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Last update 08 May 2025

Bacterial DnaK

Last update 08 May 2025

Basic Info

Synonyms-

Introduction-

Drugs associated with Bacterial DnaK

SMR peptide

Target

Bacterial DnaK

Mechanism

Bacterial DnaK inhibitors

Active Org.

Morehouse School of Medicine [+1]

Originator Org.-

Active Indication

Staphylococcus Aureus Infections

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

ML076

Target

Bacterial DnaK

Mechanism

Bacterial DnaK inhibitors

Active Org.-

Originator Org.

Sanford Burnham Prebys Medical Discovery Institute

Active Indication-

Inactive Indication

Bacterial Infections

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with Bacterial DnaK

100 Translational Medicine associated with Bacterial DnaK

0 Patents (Medical) associated with Bacterial DnaK

2,692

Literatures (Medical) associated with Bacterial DnaK

01 May 2025·International Journal of Biological Macromolecules

The impact of differential expression levels of smeE gene on antimicrobial susceptibility and other biological functions in Stenotrophomonas maltophilia CYZ

Article

Author: Han, Lujuan ; Pan, Bingxin ; Miu, Xiaojin ; Yu, Menghan ; Liu, Yawen ; Wang, Changle ; Hou, Jiahuan ; Zhao, Wenting ; Xie, Lixin ; Ding, Wenxi ; Li, Nan ; Liu, Jinxu ; Wu, Yan

Stenotrophomonas maltophilia is an important opportunistic pathogen that utilizes SmeE efflux pump to extrude structurally dissimilar antibiotics. Here, we constructed smeE gene deletion (D531) and overexpression (O531) strains of S. maltophilia CYZ, and investigated changes in biological functions by analyzing the transcriptional and expression levels of differentially expressed genes and proteins, respectively. S. maltophilia D531 showed significant susceptibility to erythromycin, quinolones, and tetracycline. The organism exhibited stronger bacterial motility, which was due to the upregulated expressions of FlhA and MotB proteins. Because the expression levels of SM01853, OhrB, DnaK, GrpE, and HslJ proteins were downregulated, S. maltophilia D531 increased susceptibilities to H₂O₂ and high temperature. Conversely, S. maltophilia O531 exhibited resistance to H₂O₂ and high temperature and enhanced biofilm-forming capacity, since the expressions of KatE, SM02481, PilO and PilQ proteins in S. maltophilia O531 were upregulated. However, both S. maltophilia D531 and O531 reduced tolerance towards Zn²⁺, and the expression of Zn transporter was found to be downregulated. Additionally, it is necessary to demonstrate whether downregulation of SmeN and SM02901 proteins resulted in S. maltophilia O531 reduced resistance to aminoglycosides. The current study may give important leads in elucidating the changes in biological functions via transcriptomic and proteomic analyses.

01 May 2025·Immunobiology

Ureaplasma urealyticum GrpE protein elicits glycolysis-mediated inflammatory responses through TLR2 in macrophages

Article

Author: Liu, Chang ; Huang, Zhemin ; Peng, Jiaofeng ; Xie, Nan ; Zheng, Kang ; Hu, Hao ; Li, Ranhui ; Du, Min ; Xie, Jing

The pathogenesis of Ureaplasma urealyticum infection is linked to the host inflammatory response; however, the specific molecular mechanisms underlying this phenomenon have not been fully elucidated. GrpE is a chaperonin that accelerates ADP release and ATP binding to DnaK, thereby enhancing the chaperone function of the HSP70 system under stress. However, alternative activities such as pro-inflammatory responses remain poorly understood. In this study, we report that the U. urealyticum GrpE exerts as a cytokine-inducing virulence factor toward macrophages. Using gene-knockout mice and specific inhibitors, we found that GrpE-induced pro-inflammatory cytokine expression was mediated by the TLR2/STAT3 pathway. We also found that glycolysis was essential for this pro-inflammatory response. Mechanistically, GrpE treatment stimulated STAT3-dependent accumulation of citric acid and acetyl-CoA, promoting histone acetylation and potent pro-inflammatory responses. Our results indicate that glycolysis plays a role in the inflammatory response induced by GrpE through the TLR2/STAT3 pathway and contributes to the glycolysis-mediated inflammatory response, offering a fresh understanding of the development of U. urealyticum infection.

18 Mar 2025·mSystems

Dual RNA-seq reveals the complement protein C3-mediated host-pathogen interaction in the brain abscess caused by Staphylococcus aureus

Article

Author: Zhang, Haifang ; Jin, Qiyuan ; Zhong, Jinqi ; Qiang, Rui ; Li, Jijie ; Ma, Xin ; Chen, Qi ; Zhao, Chenhao ; Han, Mingxiao ; Du, Hong ; Zhai, Yaxuan ; Cong, Qifei

ABSTRACT This study aimed to elucidate the complement protein C3-mediated host-pathogen interaction in the brain abscess caused by Staphylococcus aureus infection. Dual RNA-seq was employed to analyze the transcriptomic differences between C3 deficiency and wild-type mice of S. aureus- induced brain abscess model, and then we investigated the potential regulatory pathways of S. aureus- host interaction mediated by C3 and S. aureus genes associated with the pathogenesis of brain abscess. Finally, C3 deficient-mice and hla mutants of S. aureus were used to verify the specific pathogen-host interaction. In the S. aureus- induced brain abscess mouse model, the transcriptomic analysis revealed significant changes in bacterial virulence factors, such as hemolysin. Based on these data, we predicted a regulatory network formed by genes like hrcA and dnaK , which represent a possible regulation mechanism of S. aureus responding to the host. Furthermore, we identified that hla was the C3 response gene in S. aureus . From the host perspective, we observed that the absence of C3 significantly impacted the host’s inflammatory response, primarily by altering the gene expression of several key immune and inflammatory pathways. These findings suggest that C3 deficiency may impair the host’s ability to recognize and respond to external pathogens. To the best of our knowledge, this study proposed that S. aureus may affect host immune response through C3, and C3 plays a critical role in regulating inflammation and immune signaling pathways in the brain abscess caused by S. aureus infection. IMPORTANCE In this work, we employed immunofluorescence and Western blot analysis to reveal a significant upregulation of microglia-derived C3 in the brain abscess mice model caused by S. aureus infection. By integrating the individual RNA sequencing data of S. aureus and the dual RNA-seq data of S. aureus infection brain abscess mice model, the potential regulatory pathways between S. aureus and host were identified, and host C3 not only affects the immune response but also mediates the regulation network of S. aureus . This study provided the potential novel targets for therapeutic strategies in mitigating the effects of S. aureus infections and improving treatment outcomes.

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Bacterial DnaK

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