Defense-Related Enzyme Activities and Metabolomic Analysis Reveal Differentially Accumulated Metabolites and Response Pathways for Sheath Blight Resistance in Rice.

Rice sheath blight (RSB), caused by the pathogenic fungus , poses a significant threat to global food security. The defense mechanisms employed by rice against RSB are not well understood. In our study, we analyzed the interactions between rice and by comparing the phenotypic changes, ROS content, and metabolite variations in both tolerant and susceptible rice varieties during the early stages of fungal infection.

Regulation of intestinal tissue‑resident memory T cells: a potential target for inflammatory bowel disease.

Tissue-resident memory T (TRM) cells are populations which settle down in non-lymphoid tissues instead of returning to secondary lymph organs after the antigen presentation. These cells can provide rapid on-site immune protection as well as long-term tissue damage. It is reported that TRM cells from small intestine and colon exhibited distinctive patterns of cytokine and granzyme expression along with substantial transcriptional and functional heterogeneity.

PacBio full-length transcriptome analysis reveals the role of tRNA-like structures in RNA processing.

Background: Mitochondrial DNA (mtDNA) and chloroplast DNA (cpDNA) are distinct from nuclear DNA (nuDNA) in a eukaryotic cell. Animal mitochondria transcribe a single primary transcript that carries all genes from a DNA strand; In contrast, plant mitochondria and chloroplasts produce multiple primary transcripts, with each transcript carrying several genes. How primary transcripts of plant mtDNA and cpDNA are processed into mature RNAs is still unknown.

Phased chromosome-level genome provides insights into the molecular adaptation for migratory lifestyle and population diversity for Pacific saury, Cololabis saira.

The Pacific saury (Cololabis saira) is a pelagic fish commonly found in the North Pacific Ocean. Its population diversity and migratory lifestyle have long captured global attention. Despite the inherent complexity of the C.

Insights into the mA demethylases FTO and ALKBH5 : structural, biological function, and inhibitor development.

N6-methyladenosine (mA) is dynamically regulated by methyltransferases (termed "writers") and demethylases (referred to as "erasers"), facilitating a reversible modulation. Changes in mA levels significantly influence cellular functions, such as RNA export from the nucleus, mRNA metabolism, protein synthesis, and RNA splicing. They are intricately associated with a spectrum of pathologies.

The role of deacetylase SIRT1 in allergic diseases.

The silent information regulator sirtuin 1 (SIRT1) protein is an NAD-dependent class-III lysine deacetylase that serves as an important post-transcriptional modifier targeting lysine acetylation sites to mediate deacetylation modifications of histones and non-histone proteins. SIRT1 has been reported to be involved in several physiological or pathological processes such as aging, inflammation, immune responses, oxidative stress and allergic diseases. In this review, we summarized the regulatory roles of SIRT1 during allergic disorder progression.

Review of METTL3 in colorectal cancer: From mechanisms to the therapeutic potential.

N6-methyladenosine (mA), the most abundant modification in mRNAs, affects the fate of the modified RNAs at the post-transcriptional level and participants in various biological and pathological processes. Increasing evidence shows that mA modification plays a role in the progression of many malignancies, including colorectal cancer (CRC). As the only catalytic subunit in methyltransferase complex, methyltransferase-like 3 (METTL3) is essential to the performance of mA modification.

The role of the cGAS-STING pathway in metabolic diseases.

The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway is a critical innate immune pathway primarily due to its vital DNA sensing mechanism in pathogen defence. Recent research advances have shown that excessive activation or damage to the cGAS-STING pathway can exacerbate chronic inflammatory responses, playing a significant role in metabolic dysfunction and aging, leading to the development of related diseases such as obesity, osteoporosis, and neurodegenerative diseases. This article reviews the structure and biological functions of the cGAS-STING signaling pathway and discusses in detail how this pathway regulates the occurrence and development of metabolic and age-related diseases.

Circular RNA CircZNF644 Facilitates Circulating Follicular Helper T Cells Response in Patients with Graves' Disease.

Aberrant accumulation of circulating follicular helper T cells (cTfh) has been found in the peripheral blood mononuclear cells (PBMCs) of Graves' disease (GD) patients. However, the underlying mechanism that contributes to the imbalance of cTfh cells remains unknown. Previously, studies described a GD-related circular RNAs (circRNAs)-circZNF644 that might be associated with cTfh cells.

Insight into the regulatory mechanism of mA modification: From MAFLD to hepatocellular carcinoma.

