Protective Role of Bre1 in Mitochondrial Function and Energy Metabolism in Drosophila Models of Parkinson's disease.

Background: The second most common cause of autosomal recessive early-onset Parkinson's disease (PD) can be attributed to mutations in the PINK1 gene, malfunction of the mitochondria is the key pathological mechanism. Bre1 encodes an E3 ubiquitin ligase, with the discovery of Bre1's role in repairing mitochondrial damage, further investigation into its implications for PD is warranted.

Methods: We used the PINK1B9 drosophila melanogaster as the PD model.

Microtubule-Rab5 mutual-influential system screening based on gene-regulatory networks map in Rab5 RNAi eye-degeneration model.

Rabs are involved in neuronal development and protrusion formation. Existing studies support the notion that manipulation or mutation of Rab genes could lead to functional changes in neurons. However, whether Rabs gene-manipulation induced Drosophila eye-degeneration remains unknown.

Identification of diagnostic markers and molecular clusters of cuproptosis-related genes in alcohol-related liver disease based on machine learning and experimental validation.

Background And Aims: Alcohol-related liver disease (ALD) is a worldwide burden. Cuproptosis has been shown to play a key role in the development of several diseases. However, the role and mechanisms of cuproptosis in ALD remain unclear.

Mitochondrial dysfunction and NDUFS3: Insights from a PINK1 Drosophila model in Parkinson's disease pathogenesis.

PTEN-induced kinase1 (PINK1) mutation is the main cause of autosomal recessive inheritance and early-onset Parkinson's disease. Mitochondrial respiratory chain complex I (CI) functional impairment has been considered to be an important factor in the pathogenesis of PD in recent years. In addition, NDUFS3 (nicotinamide adenine dinucleotide deoxylase iron-thionein 3) is one of the core subunits of mitochondrial CI.

A label-free and rapid fluorometric strategy for microRNA detection using CRISPR-Cas12a coupled with copper nanoparticles.

CRISPR-Cas12a with robust trans-cleavage activity were employed to mitigate background fluorescence signal, achieving sensitive detection of miRNA-21. The activation of trans-cleavage activity of Cas12a was achieved by utilizing cDNA as a trigger. Upon the presence of target miRNA-21, cDNA hybridizes with it forming a DNA/RNA double-stranded structure.

RBCK1 overexpression is associated with immune cell infiltration and poor prognosis in hepatocellular carcinoma.

RBCK1 is an important E3 ubiquitin ligase, which plays an important role in many major diseases. However, the function and mechanism of RBCK1 in pan-cancer and its association with immune cell infiltration have not been reported. The purpose of this study is to find out the expression of RBCK1 in cancer, and to explore the relationship between RBCK1 and the prognosis of patients.

Icaritin greatly attenuates β-amyloid-induced toxicity in vivo.

Aims: The accumulation and deposition of β-amyloid (Aβ) has always been considered a major pathological feature of Alzheimer's disease (AD). The latest and mainstream amyloid cascade hypothesis indicates that all the main pathological changes in AD are attributed to the accumulation of soluble Aβ. However, the exploration of therapeutic drugs for Aβ toxicity has progressed slowly.

Identification and validation of potential diagnostic signature and immune cell infiltration for NAFLD based on cuproptosis-related genes by bioinformatics analysis and machine learning.

Background And Aims: Cuproptosis has been identified as a key player in the development of several diseases. In this study, we investigate the potential role of cuproptosis-related genes in the pathogenesis of nonalcoholic fatty liver disease (NAFLD).

Method: The gene expression profiles of NAFLD were obtained from the Gene Expression Omnibus database.

Vitamin K2 protects against Aβ42-induced neurotoxicity by activating autophagy and improving mitochondrial function in Drosophila.

Objective: Alzheimer disease is characterized by progressive decline in cognitive function due to neurodegeneration induced by accumulation of Aβ and hyperphosphorylated tau protein. This study was conducted to explore the protective effect of vitamin K2 against Aβ42-induced neurotoxicity.

Methods: Alzheimer disease transgenic Drosophila model used in this study was amyloid beta with the arctic mutation expressed in neurons.

Overexpressed PERK suppresses the neurodegenerative phenotypes in PINK1 flies by enhancing mitochondrial function.

PTEN-induced putative kinase 1 (PINK1) mutation induces autosomal recessive Parkinson's Disease (PD), mitochondrial dysfunction is the central pathogenic process. However, more and more studies presented the bulk of the damage to neurons with mitochondrial dysfunction stems from the endoplasmic reticulum (ER) stress. In mitochondria damaged PINK1 fly model how protein kinase RNA-like ER kinase (PERK) arm of ER stress functions remains a mystery.

Wnt2 overexpression protects against PINK1 mutant‑induced mitochondrial dysfunction and oxidative stress.

The PTEN induced putative kinase 1 (PINK1) mutation is the second most common cause of autosomal recessive adolescent Parkinson's disease (PD). Furthermore, mitochondrial disorders and oxidative stress are important mechanisms in the pathogenesis of PD. Numerous members of the Wnt family have been found to be associated with neurodegenerative diseases.

Chemical Targeting and Manipulation of Type III Secretion in the Phytopathogen Xanthomonas campestris for Control of Disease.

pv. campestris is the causative agent of black rot disease in crucifer plants. This Gram-negative bacterium utilizes the type III secretion system (T3SS), encoded by the gene cluster, to aid in its resistance to host defenses and the ability to cause disease.