Results 71 to 80 of about 64,896 (248)
ADP‐ribosylation: An emerging regulator of the epigenome
ADP‐ribosylation has emerged as a dynamic epigenetic signaling mechanism that modifies histones and chromatin‐associated proteins. Through coordinated PARylation and MARylation, it integrates with other histone modifications to regulate chromatin structure, transcription factor activity, and gene expression, influencing genome function and disease ...
Cristel V. Camacho +2 more
wiley +1 more source
Effects of anthrax lethal toxin on human primary keratinocytes [PDF]
To investigate the effects of anthrax lethal toxin (LeTx) on human primary keratinocytes.We show here that human primary keratinocytes are resistant to LeTx-triggered cytotoxicity. All but one of the MEKs (mitogen-activated protein kinase kinases) are cleaved within 3 h, and the cleavage of MEKs in keratinocytes leads to their subsequent proteasome ...
S S, Koçer +6 more
openaire +2 more sources
Aquaporin‐3 and aquaporin‐5 impact the development of pancreatic ductal adenocarcinoma spheroids
Schematic representation of the role of aquaporin‐3 (AQP3) and aquaporin‐5 (AQP5) in pancreatic ductal adenocarcinoma (PDAC). Both proteins are upregulated in PDAC and are associated with tumor progression and metastatic potential. Silencing AQP3 or AQP5 in PDAC spheroids results in decreased diameter, area, and overall growth, underscoring their key ...
Catarina Pimpão +3 more
wiley +1 more source
Anthrax Lethal Toxin Induces Endothelial Barrier Dysfunction [PDF]
Hemorrhage and pleural effusion are prominent pathological features of systemic anthrax infection. We examined the effect of anthrax lethal toxin (LT), a major virulence factor of Bacillus anthracis, on the barrier function of primary human lung microvascular endothelial cells.
Jason M, Warfel +2 more
openaire +2 more sources
Molecular characterization of covRS mutations in M1UK Streptococcus pyogenes
Group A Streptococcus (GAS) acquires covRS mutations driving a hypervirulent bacterial state, frequently associated with invasive disease‐like necrotizing fasciitis. We demonstrate that the newly emerged M1UK GAS lineage can also acquire these mutations.
Jarrad Pritchard +12 more
wiley +1 more source
How phagocytic cells kill bacteria: Lessons from a professional killer
How phagocytic cells ingest and kill bacteria has been studied for more than a century, but many questions remain unanswered. The study of the amoeba Dictyostelium discoideum brings new answers, and new questions. Professional phagocytic cells such as neutrophils and macrophages, as well as free‐living soil amoebae like Dictyostelium discoideum, employ
Otmane Lamrabet, Pierre Cosson
wiley +1 more source
Consequences and Utility of the Zinc-Dependent Metalloprotease Activity of Anthrax Lethal Toxin
Anthrax is caused by the gram-positive bacterium Bacillus anthracis. The pathogenesis of this disease is dependent on the presence of two binary toxins, edema toxin (EdTx) and lethal toxin (LeTx). LeTx, the major virulence factor contributing to anthrax,
Jennifer Bromberg-White +2 more
doaj +1 more source
Glioblastoma cells express calcitonin receptor variants (CT receptor isoforms) that may help them survive stress. Using qPCR, transcript‐specific long‐read nanopore sequencing, immunofluorescence co‐localisation and comparative sequence analysis, this study identifies a novel alternatively spliced CALCR transcript that encodes the CTb receptor isoform ...
Pragya Gupta +7 more
wiley +1 more source
Mutant NPM1 in Acute Myeloid Leukemia Initiation and Maintenance
NPM1 mutations drive acute myeloid leukemia by acting as neomorphic transcriptional regulators that cooperate with Menin–MLL and XPO1 to sustain HOX/MEIS1 expression and block differentiation. Targeting these mutant‐specific transcriptional dependencies provides a rational therapeutic strategy for NPM1‐mutated AML.
Yanan Jiang +3 more
wiley +1 more source
Chronobiology of Cancer: How Aging Fuels Oncogenesis at the Molecular Level
This graphical abstract illustrates the key biological pathways linking aging with cancer development and progression. In the upper left, cumulative exposure to ultraviolet radiation, toxins, and reactive oxygen species (ROS) causes DNA damage and genomic instability, whereas age‐related decline in repair mechanisms, such as ATM/ATR, BER, and NER ...
Anu Singh, Aroonima Misra, Sufian Zaheer
wiley +1 more source

