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Last update 23 Jan 2025

GEM

Last update 23 Jan 2025

Basic Info

Synonyms

GEM, GTP binding protein overexpressed in skeletal muscle, GTP-binding mitogen-induced T-cell protein

+ [3]

Introduction

Could be a regulatory protein, possibly participating in receptor-mediated signal transduction at the plasma membrane. Has guanine nucleotide-binding activity but undetectable intrinsic GTPase activity.

Drugs associated with GEM

CN118420782

Patent Mining

Target

GEM

Mechanism-

Active Org.

Jilin University

Originator Org.

Jilin University

Active Indication

Severe Fever With Thrombocytopenia Syndrome

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with GEM

100 Translational Medicine associated with GEM

0 Patents (Medical) associated with GEM

234

Literatures (Medical) associated with GEM

11 Nov 2024·ACS Biomaterials Science & Engineering

Quantum Insights into Partially Molecular Imprinted Microspheres for Anticancer Therapeutics: Experimental and Theoretical Studies

Article

Author: VR, Vishnu ; Thrivikraman Nair, Sreejith ; Kamalasanan, Kaladhar ; Thankappan Presanna, Aneesh

Drug solubility is a determining factor for controlled release, and solubility-dependent release kinetics can be modified by changing the drug's state in the polymer matrix through partial molecular imprinting (PMI), although research in this area remains limited. This novel PMI approach creates nanocavities within the polymer by partially retaining the imprinting molecule and trapping the drug. Such a method holds promise for developing advanced biomaterial-based drug delivery systems for anticancer therapies. In this study, we developed microspheres designed for anticancer drug delivery utilizing PMI to enhance controlled release properties. Poly(vinyl alcohol) (PVA) microspheres were partially imprinted with aspirin (ASP) to create nanocavities for gemcitabine (GEM) molecules, inducing a polymorphic shift of GEM within the polymer matrix. This novel PMI approach enhanced drug release properties by enabling control over the drug crystallinity and release rate. The PVA-ASP-GEM complex showed zero-order release kinetics, releasing 21.6% of GEM over 48 h, maintaining steady state release profile. In contrast, nonimprinted PVA-GEM microspheres exhibited first-order kinetics with a faster release of 46.85% in the same period. Quantum insights from density functional theory (DFT) calculations revealed the superior stability of the PVA-ASP-GEM complex, with a binding free energy of -56.03 kcal/mol, compared to -29.07 kcal/mol for PVA-GEM. Molecular dynamics (MD) simulations demonstrated that ASP's presence created nanocavities that restricted GEM's movement, further contributing to the controlled release. Experimental validation through differential scanning calorimetry (DSC), thermogravimetric analysis (TGA), X-ray diffraction (XRD), and Raman spectroscopy confirmed the polymorphic transitions within the PVA-ASP-GEM complex. This PMI-based approach offers a promising method for modulating drug release kinetics and improving the stability of anticancer therapeutics, paving the way for innovative biomaterial-based drug delivery systems.

08 Oct 2024·Environmental Science & Technology

Photocatalysis Inhibits the Emergence of Multidrug-Resistant Bacteria in an Antibiotic-Resistant Bacterial Community in Aquatic Environments

Article

Author: An, Taicheng ; Cai, Yiwei ; Chen, Min ; Wang, Wanjun ; Sun, Tong ; Yin, Hongliang ; Li, Guiying

Bacterial antibiotic resistance has recently attracted increasing amounts of attention. Here, an artificially antibiotic-resistant bacterial community (ARBC) combined with five different constructed antibiotic-resistant bacteria (ARB) with single antibiotic resistance, namely, kanamycin (KAN), tetracycline (TET), cefotaxime (CTX), polymyxin B (PB), or gentamicin (GEM), was studied for the stress response to photocatalysis. With photocatalytic inactivation, the transfer and diffusion of antibiotic resistance genes (ARGs) in the ARBC decreased, and fewer multidrug-resistant bacteria (MDRB) emerged in aquatic environments. After several days of photocatalytic inactivation or Luria broth cultivation, >90% ARB were transformed to antibiotic-susceptible bacteria by discarding ARGs. Bacteria with double antibiotic resistance were the dominant species (99%) of residual ARB. The changes in ARG abundance varied, decreasing for the GEM and TET resistance genes and increasing for the KAN resistance genes. The change in the antibiotic resistance level was consistent with the change in ARG abundance. Correspondingly, point mutations occurred for the KAN, CTX and PB resistance genes after photocatalytic inactivation, which might be the reason why these genes persisted longer in the studied ARBC. In summary, photocatalytic inactivation could reduce the abundance of some ARGs and inhibit the emergence of MDRB as well as block ARG transfer in the bacterial community in aquatic environments. This work highlights the advantages of long-term photocatalytic inactivation for controlling antibiotic resistance and facilitates a better understanding of bacterial communities in real aquatic environments.

01 Oct 2024·Clinical & Experimental Metastasis

GFPT2 expression is induced by gemcitabine administration and enhances invasion by activating the hexosamine biosynthetic pathway in pancreatic cancer

Article

Author: Kamei, Takashi ; Miura, Takayuki ; Sato, Satoko ; Mizuma, Masamichi ; Xun, Jingyu ; Ishida, Masaharu ; Miyazaki, Kent ; Ariake, Kyohei ; Unno, Michiaki ; Ohtsuka, Hideo ; Douchi, Daisuke ; Nakagawa, Kei

AbstractOur previous studies revealed a novel link between gemcitabine (GEM) chemotherapy and elevated glutamine-fructose-6-phosphate transaminase 2 (GFPT2) expression in pancreatic cancer (PaCa) cells. GFPT2 is a rate-limiting enzyme in the hexosamine biosynthesis pathway (HBP). HBP can enhance metastatic potential by regulating epithelial-mesenchymal transition (EMT). The aim of this study was to further evaluate the effect of chemotherapy-induced GFPT2 expression on metastatic potential. GFPT2 expression was evaluated in a mouse xenograft model following GEM exposure and in clinical specimens of patients after chemotherapy using immunohistochemical analysis. The roles of GFPT2 in HBP activation, downstream pathways, and cellular functions in PaCa cells with regulated GFPT2 expression were investigated. GEM exposure increased GFPT2 expression in tumors resected from a mouse xenograft model and in patients treated with neoadjuvant chemotherapy (NAC). GFPT2 expression was correlated with post-operative liver metastasis after NAC. Its expression activated the HBP, promoting migration and invasion. Treatment with HBP inhibitors reversed these effects. Additionally, GFPT2 upregulated ZEB1 and vimentin expression and downregulated E-cadherin expression. GEM induction upregulated GFPT2 expression. Elevated GFPT2 levels promoted invasion by activating the HBP, suggesting the potential role of this mechanism in promoting chemotherapy-induced metastasis.

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