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Cotargeting of thioredoxin 1 and glutamate-cysteine ligase in both imatinib-sensitive and imatinib-resistant CML cells.
Biochem Pharmacol
January 2025
State Key Laboratory on Technologies for Chinese Medicine Pharmaceutical Process Control and Intelligent Manufacture, Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210023, PR China; School of Pharmacy, Nanjing University of Chinese Medicine, Nanjing, PR China. Electronic address:
Chronic myeloid leukemia (CML) is a type of malignancy characterized by harboring the oncogene Bcr-Abl, which encodes the constitutively activated tyrosine kinase BCR-ABL. Although tyrosine kinase inhibitors targeting BCR-ABL have revolutionized CML therapy, native and acquired drug resistance commonly remains a great challenge. Thioredoxin 1 (Trx1) and glutamate-cysteine ligase (GCL), which are two major antioxidants that maintain cellular redox homeostasis, are potential targets for cancer therapy and overcoming drug resistance.
View Article and Find Full Text PDFInhibition of AXL ameliorates pulmonary fibrosis attenuation of M2 macrophage polarization.
Eur Respir J
January 2025
Department of Biochemistry and Molecular Biology, Brain Korea 21 Project, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea.
Rationale: Although a relationship between the Gas6/AXL pathway and pulmonary fibrosis (PF) has been suggested, the precise mechanisms and clinical implications of the AXL pathway in idiopathic pulmonary fibrosis (IPF) are still unclear.
Methods: Constitutive and conditional AXL-knockout mice were generated and injected with bleomycin (BLM) to induce pulmonary fibrosis. The expression of AXL and macrophage subtypes in BLM-injected mice and patients with IPF was analysed using flow cytometry.
Interaction of unphosphorylated PtsN with the K/H antiporter YcgO inhibits its activity in Escherichia coli.
J Biol Chem
December 2024
Laboratory of Molecular Microbiology and Genetics, BRIC-Centre for DNA Fingerprinting and Diagnostics, Hyderabad, India. Electronic address:
Genetic studies in Escherichia coli have implicated the unphosphorylated version of PtsN (unphospho-PtsN), the terminal phospho-acceptor of the PtsP-PtsO-PtsN phosphorelay, as a negative regulator of potassium (K) efflux mediated by YcgO. YcgO is a protein belonging to the CPA1 family of monovalent cation/proton antiporters. Here we show that in vivo, YcgO comprises an approximately 383 amino acid N-terminal transmembrane domain (TMD) and a 195 amino acid C-terminal cytoplasmic region (CTR).
View Article and Find Full Text PDFChromosomal instability (CIN) is common in solid tumours and fuels evolutionary adaptation and poor prognosis by increasing intratumour heterogeneity. Systematic characterization of driver events in the TRACERx non-small-cell lung cancer (NSCLC) cohort identified that genetic alterations in six genes, including FAT1, result in homologous recombination (HR) repair deficiencies and CIN. Using orthogonal genetic and experimental approaches, we demonstrate that FAT1 alterations are positively selected before genome doubling and associated with HR deficiency.
View Article and Find Full Text PDFIncreased phosphorylation of AMPKα1 S485 in colorectal cancer and identification of PKCα as a responsible kinase.
Cancer Lett
December 2024
Department of Gastroenterology, Jiangxi Provincial Key Laboratory of Digestive Diseases, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China. Electronic address:
Article Synopsis
- The study investigates how phosphorylation of AMPKα1 at S485 affects colon cancer cells and identifies PKCα as the responsible kinase.
- The results indicate that S485 phosphorylation is higher in colorectal cancer tissues compared to normal ones and is linked to increased cell growth and migration.
- The research highlights that PKCα plays a key role in this phosphorylation, as its inhibition reduces S485 phosphorylation and impacts cancer cell behaviors under various nutritional conditions.
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