The packaging of the eukaryotic genome into chromatin regulates the storage of genetic information, including the access of the cell's DNA metabolism machinery. Indeed, since the processes of DNA replication, translation, and repair require access to the underlying DNA, several mechanisms, both active and passive, have evolved by which chromatin structure can be regulated and modified. One mechanism relies upon the function of chromatin remodeling enzymes which couple the free energy obtained from the binding and hydrolysis of ATP to the mechanical work of repositioning and rearranging nucleosomes. Here, we review recent work on the nucleosome mobilization activity of this essential family of molecular machines.
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http://dx.doi.org/10.3390/ijms22010076 | DOI Listing |
Trends Genet
January 2025
Seaver Autism Center for Research and Treatment, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; The Mindich Child Health and Development Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; The Alper Center for Neural Development and Regeneration, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Electronic address:
The DEAD/DEAH-box family of RNA helicases (RHs) is among the most abundant and conserved in eukaryotes. These proteins catalyze the remodeling of RNAs to regulate their splicing, stability, localization, and translation. Rare genetic variants in DEAD/DEAH-box proteins have recently emerged as being associated with neurodevelopmental disorders (NDDs).
View Article and Find Full Text PDFRedox Biol
January 2025
Department of Pediatrics, Peking University First Hospital, Beijing, 100034, PR China. Electronic address:
Background: The binding of endothelin-1 (ET-1) to endothelin type A receptor (ETAR) performs a critical action in pulmonary arterial smooth muscle cell (PASMC) proliferation leading to pulmonary vascular structural remodeling. More evidence showed that cystathionine γ-lyase (CSE)-catalyzed endogenous hydrogen sulfide (HS) was involved in the pathogenesis of cardiovascular diseases. In this study, we aimed to explore the effect of endogenous HS/CSE pathway on the ET-1/ETAR binding and its underlying mechanisms in the cellular and animal models of PASMC proliferation.
View Article and Find Full Text PDFTransl Oncol
January 2025
State Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China. Electronic address:
Metabolic reprogramming is a hallmark of cancer. The"Warburg effect", also known as aerobic glycolysis, is an essential part of metabolic reprogramming and a central contributor to cancer progression. Moreover, hypoxia is one of the significant features of pancreatic ductal adenocarcinoma (PDAC).
View Article and Find Full Text PDFNat Commun
January 2025
Department of General Surgery, West China Hospital, Sichuan University, Chengdu, China.
Metabolic reprogramming fuels cancer cell metastasis and remodels the immunosuppressive tumor microenvironment (TME). We report here that circPETH, a circular RNA (circRNA) transported via extracellular vesicles (EVs) from tumor-associated macrophages (TAMs) to hepatocellular carcinoma (HCC) cells, facilitates glycolysis and metastasis in recipient HCC cells. Mechanistically, circPETH-147aa, encoded by circPETH in an m6A-driven manner, promotes PKM2-catalyzed ALDOA-S36 phosphorylation via the MEG pocket.
View Article and Find Full Text PDFInt J Biol Macromol
December 2024
Department of Thoracic Surgery, Affiliated Hospital of Southwest Medical University, Luzhou 646000, China. Electronic address:
Chromatin remodeling plays a pivotal role in the progression of esophageal squamous cell carcinoma (ESCC), but the precise mechanisms remain poorly understood. Here, we elucidated the critical function of staphylococcal nuclease and tudor domain-containing 1 (SND1) in modulating chromatin dynamics, thereby driving ESCC progression in both in vitro and in vivo models. Our data revealed that SND1 was markedly overexpressed in ESCC cell lines.
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