Molecular Biosciences
https://hdl.handle.net/1808/5423
2024-03-28T08:10:34ZUse of gene sequences as type for naming prokaryotes: Recommendations of the international committee on the taxonomy of chlamydiae
https://hdl.handle.net/1808/34743
Use of gene sequences as type for naming prokaryotes: Recommendations of the international committee on the taxonomy of chlamydiae
Greub, Gilbert; Pillonel, Trestan; Bavoil, Patrik M.; Borel, Nicole; Campbell, Lee Ann; Dean, Deborah; Hefty, Scott; Horn, Matthias; Morré, Servaas A.; Ouellette, Scot P.; Pannekoek, Yvonne; Puolakkainen, Mirja; Timms, Peter; Valdivia, Raphael; Vanrompay, Daisy
The International Committee on Systematics of Prokaryotes (ICSP) discussed and rejected in 2020 a proposal to modify the International Code of Nomenclature of Prokaryotes to allow the use of gene sequences as type for naming prokaryotes. An alternative nomenclatural code, the Code of Nomenclature of Prokaryotes Described from Sequence Data (SeqCode), which considers genome sequences as type material for naming species, was published in 2022. Members of the ICSP subcommittee for the taxonomy of the phylum Chlamydiae (Chlamydiota) consider that the use of gene sequences as type would benefit the taxonomy of microorganisms that are difficult to culture such as the chlamydiae and other strictly intracellular bacteria. We recommend the registration of new names of uncultured prokaryotes in the SeqCode registry.
2023-09-01T00:00:00ZRepurposing Niclosamide as a Novel Anti-SARS-CoV-2 Drug by Restricting Entry Protein CD147
https://hdl.handle.net/1808/34732
Repurposing Niclosamide as a Novel Anti-SARS-CoV-2 Drug by Restricting Entry Protein CD147
Yang, Zhe; Zhang, Qi; Wu, Xiaoqing; Hao, Siyuan; Hao, Xinbao; Jones, Elizabeth; Zhang, Yuxia; Qiu, Jianming; Xu, Liang
The outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has led to the global coronavirus disease 2019 (COVID-19) pandemic, and the search for effective treatments has been limited. Furthermore, the rapid mutations of SARS-CoV-2 have posed challenges to existing vaccines and neutralizing antibodies, as they struggle to keep up with the increased viral transmissibility and immune evasion. However, there is hope in targeting the CD147-spike protein, which serves as an alternative point for the entry of SARS-CoV-2 into host cells. This protein has emerged as a promising therapeutic target for the development of drugs against COVID-19. Here, we demonstrate that the RNA-binding protein Human-antigen R (HuR) plays a crucial role in the post-transcriptional regulation of CD147 by directly binding to its 3′-untranslated region (UTR). We observed a decrease in CD147 levels across multiple cell lines upon HuR depletion. Furthermore, we identified that niclosamide can reduce CD147 by lowering the cytoplasmic translocation of HuR and reducing CD147 glycosylation. Moreover, our investigation revealed that SARS-CoV-2 infection induces an upregulation of CD147 in ACE2-expressing A549 cells, which can be effectively neutralized by niclosamide in a dose-dependent manner. Overall, our study unveils a novel regulatory mechanism of regulating CD147 through HuR and suggests niclosamide as a promising therapeutic option against COVID-19.
2023-07-18T00:00:00ZTargeting RNA-binding protein HuR to inhibit the progression of renal tubular fibrosis
https://hdl.handle.net/1808/34576
Targeting RNA-binding protein HuR to inhibit the progression of renal tubular fibrosis
Huang, Zhimin; Liu, Simeng; Tang, Anna; Wu, Xiaoqing; Aube, Jeffrey; Xu; Huang, Yufeng
Background
Upregulation of an RNA-binding protein HuR has been implicated in glomerular diseases. Herein, we evaluated whether it is involved in renal tubular fibrosis.
Methods
HuR was firstly examined in human kidney biopsy tissue with tubular disease. Second, its expression and the effect of HuR inhibition with KH3 on tubular injury were further assessed in a mouse model induced by a unilateral renal ischemia/reperfusion (IR). KH3 (50 mg kg−1) was given daily via intraperitoneal injection from day 3 to 14 after IR. Last, one of HuR-targeted pathways was examined in cultured proximal tubular cells.
Results
HuR significantly increases at the site of tubular injury both in progressive CKD in patients and in IR-injured kidneys in mice, accompanied by upregulation of HuR targets that are involved in inflammation, profibrotic cytokines, oxidative stress, proliferation, apoptosis, tubular EMT process, matrix remodeling and fibrosis in renal tubulointerstitial fibrosis. KH3 treatment reduces the IR-induced tubular injury and fibrosis, accompanied by the remarkable amelioration in those involved pathways. A panel of mRNA array further revealed that 519 molecules in mouse kidney following IR injury changed their expression and 71.3% of them that are involved in 50 profibrotic pathways, were ameliorated when treated with KH3. In vitro, TGFβ1 induced tubular HuR cytoplasmic translocation and subsequent tubular EMT, which were abrogated by KH3 administration in cultured HK-2 cells.
Conclusions
These results suggest that excessive upregulation of HuR contributes to renal tubulointerstitial fibrosis by dysregulating genes involved in multiple profibrotic pathways and activating the TGFß1/HuR feedback circuit in tubular cells. Inhibition of HuR may have therapeutic potential for renal tubular fibrosis.
2023-06-30T00:00:00ZProtein folds vs. protein folding: Differing questions, different challenges
https://hdl.handle.net/1808/34361
Protein folds vs. protein folding: Differing questions, different challenges
Chen, Shi-Jie; Hassan, Mubashir; Jernigan, Robert L.; Jia, Kejue; Kihara, Daisuke; Kloczkowski, Andrzej; Kotelnikov, Sergei; Kozakov, Dima; Liang, Jie; Liwo, Adam; Matysiak, Silvina; Meller, Jarek; Micheletti, Cristian; Mitchell, Julie C.; Mondal, Sayantan; Nussinov, Ruth; Okazaki, Kei-ichi; Padhorny, Dzmitry; Skolnick, Jeffrey; Sosnick, Tobin R.; Stan, George; Vakser, Ilya; Zou, Xiaoqin; Rose, George D.
2022-12-29T00:00:00Z