Increased CD4⁺CXCR5⁺T follicular helper cells in diabetic nephropathy by Nan Zhang (46264)

“…Post-treatment, there was a significant reduction in the CD4⁺CXCR5⁺PD-1⁺ Tfh cell counts and its subsets, with a corresponding decrease in plasma levels of IL-6 and IL-17A (<i>p</i> < 0.05) in DN patients, as compared to the HCs. …”

Fig 3 - by Sumei Luo (9570740)

Data_Sheet_1_Functional Change of Effector Tumor-Infiltrating CCR5+CD38+HLA-DR+CD8+ T Cells in Glioma Microenvironment.docx by Pin-Yuan Chen (391703)

“…However, little is known about the characteristics of peripheral and tumor-infiltrating CD8⁺ T cells in patients with glioma. In this study, we examined the level of CD8⁺ T-cell activation in a group of 143 patients with glioma and determined that peripheral CD3⁺ T cells decreased in accordance with disease severity. …”

Trabectedin induced apoptosis in a dose-dependent manner as measured by the Muse™ Annexin V and Dead Cell assay. by Eda Acikgoz (816259)

The effect of (A) mean sequencing depth (genome coverage) and (B) average number of nucleotide differences per site (<i>π</i>) on accuracy of genetic similarity estimates in simula... by Kevin D. Murray (759583)

Table_4_Aneuploidy enables cross-tolerance to unrelated antifungal drugs in Candida parapsilosis.DOCX by Liu-liu Sun (15205327)

“…In clinical isolates, tolerance to echinocandins in Candida species is mostly due to point mutations of FKS genes, which encode the target protein of echinocandins. However, here, we found chromosome 5 trisomy was the major mechanism of adaptation to the echinocandin drug caspofungin, and FKS mutations were rare events. …”

Table_2_Aneuploidy enables cross-tolerance to unrelated antifungal drugs in Candida parapsilosis.DOCX by Liu-liu Sun (15205327)

“…In clinical isolates, tolerance to echinocandins in Candida species is mostly due to point mutations of FKS genes, which encode the target protein of echinocandins. However, here, we found chromosome 5 trisomy was the major mechanism of adaptation to the echinocandin drug caspofungin, and FKS mutations were rare events. …”

Table_3_Aneuploidy enables cross-tolerance to unrelated antifungal drugs in Candida parapsilosis.XLSX by Liu-liu Sun (15205327)

“…In clinical isolates, tolerance to echinocandins in Candida species is mostly due to point mutations of FKS genes, which encode the target protein of echinocandins. However, here, we found chromosome 5 trisomy was the major mechanism of adaptation to the echinocandin drug caspofungin, and FKS mutations were rare events. …”

Image_1_Aneuploidy enables cross-tolerance to unrelated antifungal drugs in Candida parapsilosis.TIF by Liu-liu Sun (15205327)

“…In clinical isolates, tolerance to echinocandins in Candida species is mostly due to point mutations of FKS genes, which encode the target protein of echinocandins. However, here, we found chromosome 5 trisomy was the major mechanism of adaptation to the echinocandin drug caspofungin, and FKS mutations were rare events. …”

Table_1_Aneuploidy enables cross-tolerance to unrelated antifungal drugs in Candida parapsilosis.DOCX by Liu-liu Sun (15205327)

“…In clinical isolates, tolerance to echinocandins in Candida species is mostly due to point mutations of FKS genes, which encode the target protein of echinocandins. However, here, we found chromosome 5 trisomy was the major mechanism of adaptation to the echinocandin drug caspofungin, and FKS mutations were rare events. …”

Image_3_Aneuploidy enables cross-tolerance to unrelated antifungal drugs in Candida parapsilosis.TIF by Liu-liu Sun (15205327)

“…In clinical isolates, tolerance to echinocandins in Candida species is mostly due to point mutations of FKS genes, which encode the target protein of echinocandins. However, here, we found chromosome 5 trisomy was the major mechanism of adaptation to the echinocandin drug caspofungin, and FKS mutations were rare events. …”

Image_2_Aneuploidy enables cross-tolerance to unrelated antifungal drugs in Candida parapsilosis.TIF by Liu-liu Sun (15205327)

“…In clinical isolates, tolerance to echinocandins in Candida species is mostly due to point mutations of FKS genes, which encode the target protein of echinocandins. However, here, we found chromosome 5 trisomy was the major mechanism of adaptation to the echinocandin drug caspofungin, and FKS mutations were rare events. …”

Image_4_Aneuploidy enables cross-tolerance to unrelated antifungal drugs in Candida parapsilosis.TIFF by Liu-liu Sun (15205327)

“…In clinical isolates, tolerance to echinocandins in Candida species is mostly due to point mutations of FKS genes, which encode the target protein of echinocandins. However, here, we found chromosome 5 trisomy was the major mechanism of adaptation to the echinocandin drug caspofungin, and FKS mutations were rare events. …”

Loss of RBM-26 function causes a reduction in the density of mitochondria in the PLM axon. by Tamjid A. Chowdhury (14149846)

Down-regulation of HCP5 inhibits cell proliferation, migration, and invasion through regulating EPHA7 by competitively binding miR-101 in osteosarcoma by Yangmao Tu (10461966)

“…Long non-coding RNAs (lncRNAs) have been reported to be associated with tumorigenesis and metastasis. In this study, we investigated the expression and roles of lncRNA human histocompatibility leukocyte antigen (HLA) complex P5 (HCP5) in OS, aiming to provide a novel molecular mechanism for OS. …”

T37A mutation protects M1 protein of BJ/3/99 virus from degradation directed by PKG and increases the viral replication. by Chenxi Wang (284364)

Propofol attenuates sepsis-induced acute kidney injury by regulating miR-290-5p/CCL-2 signaling pathway by Guodong Zheng (714597)

“…We found that miR-290-5p was a direct regulator of CCL-2 in MPC5. …”

Lipid Droplet-Binding Protein TIP47 Regulates Hepatitis C Virus RNA Replication through Interaction with the Viral NS5A Protein by Dorothee A. Vogt (247917)

“…To identify host proteins that interact with NS5A, we performed a yeast two-hybrid screen with the N-terminus of NS5A (amino acids 1–31), a well-studied α-helical domain important for the membrane tethering of NS5A. …”

M1-37T protein is degraded in a lysosome-independent manner, and its ubiquitination is not through K48 linkage. by Chenxi Wang (284364)

M1 protein harboring T37 is susceptible to ubiquitination at K187. by Chenxi Wang (284364)