Similar Datasets
Project description:To further explore the overall development and progression of hepatic steatosis induced by HiAlc Kpn, we examined liver transcriptional profiles derived HiAlc Kpn-fed, pair-fed, or ethanol-fed mice for the 4th, 6th and 8th week post gavage. The liver gene expressions in mice both with HiAlc Kpn-fed and ethanol-fed have been showed large diversities to pair-fed mice. These results clearly illustrated a process of chronic liver injury, which is consistent with previous “two-hits” insulin hypothesis, and suggested that endogenous ethanol produced by HiAlc Kpn play important roles in the steatohepatitis, as well as alcohol intake.
2020-08-10 | GSE102489 | GEO
Project description:The emergence and spread of carbapenem-resistant Klebsiella pneumoniae (CR-KPN) infections have worsened the current situation worldwide. Clinically, cotrimoxazole (CTX) and amikacin (AMI) are considered to be the preferred drugs in the treatment of (CR-KPN). But for now, the extensive use of cotrimoxazole (CTX) and amikacin (AMI) During the course of treatment leads to the emergence of cotrimoxazole- and amikacin-resistant infections, which is of great clinical concern. Previous evidence has shown that bacteria with reduced metabolism tend to be resistant to antibiotics, however, the mechanism remains unclear. In the present study, proteomics was performed on the sensitive, cotrimoxazole-resistant, amikacin-resistant and cotrimoxazole/amikacin-both-resistant KPN clinical isolates, and 2266 proteins were identified in total by liquid chromatography coupled with tandem mass spectrometry (LC–MS/MS) analysis. Further bioinformatic analysis showed down-regulation of tricarboxylic acid cycle pathway and up-regulation of alcohol metabolic or glutathione metabolism processes, which may contribute to ROS clearance and cell survival, in drug-resistant isolates. Finally, combined with minimum inhibitory concentration (MIC) of Amikacin and Cotrimoxazole on different KPN isolates, we identified nine proteins contributed mostly to such an alteration and the survival of bacteria under drug pressure, which could reveal novel mechanisms or pathways involved in drug resistance. These proteins and their pathways might be used as targets for the development of novel therapeutics against antimicrobial-resistant (AMR) infections.
2021-11-25 | PXD028544 | Pride
Project description:We aimed to investigate gene expression changes in intestinal organoids from different mouse genotypes after treatment with TGF-beta. Wild-type, villinCreER;KrasG12D/+;Trp53fl/flRosa26N1icd/+ (KPN), and villinCreER;Apcfl/fl;KrasG12D/+;Trp53fl/flTgfbrIfl/fl (AKPT) intestinal organoids were plated, and the media was supplemented with 5ng/mL of recombinant mouse TGFß1 protein on Day 3. RNA was collected 24h later and processed for RNA sequencing.
2022-06-30 | E-MTAB-11784 | biostudies-arrayexpress
Project description:We aimed to investigate gene expression changes in intestinal organoids from different mouse genotypes after treatment with interferon-gamma. Wild-type, villinCreER;KrasG12D/+;Trp53fl/flRosa26N1icd/+ (KPN), and villinCreER;Apcfl/fl;KrasG12D/+;Trp53fl/flTgfbrIfl/fl (AKPT) intestinal organoids were plated, and the media was supplemented with 1 ng/mL of recombinant mouse interferon-gamma protein on Day 3. RNA was collected 24h later and processed for RNA sequencing.
2022-06-30 | E-MTAB-11769 | biostudies-arrayexpress
Project description:Colorectal cancer (CRC) can be divided into 4 subtypes of which consensus molecular subtype 4 (CMS4) is associated with metastasis and poor survival. Previously, we reported that the KPN mouse model resembles human CMS4. Strikingly, although tumor formation in this model is slow and limited, effective metastasis is observed. To understand this aggressive behavior, we compared two distinct in vitro KPN models, organoids and tumoroids. The organoid model only carries the original mutations, while the tumoroids are derived from in vivo grown tumors that underwent selection during development. Here, we reveal that tumoroids harbor endogenous WNT pathway activity, which can be driven by tankyrase activity and Cdx2 downregulation. Importantly, WNT pathway activation was heterogeneous in nature, subject to regulation and allowed for a mixture of WNT-driven and YAP-driven cells within tumoroids. This unique type of WNT pathway activation is not crucial for colonic tumor growth, but results in metastatic spreading. Intriguingly, these findings reflect a specific subset of aggressive human CMS4 cancers that display low CDX2 expression and lack of classical WNT pathway mutations, while having a higher tendency to metastasize. Together, these data propose a novel mechanism for WNT pathway activation that drives metastasis formation in aggressive CRC.
2025-02-03 | GSE277663 | GEO
Project description:Klebsiella pneumoniae strain:Kpn-A76 Genome sequencing
| PRJNA1206744 | ENA
Project description:Klebsiella pneumoniae strain:Kpn-A45 Genome sequencing
| PRJNA1225901 | ENA
Project description:Klebsiella pneumoniae strain:KPN.355 Genome sequencing
| PRJNA1413901 | ENA