AMPKα1: SUMO Wrestling Runx2 as a Strategy to Inhibit Arteriosclerotic Calcification.

Circ Res

From the Endocrine Division, Department of Internal Medicine, UT Southwestern Medical Center, Dallas, TX.

Published: July 2016

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5051572PMC
http://dx.doi.org/10.1161/CIRCRESAHA.116.309237DOI Listing

Publication Analysis

Top Keywords

ampkα1 sumo
4
sumo wrestling
4
wrestling runx2
4
runx2 strategy
4
strategy inhibit
4
inhibit arteriosclerotic
4
arteriosclerotic calcification
4
ampkα1
1
wrestling
1
runx2
1

Similar Publications

The SUMO fusion technology has immensely contributed to the soluble production of therapeutics and other recombinant proteins in E. coli. The structure-based functionality of SUMO protease has remained the primary determinant for choosing SUMO as a solubility enhancer tag.

View Article and Find Full Text PDF

Age-related p53 SUMOylation accelerates senescence and tau pathology in Alzheimer's disease.

Cell Death Differ

January 2025

Department of Pathophysiology, School of Basic Medicine, Key Laboratory of Education Ministry/Hubei Province of China for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Aging is a major risk factor for Alzheimer's disease (AD). With the prevalence of AD increased, a mechanistic linkage between aging and the pathogenesis of AD needs to be further addressed. Here, we report that a small ubiquitin-related modifier (SUMO) modification of p53 is implicated in the process which remarkably increased in AD patient's brain.

View Article and Find Full Text PDF

Site-selective photo-crosslinking for the characterisation of transient ubiquitin-like protein-protein interactions.

PLoS One

January 2025

Manchester Cancer Research Centre, Division of Cancer Sciences, School of Medical Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, United Kingdom.

Non-covalent protein-protein interactions are one of the most fundamental building blocks in cellular signalling pathways. Despite this, they have been historically hard to identify using conventional methods due to their often weak and transient nature. Using genetic code expansion and incorporation of commercially available unnatural amino acids, we have developed a highly accessible method whereby interactions between biotinylated ubiquitin-like protein (UBL) probes and their binding partners can be stabilised using ultraviolet (UV) light-induced crosslinks.

View Article and Find Full Text PDF

Background: This study investigates the role of small ubiquitin-like modifier (SUMO)-specific peptidase 5 (SENP5), a key regulator of SUMOylation, in esophageal squamous cell carcinoma (ESCC), a lethal disease, and its underlying molecular mechanisms.

Methods: Differentially expressed genes between ESCC mouse oesophageal cancer tissues and normal tissues were analysed via RNA-seq; among them, SENP5 expression was upregulated, and this gene was selected for further analysis. Immunohistochemistry and western blotting were then used to validate the increased protein level of SENP5 in both mouse and human ESCC samples.

View Article and Find Full Text PDF

The intricate relationship between SUMOylation and gliomas: a review with a perspective on natural compounds.

Nat Prod Res

January 2025

Programa de Pós-Graduação em Biologia Celular e do Desenvolvimento, Universidade Federal de Santa Catarina, Florianópolis, Brazil.

Gliomas are tumours that affect the nervous system, with glioblastoma, also known as grade IV astrocytoma, being the most aggressive type, associated with poor prognosis. Glioblastoma is characterised by its highly invasive nature, rapid growth, and resistance to conventional chemotherapy and radiation treatments, resulting in a median survival of about 14 months. To improve patient outcomes, novel therapeutic approaches are needed.

View Article and Find Full Text PDF

Want 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!