Results 161 to 170 of about 62,168 (302)

Dimerization‐dependent NOTCH receptor transactivation unveils a class of highly selective NOTCH signalling inhibitors

open access: yesThe FEBS Journal, EarlyView.
NOTCH signalling is indispensable for tissue homeostasis and, consequently, corruption of its normal function promotes numerous diseases, including cancer. However, the development of targeted therapies has been hampered by inefficacy and overt toxicity. Here, we show that NOTCH receptor dimerization is necessary for receptor transactivation, which has
Xinxin Liu   +9 more
wiley   +1 more source

Engineering a DYRK1B R102C mutation: insights into metabolic syndrome pathogenesis through lentiviral gene delivery [PDF]

open access: yesMedical Laboratory Journal
Background: A rare heterozygous DYRK1B mutation (R102C) recently linked to a familial form of metabolic syndrome prompted this study to introduce the R102C mutation into the mouse DYRK1B gene, utilizing recombinant lentiviruses for long-term gene ...
Afrooz Daneshparvar   +6 more
doaj  

LIN28A blocks the EndMT process of high glucose‐induced HRMECs by stabilizing SIRT6 mRNA

open access: yesJournal of Diabetes Investigation, EarlyView.
LIN28A promotes mRNA stability of SIRT6 to activate the AMPK signaling, thereby inhibiting the EndMT process induced by HG in HRMECs. ABSTRACT Background Diabetic retinopathy (DR) is a microvascular condition resulting from microangiopathy, causing gradual retinal damage and potential blindness.
Xueying Wang   +5 more
wiley   +1 more source

FNDC1 Competitively Binds Gβ2 to Suppress the β‐Catenin–Destruction Complex and Promote Gastric Cancer Malignancy

open access: yesThe FASEB Journal, Volume 40, Issue 6, 31 March 2026.
FNDC1 competitively binds Gβ2 to suppress the β‐catenin–destruction complex and promote the malignant behavior of gastric cancer (GC) by the following mechanism: elevated FNDC1 competes with Dvl for binding to Gβ2, thereby reducing Dvl–Gβ2 interaction; this reduction inhibits Dvl degradation in the cytoplasm; increased Dvl recruits Axin1, thereby ...
Wenyu Gao   +9 more
wiley   +1 more source

NOTCH3 CADASIL Variant Receptor Aggregation Requires NOTCH3 Wild‐Type Receptors: Identification of Highly Selective Inhibitors That Block the Process

open access: yesThe FASEB Journal, Volume 40, Issue 6, 31 March 2026.
CADASIL is the major cause of early‐onset stroke and cognitive dysfunction, including dementia. It is caused by mutations in the NOTCH3 receptor that result in the formation of protein aggregates in the small vessel walls of the brain. We demonstrated that NOTCH3 CADASIL variant receptor aggregation is strictly dependent on interactions with NOTCH3 ...
Haijiang Wang   +9 more
wiley   +1 more source

Decoding the Cellular Heterogeneity and Malignant Progression of Human Penile Squamous Cell Carcinoma by Single‐Cell RNA Sequencing

open access: yesAdvanced Science, Volume 13, Issue 14, 9 March 2026.
Single‐cell transcriptomic and functional analyses identify SEMA3C as a key regulator of tumor progression and tumor microenvironment remodeling in penile squamous cell carcinoma. SEMA3C promotes epithelial–mesenchymal transition, tumor growth, and invasion while shaping an immunosuppressive microenvironment, highlighting its potential as a prognostic ...
Xiheng Hu   +21 more
wiley   +1 more source

NDST3‐Induced Epigenetic Reprogramming Reverses Neurodegeneration in Parkinson's Disease

open access: yesAdvanced Science, Volume 13, Issue 14, 9 March 2026.
NDST3‐mediated epigenetic reprogramming revitalizes neuronal circuits in the substantia nigra and striatum to halt dopaminergic neuron degeneration and restore motor function in Parkinson's disease models. This strategy promotes neuronal maintenance and functional recovery, highlighting NDST3's therapeutic potential in neurodegenerative disorders ...
Yujung Chang   +18 more
wiley   +1 more source

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