Results 101 to 110 of about 5,538,011 (302)
Self‐assembled, scaffold‐free full‐thickness skin equivalents with monoclonal, genetically modified N/TERT‐1 keratinocytes represent a novel in vitro model of human skin and skin diseases. The model is highly robust, reproducible, physiologically relevant, and suitable for high‐throughput applications.
Marta Slaufova +4 more
wiley +1 more source
Chromosomal Instability Drives Glioblastoma Heterogeneity and Therapeutic Opportunities
ABSTRACT Glioblastoma, the most aggressive and lethal form of brain cancer, is defined by profound genomic instability, with Chromosomal Instability (CIN) playing a central role in driving tumor progression, therapy resistance, and poor prognosis. CIN is characterized by numerical and structural alterations, is driven by mechanisms such as mitotic ...
Amarnath Pal +3 more
wiley +1 more source
Ubiquitination of caspase‐8 regulates TNF‐related apoptosis‐inducing ligand (TRAIL) sensitivity in cancer cells, and the preligand assembly complex plays a role in caspase‐8 polyubiquitination.
Ling Xu +16 more
doaj +1 more source
Our study reveals the protective role of GPR124 in maintaining BBB integrity and promoting neurological recovery following TBI. It makes a significant contribution by uncovering a novel molecular interaction between GPR124 and FGFBP1 and linking this to activation of the Wnt/β‐catenin signaling pathway in vascular repair mechanisms.
Chen Wang +13 more
wiley +1 more source
Hepatocellular carcinomas will emerge as a major form of malignancy in the coming decades. When these tumors are in advanced stages, few therapeutic options are available.
Neveen Abd El Moneim Hussein +6 more
doaj +1 more source
Malectin alleviates high glucose‐induced ER stress and damage in placental trophoblasts, a function dependent on its six critical carbohydrate‐binding residues. In a GDM mouse model, administration of TAT‐Malectin ameliorated hyperglycemia and placental ER stress and prevented fetal macrosomia.
Jiahui Zhu +12 more
wiley +1 more source
Summary: The caspase activation and recruitment domain (CARD)-based inflammasome sensors NLRP1b and NLRC4 induce caspase-1-dependent pyroptosis independent of the inflammasome adaptor ASC.
Nina Van Opdenbosch +14 more
doaj +1 more source
Caspase-8 self-cleavage is necessary for apoptosis but not cytokine responses.
(A) Schematic of strategy used to generate Casp8DA/DA mice using CRISPR/Cas9. GuideRNA is in blue. (B) Casp8+/+, Casp8DA/+, Casp8DA/DA and Ripk3-/-Casp8-/- BMDMs were infected with YopJ-deficient (ΔYopJ) and wild type Yersinia and caspase-8 processing ...
Melanie Santos-Marrero (3217635) +16 more
core +1 more source
Perivascular matrix densification promotes the emergence of aberrant endothelial tip cells (ATECs) that invade and persist within fibrotic microenvironments. Using in vivo lineage tracing and a human microvessel model, this study shows that fibrous matrix cues destabilize VE‐cadherin–mediated junctions to gate TGF‐β signaling, inducing a pro ...
Jingyi Xia +17 more
wiley +1 more source
SETDB1 is progressively downregulated in ALD, correlating with disease severity. SETDB1 deficiency impairs LAP by disrupting Rubicon membrane localization, leading to defective lipid droplet clearance. Concurrently, loss of SETDB1 reduces nuclear LC3B, causing R‐loop accumulation and cGAS‐STING‐driven inflammation. Lipidated LC3B mediates LAP‐dependent
Yi Zhang +17 more
wiley +1 more source

