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Piceatannol upregulates USP14-mediated GPX4 deubiquitination to inhibit neuronal ferroptosis caused by cerebral ischemia-reperfusion in mice.

Food Chem Toxicol

January 2025

Department of Pharmacology, Key Laboratory of Anti-Inflammatory and Immunopharmacology of Ministry of Education, Key Laboratory of Chinese Medicine Research and Development of State Administration of Traditional Chinese Medicine, Anhui Medical University, Hefei, Anhui, People's Republic of China. Electronic address:

Ischemic stroke is a very common brain disorder. This study aims to assess the neuroprotective effects of piceatannol (PCT) in preventing neuronal injury resulting from cerebral ischemia and reperfusion (I/R) in mice. Additionally, we investigated the underlying mechanisms through which PCT inhibits neuronal ferroptosis by modulating the USP14/GPX4 signaling axis.

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Background: Ferroptosis has emerged as a promising therapeutic target in cancer treatment. CEP55, a key regulator of cell mitosis, plays a significant role in the tumorigenesis of many malignancies. In this study, we elucidated the function of CEP55 in the ferroptosis of breast cancer (BC).

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UBE2Q2 promotes tumor progression and glycolysis of hepatocellular carcinoma through NF-κB/HIF1α signal pathway.

Cell Oncol (Dordr)

January 2025

Department of Hepatobiliary and Pancreatic Surgery, Zhongnan Hospital of Wuhan University, 169 Donghu Road, Wuhan, Hubei, 430071, PR China.

Purpose: Metabolic reprogramming, particularly the Warburg effect, plays a crucial role in the onset and progression of tumors. The ubiquitin-conjugating enzyme E2 Q2 (UBE2Q2) has been identified overexpressed in hepatocellular carcinoma (HCC). Our aim was to determine if UBE2Q2 plays a role in regulating glycolysis, contributing to the carcinogenesis of HCC.

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Neuronal excitation-transcription (E-T) coupling pathways can be initiated by local increases of Ca concentrations within a nanodomain close to the L-type voltage-gated Ca channel (LTCC). However, molecular mechanisms controlling LTCC organization within the plasma membrane that help creation these localized signaling domains remain poorly characterized. Here, we report that neuronal depolarization increases Ca1.

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(-) - (11R, 12S)-mefloquine ameliorates neuropathic pain by modulating Cx36-ER stress interaction in the pain-related central nervous system in rats.

Life Sci

January 2025

Key Laboratory of Brain Functional Genomics, Ministry of Education, School of Life Sciences, East China Normal University, Shanghai 200062, China; Shanghai Engineering Research Center of Molecular Therapeutics and New Drug Development, School of Chemistry and Molecular Engineering, East China Normal University, Shanghai 200062, China. Electronic address:

Article Synopsis
  • The study investigates how (-) - Mefloquine affects the interactions between Connexin 36 (Cx36) and endoplasmic reticulum stress (ERS) in rat models of neuropathic pain and cell cultures.
  • Researchers induced neuropathic pain in rats and ERS in specific cells to observe the effects of Mefloquine through various biological techniques.
  • Findings indicate that Mefloquine can reduce neuropathic pain by modifying Cx36 and its relationship with ERS, offering insights into potential new treatments for pain management.
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