Nucleosomes play a vital role in chromatin organization and gene regulation,acting as key hubs that inter-act with various chromatin-associated factors through diverse binding mechanisms.Recent research has highlighte...Nucleosomes play a vital role in chromatin organization and gene regulation,acting as key hubs that inter-act with various chromatin-associated factors through diverse binding mechanisms.Recent research has highlighted the prevalence of mutations in linker histones across different types of cancer,emphasizing their critical involvement in cancer progression.These cancer-associated mutations in linker histones have been shown to disrupt nucleosome stacking and the formation of higher-order chromatin structures,which in turn significantly affect epigenetic regulatory processes.In this review,we provide a comprehensive analysis of how cancer-associated linker histone mutations alter their physicochemical properties,influencing their binding to nucleosomes,and overall chromatin architecture.Additionally,we explore the significant impact of mutations near post-translational modification sites,which further modulate chromatin dynamics and regulatory functions,offering insights into their role in oncogenesis and potential therapeutic targets.展开更多
We consider large-time behaviors of weak solutions to the evolutionary p-Laplacian with logarithmic source of time-dependent coefficient.We find that the weak solutions may neither decay nor blow up,provided that the ...We consider large-time behaviors of weak solutions to the evolutionary p-Laplacian with logarithmic source of time-dependent coefficient.We find that the weak solutions may neither decay nor blow up,provided that the initial data u(·,t_(0))is on the Nehari manifold N:={v∈W_(0)^(1,p)(Ω):I(v,to)=0,||▽v||P^(P)≠0}.This is quite different from the known results that the weak solutions may blow up as,u(·,to)∈N^(+):={v∈W_(0)^(1,p)(Ω):I(v,t_(0))<0}and weak solutions may decay as u(·,t_(0))∈N^(+):={v∈W_(0)^(1,p)(Ω):I(v,t_(0))>0}.展开更多
Placental growth factor(PlGF)is a glycosylated dimeric protein that is homologous to vascular endothelial growth factor(VEGF).PlGF expression is upregulated in patients with bronchial asthma,suggesting that it plays a...Placental growth factor(PlGF)is a glycosylated dimeric protein that is homologous to vascular endothelial growth factor(VEGF).PlGF expression is upregulated in patients with bronchial asthma,suggesting that it plays a role in the pathogenesis of asthma.Bronchial asthma is characterized by chronic airway inflammation and airway hyperresponsiveness(AHR).After recurrent asthma attacks,pulmonary fibrosis develops and leads to airway remo-deling and a further decline in lung function.In this review,we focused on the pivotal role of PlGF in chronic airway inflammation,AHR,and airway remodeling during bronchial asthma.Furthermore,we summarized data showing that PlGF may be a potential therapeutic target in bronchial asthma.展开更多
基金supported by the National Natural Science Foundation of China(No.12205112)financially supported by self-determined research funds of CCNU from the colleges’basic research and operation of MOE(CCNU24JC012)supported by Natural Science Foundation of Wuhan(No.2024040801020302).
文摘Nucleosomes play a vital role in chromatin organization and gene regulation,acting as key hubs that inter-act with various chromatin-associated factors through diverse binding mechanisms.Recent research has highlighted the prevalence of mutations in linker histones across different types of cancer,emphasizing their critical involvement in cancer progression.These cancer-associated mutations in linker histones have been shown to disrupt nucleosome stacking and the formation of higher-order chromatin structures,which in turn significantly affect epigenetic regulatory processes.In this review,we provide a comprehensive analysis of how cancer-associated linker histone mutations alter their physicochemical properties,influencing their binding to nucleosomes,and overall chromatin architecture.Additionally,we explore the significant impact of mutations near post-translational modification sites,which further modulate chromatin dynamics and regulatory functions,offering insights into their role in oncogenesis and potential therapeutic targets.
文摘We consider large-time behaviors of weak solutions to the evolutionary p-Laplacian with logarithmic source of time-dependent coefficient.We find that the weak solutions may neither decay nor blow up,provided that the initial data u(·,t_(0))is on the Nehari manifold N:={v∈W_(0)^(1,p)(Ω):I(v,to)=0,||▽v||P^(P)≠0}.This is quite different from the known results that the weak solutions may blow up as,u(·,to)∈N^(+):={v∈W_(0)^(1,p)(Ω):I(v,t_(0))<0}and weak solutions may decay as u(·,t_(0))∈N^(+):={v∈W_(0)^(1,p)(Ω):I(v,t_(0))>0}.
基金supported by the National Science Foundation of Guangdong Province,China(No.2022A1515011731,2021A1515011062)Guangdong Provincial Administration of Traditional Chinese Medicine(China)(No.20221211)+1 种基金Project of Zhanjiang City,Guangdong,China(No.2020A01016,2020B01346,2021A05077,2016B01062)Affiliated Hospital of Guangdong Medical University(China)(No.4SG21231G,LCYJ2017A003,CLP202113001,CLP2021B001,LCYJ2020B008,BK201616).
文摘Placental growth factor(PlGF)is a glycosylated dimeric protein that is homologous to vascular endothelial growth factor(VEGF).PlGF expression is upregulated in patients with bronchial asthma,suggesting that it plays a role in the pathogenesis of asthma.Bronchial asthma is characterized by chronic airway inflammation and airway hyperresponsiveness(AHR).After recurrent asthma attacks,pulmonary fibrosis develops and leads to airway remo-deling and a further decline in lung function.In this review,we focused on the pivotal role of PlGF in chronic airway inflammation,AHR,and airway remodeling during bronchial asthma.Furthermore,we summarized data showing that PlGF may be a potential therapeutic target in bronchial asthma.
