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Last update 08 May 2025

GRPEL1

Last update 08 May 2025

Basic Info

Synonyms

FLJ25609, GREPEL1, GrpE

+ [5]

Introduction

Essential component of the PAM complex, a complex required for the translocation of transit peptide-containing proteins from the inner membrane into the mitochondrial matrix in an ATP-dependent manner (By similarity). Seems to control the nucleotide-dependent binding of mitochondrial HSP70 to substrate proteins (PubMed:11311562).

Drugs associated with GRPEL1

CN116023505

Patent Mining

Target

GRPEL1

Mechanism-

Active Org.

Lanzhou University

Originator Org.

Lanzhou University

Active Indication

Infectious Diseases

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with GRPEL1

100 Translational Medicine associated with GRPEL1

0 Patents (Medical) associated with GRPEL1

681

Literatures (Medical) associated with GRPEL1

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.

11 Mar 2025·Blood Advances

Genome-wide CRISPR/Cas9 screen identifies AraC-daunorubicin-etoposide response modulators associated with outcomes in pediatric AML

Article

Author: Rafiee, Roya ; Rubnitz, Jeffrey ; Parcha, Phani K. ; Tagmount, Abderrahmane ; Vulpe, Christopher D. ; Ribeiro, Raul ; Lamba, Jatinder K. ; Nguyen, Nam H. K. ; Pounds, Stanley B. ; Cao, Xueyuan

AbstractCytarabine, daunorubicin, and etoposide (ADE) have been the standard backbone of induction chemotherapy regimen for patients with pediatric acute myeloid leukemia (pAML) for >5 decades. However, chemoresistance is still a major concern, and a significant proportion of pAML becomes resistant to ADE treatment and relapse, leading to poor survival. Therefore, there is a considerable need to identify mechanisms mediating drug resistance for overcoming chemoresistance. Herein, we performed synthetic lethal CRISPR/Cas9 screens using the ADE components to identify response markers. We further integrated significant markers in 3 independent pAML clinical cohorts treated with only an ADE regimen to identify drug response biomarkers with prognostic significance. We were able to identify several mediators that represent clinically and biologically significant marker genes for ADE treatment, such as BCL2, CLIP2, and VAV3, which are resistant markers to ADE, with high expression associated with poor outcomes in pAML treated with ADE, and GRPEL1, HCFC1, and TAF10, which are sensitive markers to ADE, with high expression showing beneficial outcomes. Notably, BCL2, CLIP2, and VAV3 knockdowns in their expression in AML cell lines sensitized the cells more to the ADE components, suggesting that these modulators should be further studied as potential therapeutic targets to overcome chemoresistance.

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GRPEL1

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