AI Article Synopsis
- Familial adenomatous polyposis (FAP) leads to numerous colorectal polyps that can turn into cancer, making it important for cancer research.
- A specific patient had a 1 bp deletion in the APC gene, which results in a faulty protein that contributes to FAP.
- By reprogramming blood cells from this patient into induced pluripotent stem cells, researchers can better model the disease in the lab.
Article Abstract
Familial adenomatous polyposis (FAP) is a disorder characterized by the development of numerous colorectal adenomatous polyps progressing to colorectal cancers and has been used as an important model to study the neoplasia formation. The peripheral blood mononuclear cells from a patient carrying a heterozygous 1 bp deletion in Exon 17 of the APC gene were reprogrammed using the Sendai Reprogramming Kit. This frameshift mutation in APC is expected to produce an aberrant truncated protein which is responsible for FAP. The established human induced pluripotent cell line will enable proper in vitro disease modelling of FAP.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.scr.2022.102867 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Protocol for differentiating hematopoietic progenitor cells from human pluripotent stem cells in chemically defined monolayer culture.
STAR Protoc
January 2025
State Key Laboratory of Experimental Hematology, National Clinical Research Center for Blood Diseases, Haihe Laboratory of Cell Ecosystem, Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin 300020, China. Electronic address:
Human pluripotent stem cells (hPSCs) provide a powerful platform for generating hematopoietic progenitor cells (HPCs) and investigating hematopoietic development. Here, we present a protocol for maintaining hPSCs and inducing their differentiation into HPCs through the endothelial-to-hematopoietic transition (EHT) on vitronectin-coated plates. We outline steps for evaluating the efficiency of HPC generation and assessing their potential to differentiate into various hematopoietic lineages.
View Article and Find Full Text PDFCadmium Reduces VE-Cadherin Expression in Endothelial Cells Through Activation of the Notch Signaling Pathway.
J Biochem Mol Toxicol
January 2025
Laboratory of Translational Medicine in Microvascular Regulation, Medical Research Center, The First Affiliated Hospital of Shandong First Medical University and Shandong Provincial Qianfoshan Hospital; Shandong Provincial Key Laboratory of Medicine in Microvascular Ageing; Laboratory of Future Industry of Gene Editing in Vascular Endothelial Cells of Universities in Shandong Province, Jinan, China.
Cadmium (Cd) is a toxic heavy metal which induces vascular disorders. Previous studies suggest that Cd in the bloodstream affects vascular endothelial cells (ECs), potentially contributing to vascular-related diseases. However, the molecular mechanisms of effects of Cd on ECs remain poorly understood.
View Article and Find Full Text PDFNaringenin Inhibits Ferroptosis in Renal Tubular Epithelial Cells of Diabetic Nephropathy Through SIRT1/FOXO3a Signaling Pathway.
Drug Dev Res
February 2025
Graduate School, Fujian University of Traditional Chinese Medicine, Fuzhou City, People's Republic of China.
Naringenin has the potential to regulate ferroptosis and mitigate renal damage in diabetic nephropathy (DN). However, it remains unclear whether the naringenin's effects in DN are linked to its ability to regulate ferroptosis. This study investigated the potential anti-ferroptosis properties of naringenin in high glucose (HG)-induced renal tubular epithelial cell models.
View Article and Find Full Text PDFInhibition of GPR4 Attenuates the Formation of Abdominal Aortic Aneurysm Through Inhibiting the SP-1/VEGF-A Signaling.
J Biochem Mol Toxicol
January 2025
Department of Cardiothoracic Surgery, Jingzhou Hospital Affiliated to Yangtze University, Jingzhou City, Hubei Province, China.
Abdominal aortic aneurysm (AAA) is a severe cardiovascular disease (CVD) that is partly attributable to endothelial dysfunction, inflammatory response, and angiogenesis. G protein-coupled receptor 4 (GPR4), a proton-sensitive G protein-coupled receptor that is abundantly expressed in vascular endothelial cells, has been associated with numerous physiological functions. Nevertheless, its potential involvement in the development of AAA remains unexplored.
View Article and Find Full Text PDFExploring the regulatory role of small RNAs in modulating host-pathogen interactions: implications for bacterial and viral infections.
Mol Biol Rep
January 2025
Mahatma Gandhi Medical Advanced Research Institute (MGMARI), Sri Balaji Vidyapeeth (Deemed to be University), Puducherry, 607402, India.
MicroRNAs (miRNAs) and transfer RNA-derived stress-induced RNAs (tiRNAs) have emerged as crucial players in the post-transcriptional regulation of gene expression in various cellular processes, including immunity and host defense against infections. In recent years, increasing evidence has highlighted their complex role in influencing the host response during viral and bacterial infections. miRNAs have been shown to play multiple roles in host-pathogen interaction like TLR activation and altered disease virulence during bacterial infections.
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!