and electrophysiological studies indicated that RECS1 is a pH-regulated calcium channel, an activity that is essential to trigger cell death. RECS1 also sensitizes whole animals to stress in vivo in and zebrafish models. Our results unveil an unanticipated function for RECS1 as a proapoptotic component of the TMBIM family that ignites cell death programs at lysosomes.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8589314 | PMC |
| http://dx.doi.org/10.1126/sciadv.abe5469 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Immunophenotypic Characterization of Neoplastic T Follicular Helper Cells by Flow Cytometry.
Int J Lab Hematol
September 2025
Department of Hematology, Tongde Hospital of Zhejiang Province, Hangzhou, China.
Background: T follicular helper (TFH) cell lymphoma is complex, and we hope to provide a new perspective for its diagnosis.
Methods: We analysed the immunophenotypes of 89 mature T-cell lymphomas, including 52 nodal lymphomas of TFH origin, as well as 32 benign lymph node samples and 30 healthy bone marrow samples, by flow cytometry (FCM).
Results: Among pan-T cell markers, CD4CD5CD3 is the typical pattern that distinguishes TFH lymphoma from other T-cell lymphomas.
A Promising Frontier in Cancer Therapy - Combining Endothelial Colony Forming Cells, Nanotechnology, and Hyperthermia for Precision Oncology.
Stem Cell Rev Rep
September 2025
Paris Cité University, INSERM UMR-S 970, Paris Cardiovascular Research Centre, Paris, France.
Endothelial Colony-Forming Cells (ECFCs) are recognized as key vasculogenic progenitors in humans and serve as valuable liquid biopsies for diagnosing and studying vascular disorders. In a groundbreaking study, Anceschi et al. present a novel, integrative strategy that combines ECFCs loaded with gold nanorods (AuNRs) to enhance tumor radiosensitization through localized hyperthermia.
View Article and Find Full Text PDFShigella type-III secretion system effectors counteract the induction of host inflammation and cell death.
EMBO J
September 2025
Department of Bacterial Infection and Host Response, Graduate School of Medical and Dental Sciences, Institute of SCIENCE TOKYO, 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan.
Many enteric bacterial pathogens deliver virulence effectors to counteract host innate immune responses, such as inflammation and cell death, and colonize the intestinal epithelium. However, host cells recognize the disruption of their innate immune signaling by bacterial effectors and induce alternative immune responses, collectively termed "effector-triggered immunity", to clear bacterial pathogens. Here, we describe a mechanism of cell death induction via effector-triggered immunity and the bacterial countermeasures of the pathogen Shigella flexneri.
View Article and Find Full Text PDFProteasome 20S beta 8 (PSMB8) as a metabolic switcher of neuronal ferroptosis in multiple sclerosis.
Cell Death Differ
September 2025
Department of Neurology, China National Clinical Research Center for Neurological Diseases, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.
RNF128 regulates the adaptive metabolic response to fasting by modulating PPARα function.
Cell Death Differ
September 2025
Graduate Institute of Physiology, College of Biomedical Sciences, National Defense Medical University, Taipei, Taiwan, Republic of China.
Peroxisome proliferator-activated receptor alpha (PPARα) is a crucial transcriptional factor that regulates fatty acid β-oxidation and ketogenesis in response to fasting. However, the mechanisms underlying PPARα function remain unclear. This study identified a novel PPARα-binding protein-RING finger protein 128 (RNF128)-that facilitates PPARα polyubiquitination, resulting in the degradation and suppression of PPARα function during fasting.
View Article and Find Full Text PDF