2024 Top Research Publications Roundup

Ubigene's 2024 Top Research Publications Roundup

Looking back on 2024, thank you all for choosing Ubigene to assist in scientific challenges and breakthroughs together. Our growth and progress cannot be separated from the trust and support of the vast number of researchers!

During the year 2024, Ubigene assisted researchers in publishing 115 high-quality articles, with a total impact factor of over 1000, covering various services and products such as KO cells, point mutation cells, gene-editing microbe, Luciferase expressing cells, etc. These articles are not only genuine feedback from customers on our products and services, but also a source of motivation for us to keep moving forward. We have selected some top research articles that cite the services and products of Ubigene in 2024, and have organized and briefly interpreted them, hoping to provide experimental ideas and references for more researchers!

1.

Title: Deep whole-genome analysis of 494 hepatocellular carcinomas

Published in Nature

IF: 50.5

Cited Service/Products: PPP1R12B, KCNJ12, FGA gene knockout cells and overexpression lentivirus carrying mutation sites

Abstract: In this study, 494 HCC patients' tumor tissues from different regions of China were subjected to high-depth whole genome sequencing (average depth, 120x), and the coding and non-coding driver genes, mutational signatures, copy number variations, clustered alternation: chromothripsis, chromoplexy and kataegis, extrachromosomal circular DNA (ecDNA), and the characteristics of mutation evolution were analyzed in depth. Three newly identified potential driver events were also selected for detailed functional verification. Based on CRISPR site directed mutagenesis and knockdown / knockout experiments in multiple cell lines, it was found that mutations in the above genes were sufficient to cause significant changes in gene expression levels, and were involved in regulating various malignant phenotypes of hepatocellular carcinoma, These results confirm the validity of the new driving events found based on data analysis.

Candidate driver landscape

2.

Title: Nondigestible stachyose binds membranous HSP90β on small intestinal epithelium to regulate the exosomal miRNAs: a new function & mechanism

Published in Cell Metabolism

IF: 27.7

Cited Service/Products: HSP90β gene knockout Mode-K cells

Abstract: This study found for the first time that although oligosaccharide stachyose did not enter the small intestinal epithelial cells but accumulated significantly on the cell membrane surface and bound to the heat shock protein HSP90β on the small intestinal epithelial cell membrane. HSP90 is known as the regulatory "switch" for extracellular vesicle secretion. Extracellular vesicles act as important messengers for intercellular communication, transmitting their miRNA, protein and other signaling molecules to recipient cells, activating intracellular signaling pathways, and regulating physiological functions of the body. The team further investigated and revealed a novel nutritional function of stachyose by directly acting on the HSP90β membrane of small intestinal epithelial cells to reorganize their extracellular vesicle miRNA expression profile, and was the first to elucidate the indirect probiotic mechanism by which stachyose regulate gut microbiota through this novel function.

Knockout of HSP90β in MODE-K cells eliminates the accumulation of stachyose on the cell membrane and the regulatory effects of stachyose on the exosomal miRNA expression

3.

Title: Nuclear miR-204-3p mitigates metabolic dysfunction-associated steatotic liver disease in mice

Published in Journal of Hepatology

IF: 26.8

Cited Service/Products: TLR4 gene knockout THP-1 cells

Abstract: This study demonstrates a new discovery of the role of miR-204-3p in macrophages, which depends on transcriptional regulation of ULK1 expression. It can increase autophagic flux, reduce inflammatory response, and thus limit fatty liver disease. Therefore, miR-204-3p and potential specific ULK1 drug agonists may become new therapeutic targets for metabolic dysfunction-associated steatotic liver disease (MASLD).

Graphical abstract

1.

Title: Acetate reprogrammes tumour metabolism and promotes PD-L1 expression and immune evasion by upregulating c-Myc

Published in Nature Metabolism

IF: 18.9

Cited Service/Products: MYC gene mutated (p.K148R) A549 cells, MYC gene mutated (p.K148Q) A549 cells

Abstract: This study reveals the important mechanism by which acetic acid taken up by tumor cells reprograms tumor cell metabolism and promotes immune evasion by upregulating c-Myc levels. Importantly, the efficacy of immune checkpoint inhibitor therapy is enhanced by regulating the tumor acetic acid metabolism pathway.

Graphical abstract

2.

Title: FOXP1 phosphorylation antagonizes its O-GlcNAcylation in regulating ATR activation in response to replication stress

Published in The EMBO Journal

IF: 9.4

Cited Service/Products: FOXP1 gene mutated (S396A and S396D) HEK293 cells

Abstract: This study reveals a novel mechanism by which the forkhead box (FOX) transcription factor FOXP1 promotes ATR-CHK1 activation under replication stress. This function is independent of the transcriptional regulatory activity of FOXP1 and is regulated by the interaction between phosphorylation and glycosylation modifications of FOXP1.

Graphical abstract

Title: YjgA plays dual roles in enhancing PTC maturation

Published in Nucleic Acids Research

IF: 16.6

Cited Service/Products: YigA gene knockout E.coli

Abstract: This study observed the accumulation of pre50S particles by knocking out the expression of YjgA or its N-loop in Escherichia coli. These particles mainly exhibit structural abnormalities in the peptidyl transferase center (PTC) and H68/69 region. The study reveals the key function of the small protein YjgA in the late stage of ribosome subunit 50S assembly, providing new insights into the complex process of ribosome biosynthesis.

YjgA promotes the maturation of PTC through its dual function of preventing H68 from entering and recruiting uL16

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