LuxS/AI-2 system facilitates the dissemination of antibiotic-resistant plasmids in Klebsiella pneumoniae.

Plasmid conjugation is a central mechanism driving the dissemination of antibiotic resistance in Klebsiella pneumoniae. However, the conjugative operon requires specific stimuli for activation. Identifying signals and elucidating the underlying mechanisms is crucial in combating plasmid spread.

The roles of cell wall inhibition responsive protein CwrA in the pathogenicity of .

The ability to form robust biofilms and secrete a diverse array of virulence factors are key pathogenic determinants of , causing a wide range of infectious diseases. Here, we characterized as a VraR-regulated gene encoding a cell wall inhibition-responsive protein (CwrA) using electrophoretic mobility shift assays. We constructed deletion mutants in the genetic background of methicillin-resistant (MRSA) and methicillin-sensitive (MSSA) strains.

Insights into small-molecule compound CY-158-11 antibacterial activity against .

Unlabelled: The widespread prevalence and dissemination of antibiotic-resistant bacteria, coupled with the diminishing supply of new antibiotics, emphasize the pressing necessity for the exploration of innovative antibacterial agents. Previously, we detailed the impact of the small-molecule compound CY-158-11 on biofilm. By hindering adhesion and PIA-mediated biofilm formation, subinhibitory concentrations of CY-158-11 exhibit antibiofilm activity toward .

Intron Retention of DDX39A Driven by SNRPD2 is a Crucial Splicing Axis for Oncogenic MYC/Spliceosome Program in Hepatocellular Carcinoma.

RNA splicing is a dynamic molecular process in response to environmental stimuli and is strictly regulated by the spliceosome. Sm proteins, constituents of the spliceosome, are key components that mediate splicing reactions; however, their potential role in hepatocellular carcinoma (HCC) is poorly understood. In the study, SNRPD2 (PD2) is found to be the most highly upregulated Sm protein in HCC and to act as an oncogene.

Characteristic of KPC-12, a KPC Variant Conferring Resistance to Ceftazidime-Avibactam in the Carbapenem-Resistant ST11-KL47 Clone Background.

Background: Carbapenem-resistant (CRKP) infections are a great threat to public health worldwide. Ceftazidime-avibactam (CZA) is an effective -lactam/-lactamase inhibitors against CRKP. However, reports of resistance to CZA, mainly caused by carbapenemase (KPC) variants, have increased in recent years.

The Wnt-dependent and Wnt-independent functions of BCL9 in development, tumorigenesis, and immunity: Implications in therapeutic opportunities.

B-cell CLL/lymphoma 9 (BCL9) is considered a key developmental regulator and a well-established oncogenic driver in multiple cancer types, mainly through potentiating the Wnt/β-catenin signaling. However, increasing evidences indicate that BCL9 also plays multiple Wnt-independent roles. Herein, we summarized the updates of the canonical and non-canonical functions of BCL9 in cellular, physiological, or pathological processes.

Targeted profiling of polar metabolites in cancer metabolic reprogramming by hydrophilic interaction liquid chromatography-tandem mass spectrometry.

Metabolic reprogramming of cancer cells is a hallmark of cancer, in which the polar metabolites involving aerobic glycolysis, pentose phosphate pathway (PPP), tricarboxylic acid (TCA) cycle, and glutaminolysis play a crucial role in the occurrence and development of cancer. Therefore, targeted analysis of the polar metabolites in these pathways is of great value for understanding cancers, finding diagnostic biomarkers, and identifying therapeutic targets. However, it is still challenging to directly determine polar metabolites in these pathways without derivatization due to their diverse chemical properties, isomers, and strong polarity.

Bacteria-mediated cancer therapy: A versatile bio-sapper with translational potential.

Bacteria are important symbionts for humans, which sustain substantial influences on our health. Interestingly, some bastrains have been identified to have therapeutic applications, notably for antitumor activity. Thereby, oncologists have developed various therapeutic models and investigated the potential antitumor mechanisms for bacteria-mediated cancer therapy (BCT).

The aberrant upregulation of exon 10-inclusive SREK1 through SRSF10 acts as an oncogenic driver in human hepatocellular carcinoma.

Deregulation of alternative splicing is implicated as a relevant source of molecular heterogeneity in cancer. However, the targets and intrinsic mechanisms of splicing in hepatocarcinogenesis are largely unknown. Here, we report a functional impact of a Splicing Regulatory Glutamine/Lysine-Rich Protein 1 (SREK1) variant and its regulator, Serine/arginine-rich splicing factor 10 (SRSF10).