In recent years, there has been a significant increase in the incidence of metabolic-associated fatty liver disease (MAFLD), which has been attributed to the increasing prevalence of type 2 diabetes mellitus (T2DM) and obesity. MAFLD affects more than one-third of adults worldwide, making it the most prevalent liver disease globally. Moreover, MAFLD is considered a significant risk factor for hepatocellular carcinoma (HCC), with MAFLD-related HCC cases increasing.

Inhibition of NLRP3 inflammasome alleviates cognitive deficits in a mouse model of anti-NMDAR encephalitis induced by active immunization.

Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is a neurological disorder, characterized by cognitive deficits as one of its vital features. The nucleotide-binding oligomerization domain-like receptor (NLRP3) inflammasome is a key contributor to neuroinflammation and cognitive deficits in neurological diseases. However, the underlying mechanism of anti-NMDAR encephalitis remains unclear, and the biological function of the NLRP3 inflammasome in this condition has not been elucidated.

Sequential glycosylations at the multibasic cleavage site of SARS-CoV-2 spike protein regulate viral activity.

The multibasic furin cleavage site at the S1/S2 boundary of the spike protein is a hallmark of SARS-CoV-2 and plays a crucial role in viral infection. However, the mechanism underlying furin activation and its regulation remain poorly understood. Here, we show that GalNAc-T3 and T7 jointly initiate clustered O-glycosylations in the furin cleavage site of the SARS-CoV-2 spike protein, which inhibit furin processing, suppress the incorporation of the spike protein into virus-like-particles and affect viral infection.

Effects of Hydrogen Inhalation on Neurological Function Indicators, Oxidative Stress Markers, and E-Cadherin Levels in Patients with Brain Glioma.

Objective: This study aims to evaluate the effects of hydrogen therapy on nerve function and tumor progression markers in glioma patients, focusing on the modulation of oxidative stress and cadherin expression to establish its potential as a complementary treatment.

Methods: 100 glioma patients were enrolled and divided into two groups using the random number table: routine treatment (50) and hydrogen inhalation plus routine treatment (50). After 2 weeks of treatment, clinical curative effect, levels of nerve function indexes [national institute of health stroke scale (NIHSS), central nervous specific protein (S100β), neuron-specific enolase (NSE), glial fibrillary acidic protein (GFAP)], oxidative stress indexes [malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT)] and E-cadherin before and after treatment, and occurrence of adverse reactions during treatment were compared between the two groups.

Tfh cell-derived small extracellular vesicles exacerbate the severity of collagen-induced arthritis by enhancing B-cell responses.

Soluble components secreted by Tfh cells are critical for the germinal center responses. In this study, we investigated whether Tfh cells could regulate the B-cell response by releasing small extracellular vesicles (sEVs). Our results showed that Tfh cells promote B-cell differentiation and antibody production through sEVs and that CD40L plays a crucial role in Tfh-sEVs function.

The Role of Citrullination Modification in CD4 T Cells in the Pathogenesis of Immune-Related Diseases.

The post-translational modifications (PTMs) of proteins play a crucial role in increasing the functional diversity of proteins and are associated with the pathogenesis of various diseases. This review focuses on a less explored PTM called citrullination, which involves the conversion of arginine to citrulline. This process is catalyzed by peptidyl arginine deiminases (PADs).

ALKBH5 regulates arginase 1 expression in MDSCs and their immunosuppressive activity in tumor-bearing host.

Myeloid-derived suppressor cells (MDSCs) are closely related to the occurrence and development of many cancers, but the specific mechanism is not fully understood. It has been found that N6-methyladenosine (mA) plays a key role in RNA metabolism, but its function in MDSCs has yet to be revealed. In this study, we found that MDSCs in mice with colorectal cancer (CRC) have significantly elevated levels of mA, while ALKBH5 expression is decreased.

Rapamycin alleviates mitochondrial dysfunction in anti-NMDAR encephalitis mice.

Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is one of the most prevalent forms of autoimmune encephalitis, characterized by a series of neurological and psychiatric symptoms, including cognitive impairment, seizures and psychosis. The underlying mechanism of anti-NMDAR encephalitis remains unclear. In the current study, the mouse model of anti-NMDAR encephalitis with active immunization was performed.

Correction: Enhancing Specific-Antibody Production to the ragB Vaccine with GITRL That Expand Tfh, IFN-γ+ T Cells and Attenuates Porphyromonas gingivalis Infection in Mice.

[This corrects the article DOI: 10.1371/journal.pone.