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The histone demethylase KDM5C enhances the sensitivity of acute myeloid leukemia cells to lenalidomide by stabilizing cereblon.
Cell Mol Biol Lett
January 2025
Jiangsu Key Laboratory of Neuropsychiatric Diseases and College of Pharmaceutical Sciences, Jiangsu Province Engineering Research Center of Precision Diagnostics and Therapeutics Development, Jiangsu Key Laboratory of Preventive and Translational Medicine for Geriatric Diseases, Suzhou Key Laboratory of Drug Research for Prevention and Treatment of Hyperlipidemic Diseases, Soochow University, 199 Ren'ai Road, Suzhou, 215123, Jiangsu, China.
Background: The protein cereblon (CRBN) mediates the antileukemia effect of lenalidomide (Len). Len binds to CRBN, recruits IKZF1/IKZF3, and promotes their ubiquitination and degradation, through which Len exhibits its antileukemia and antimyeloma activity. Therefore, the protein level of CRBN might affect the antiproliferative effect of Len.
View Article and Find Full Text PDFSodium butyrate regulates macrophage polarization by TGR5/β-arrestin2 in vitro.
Mol Med
January 2025
Department of Critical Care Medicine, Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuchang, Wuhan, 430060, Hubei, China.
Background: Macrophages play an important role in the pathogenesis of ulcerative colitis (UC). We will explore the effects of sodium butyrate (SB) on macrophage function.
Methods: The targets of butyric acid were identified using SwissTargetPrediction database and surface plasmon resonance (SPR).
Spinal ADAM17 contributes to the pathogenesis of painful diabetic neuropathy in leptin receptor-deficient mice.
Biochem Pharmacol
January 2025
Division of Pharmacology, Faculty of Pharmaceutical Sciences, Tohoku Medical and Pharmaceutical University, Japan.
The pathogenesis of painful diabetic neuropathy (PDN) is complicated and remains not fully understood. A disintegrin and metalloprotease 17 (ADAM17) is an enzyme that is responsible for the degradation of membrane proteins. ADAM17 is known to be activated under diabetes, but its involvement in PDN is ill defined.
View Article and Find Full Text PDFKnockout or treatment with an antagonist of formyl peptide receptor 1 protects mice from sepsis by inhibiting inflammation.
Cytokine
January 2025
Department of Gastroenterology, General Hospital of Ningxia Medical University (The First Clinical Medical College of Ningxia Medical University), 750004 Yinchuan, China.
Background: Sepsis is an infection-related systemic inflammation with high mortality rates. Activation of formyl peptide receptor 1 (FPR1) in immune cells can promote their chemotaxis and inflammatory response, which imbalances immune response during the process of sepsis. FPR1 blockade did diminish systemic inflammatory response during bacterial infection.
View Article and Find Full Text PDFSynthesis and biological evaluation of new dual APN/NEP inhibitors as potent analgesics.
Bioorg Chem
January 2025
School of Pharmaceutical Sciences, Cheeloo College of Medicine, Shandong University, Jinan 250012, China. Electronic address:
An alternative approach for the management of acute and chronic pains involves prolonging the half-life of endogenous opiates, such as enkephalins that are released in response to nociceptive stimuli. This can be achieved through the inhibition of enzymatic pathways responsible for the hydrolysis of these peptides, particularly targeting Aminopeptidase N (APN) and Neutral Endopeptidase (NEP). In this study, we designed and synthesized a series of dual enkephalinase inhibitors (DENKIs) targeting both APN and NEP as novel analgesic treatments.
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