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http://dx.doi.org/10.5114/aoms/193392 | DOI Listing |
Biomark Res
January 2025
Department of Breast Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
Background: Although immunotherapy has achieved great progress in advanced triple-negative breast cancer (TNBC), there are still numerous patients who do not benefit from immunotherapy. Therefore, identification of the key molecule that induces immune escape and clarification of its specific mechanism in TNBC are urgently needed.
Methods: In this research, single cell sequencing and bulk sequencing were conducted for biomarker screening.
J Mol Neurosci
December 2024
Centre for Drug and Herbal Development, Faculty of Pharmacy, Universiti Kebangsaan Malaysia, Jalan Raja Muda Abdul Aziz, 50300, Kuala Lumpur, Malaysia.
Elevated inflammatory reactions are a significant component in cerebral ischemia-reperfusion injury (CIRI). Activation of α7-Nicotinic Acetylcholine Receptor (α7nAChR) reduces stroke-induced inflammation in rats, but the anti-inflammatory pathway in microglia under CIRI condition remains unclear. This study employed qRT-PCR, protein assays, NanoString analysis, and bioinformatics to examine the effects of PNU282987 treatment (α7nAChR agonist) on BV2 microglial functional differentiation in oxygen-glucose deprivation/reoxygenation (OGDR) condition.
View Article and Find Full Text PDFArch Med Sci
October 2024
Department of Obstetrics and Gynecology, Putuo District Central Hospital, Shanghai Putuo Hospital, Shanghai University of Traditional Chinese Medicine, China.
Cell Mol Biol (Noisy-le-grand)
November 2024
Stem Cells and Regenerative Medicine, Cell Therapy and Cancer Research (CTCR), King Abdullah International Medical Research Center (KAIMRC), King Abdulaziz Medical City P.O. Box 22490, Riyadh 11426, Saudi Arabia.
Cell Commun Signal
November 2024
Department of Oral Pathobiological Science, Microbiology, Graduate School of Dental Medicine, Hokkaido University, Kita13 Nishi7, Kita-Ku, Sapporo, 060-8586, Japan.
Understanding the intricate cellular interactions involved in bone restoration is crucial for developing effective strategies to promote bone healing and mitigate conditions such as osteoporosis and fractures. Here, we provide compelling evidence supporting the anabolic effects of a pharmacological Pyk2 inhibitor (Pyk2-Inh) in promoting bone restoration. In vitro, Pyk2 signaling inhibition markedly enhances alkaline phosphatase (ALP) activity, a hallmark of osteoblast differentiation, through activation of canonical Wnt/β-catenin signaling.
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