Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC173522 | PMC |
| http://dx.doi.org/10.1128/iai.63.9.3736-3738.1995 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Inhibition of DEK restores hematopoietic stem cell function in Fanconi anemia.
J Exp Med
March 2025
Department of Hematology, The Second Affiliated Hospital of Chongqing Medical University, School of Basic Medical Sciences, Chongqing Medical University, Chongqing, China.
Hematopoietic stem cells (HSCs) are susceptible to replication stress, which is a major contributor to HSC defects in Fanconi anemia (FA). Here, we report that HSCs relax the global chromatin by downregulating the expression of a chromatin architectural protein, DEK, in response to replication stress. DEK is abnormally accumulated in bone marrow (BM) CD34+ cells from patients with FA and in Fancd2-deficient HSCs.
View Article and Find Full Text PDFAnnexin A8 deficiency delays atherosclerosis progression.
Clin Transl Med
January 2025
Vascular Research Laboratory, IIS-Fundación Jiménez Díaz, Madrid, Spain.
Background: Atherosclerosis is a chronic inflammatory disease characterized by the accumulation of lipids and leukocytes within the arterial wall. By studying the aortic transcriptome of atherosclerosis-prone apolipoprotein E (ApoE) mice, we aimed to identify novel players in the progression of atherosclerosis.
Methods: RNA-Seq analysis was performed on aortas from ApoE and wild-type mice.
CPT1 deficiency blocks autophagic flux to promote lipid accumulation induced by co-exposure to polystyrene microplastic and cadmium.
Front Pharmacol
January 2025
College of Veterinary Medicine, Yangzhou University, Yangzhou, China.
Introduction: Cadmium (Cd) and polystyrene microplastics (PS-MPs), two ubiquitous environmental contaminants, produce unique synergistic toxicity when co-existing. Key unanswered questions include specific effects on liver function and potential mechanisms.
Methods: In this study, C57BL/6 mice and AML12 cells were used to establish and models to elucidate the effects of combined exposure to PS-MPs and Cd on the liver and their mechanisms.
Role of GLCCI1 in inhibiting PI3K-induced NLRP3 inflammasome activation in asthma.
Chin Med J Pulm Crit Care Med
December 2024
Department of Respiratory Medicine, National Key Clinical Specialty, Branch of National Clinical Research Center for Respiratory Disease, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China.
Background: Glucocorticoid-induced transcript 1 (GLCCI1) has been reported to be associated with the efficiency of inhaled glucocorticoids in patients with asthma. This study aimed to investigate the role of GLCCI1 in the regulation of nucleotide-binding oligomerization domain (NOD)-like receptor (NLR) family pyrin domain-containing 3 (NLRP3) by the phosphatidylinositol 3-kinase (PI3K) pathway in the pathogenesis of allergic asthma.
Methods: The expression levels of genes encoding GLCCI1, NLRP3 inflammasome components, and PI3K pathway-related indicators were detected in cells isolated from induced sputum from patients with asthma and healthy controls.
Parkin deficiency aggravates inflammation-induced acute lung injury by promoting necroptosis in alveolar type II cells.
Chin Med J Pulm Crit Care Med
December 2024
Medical Research Center; The Zhejiang Key Laboratory of Intelligent Cancer, Biomarker Discovery and Translation, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, China.
Background: Necroptosis is a form of programmed cell death resulting in tissue inflammation due to the release of intracellular contents. Its role and regulatory mechanism in the context of acute lung injury (ALI) are unclear. Parkin (Prkn), an E3 ubiquitin ligase, has recently been implicated in the regulation of necroptosis.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!