Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/0005-2787(66)90133-x | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Targeting of the G9a, DNMT1 and UHRF1 epigenetic complex as an effective strategy against pancreatic ductal adenocarcinoma.
J Exp Clin Cancer Res
January 2025
Hepatology Laboratory, Solid Tumors Program, CIMA, CCUN, University of Navarra, Pamplona, Spain.
Background: Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive cancer with limited treatment options and a poor prognosis. The critical role of epigenetic alterations such as changes in DNA methylation, histones modifications, and chromatin remodeling, in pancreatic tumors progression is becoming increasingly recognized. Moreover, in PDAC these aberrant epigenetic mechanisms can also limit therapy efficacy.
View Article and Find Full Text PDFSIRT1/PGC-1α-mediated mitophagy participates the improvement roles of BMAL1 in podocytes injury in diabetic nephropathy: evidences from in vitro experiments.
Eur J Med Res
January 2025
Department of Nephrology, Affiliated Hospital of Jiaxing University (The First Hospital of Jiaxing), No.1882, Zhonghuan North Road, Jiaxing, 314000, Zhejiang, China.
Background: Dysfunction in podocyte mitophagy has been identified as a contributing factor to the onset and progression of diabetic nephropathy (DN), and BMAL1 plays an important role in the regulation of mitophagy. Thus, this study intended to examine the impact of BMAL1 on podocyte mitophagy in DN and elucidate its underlying mechanisms.
Materials And Methods: High D-glucose (HG)-treated MPC5 cells was used as a podocyte injury model for investigating the potential roles of BMAL1 in DN.
High interstitial fluid pressure enhances USP1-dependent KIF11 protein stability to promote hepatocellular carcinoma progression.
J Transl Med
January 2025
Department of General Surgery, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, No.1, Minde Road, Nanchang, 330006, Jiangxi, China.
Background: HCC is characterized by a high interstitial fluid pressure (HIFP) environment, which appears to support cancer cell survival. However, the mechanisms behind this phenomenon are not fully understood.
Methods: This study investigates the role of kinesin family member 11 (KIF11) in HCC under HIFP conditions, using both in vivo and in vitro models.
A strategy for controlling Hypervirulent Klebsiella pneumoniae: inhibition of ClpV expression.
BMC Microbiol
January 2025
The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, China.
The emergence and prevalence of hypervirulent Klebsiella pneumoniae (hvKP) have proposed a great challenge to control this infection. Therefore, exploring some new drugs or strategies for treating hvKP infection is an urgent issue for scientific researchers. In the present study, the clpV gene deletion strain of hvKP (ΔclpV-hvKP) was constructed using CRISPR-Cas9 technology, and the biological characteristics of ΔclpV-hvKP were investigated to explore the new targets for controlling this pathogen.
View Article and Find Full Text PDFPLAC8 attenuates pulmonary fibrosis and inhibits apoptosis of alveolar epithelial cells via facilitating autophagy.
Commun Biol
January 2025
Department of Pulmonary and Critical Care Medicine, Shengjing Hospital of China Medical University, Shenyang, Liaoning, China.
Idiopathic pulmonary fibrosis (IPF) is an irreversible lung condition that progresses over time, which ultimately results in respiratory failure and mortality. In this study, we found that PLAC8 was downregulated in the lungs of IPF patients based on GEO data, in bleomycin (BLM)-induced lungs of mice, and in primary murine alveolar epithelial type II (pmATII) cells and human lung epithelial cell A549 cells. Overexpression of PLAC8 facilitated autophagy and inhibited apoptosis of pmATII cells and A549 cells in vitro.
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!