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ACK1/TNK2 kinase: molecular mechanisms and emerging cancer therapeutics.
Trends Pharmacol Sci
December 2024
Division of Urologic Surgery, Department of Surgery, Washington University at St. Louis, St. Louis, MO 63110, USA; Siteman Cancer Center, Cancer Research Building, Washington University at St. Louis, St. Louis, MO 63110, USA. Electronic address:
Activated CDC42-associated kinase 1 (ACK1), encoded by the TNK2 gene, is a cytoplasmic non-receptor tyrosine kinase whose aberrant activation correlates positively with cancer severity. Recent research has revealed the functional relevance of this oncokinase - it is an epigenetic regulator that drives cancer progression in multiple malignancies. Although ACK1 is an attractive target for therapeutic intervention, incomplete knowledge of its diverse signaling mechanisms and the lack of specific inhibitors have challenged its clinical success.
View Article and Find Full Text PDFKif15 regulates Coro1a cell migration and phagocytosis in zebrafish after spinal cord injury.
Int Immunopharmacol
December 2024
Key Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, Co-innovation Center of Neuroregeneration, Nantong University, Nantong Jiangsu 226001, China. Electronic address:
The role of immune cells is crucial in nerve regeneration following spinal cord injury. Kif15, a member of the kinesin family, has been shown to enhance macrophage phagocytosis. This study investigates the impact of Kif15 deficiency on immune cells in zebrafish with spinal cord injury.
View Article and Find Full Text PDFA PDZ-kinase allosteric relay mediates Par complex regulator exchange.
J Biol Chem
December 2024
Institute of Molecular Biology Department of Chemistry and Biochemistry 1229 University of Oregon Eugene, OR 97403. Electronic address:
The Par complex polarizes the plasma membrane of diverse animal cells using the catalytic activity of atypical Protein Kinase C (aPKC) to pattern substrates. Two upstream regulators of the Par complex, Cdc42 and Par-3, bind separately to the complex to influence its activity in different ways. Each regulator binds a distinct member of the complex, Cdc42 to Par-6 and Par-3 to aPKC, making it unclear how they influence one another's binding.
View Article and Find Full Text PDFaPKC/Par3/Par6 polarity complexes regulate podocyte motility and crescent formation in the progression of ANCA-associated vasculitis.
Rheumatology (Oxford)
December 2024
Renal Division, Department of Medicine, Peking University First Hospital, Peking University Institute of Nephrology, Key Laboratory of Renal Disease, Ministry of Health of China, Key Laboratory of Chronic Kidney Disease Prevention and Treatment (Peking University), Ministry of Education, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, China.
Objectives: Podocyte bridging may be a key initial event occurring early in crescent formation. This study aims to probe the underlying mechanism of atypical protein kinase C (aPKC)/protease-activated receptor 3(Par3)/Par6 polarity complexes on podocyte motility and crescent formation during the progression of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV).
Methods: The effects of anti-TNF-α monoclonal antibody (mAb) on the crescent formation, localization and expression of aPKC/Par3/Par6 polarity complexes, and activities of small GTPases (Rho/Rac1/Cdc42) were explored in an AAV mouse model.
and in prostate cancer: from molecular pathways to therapeutic targets: a narrative review.
Transl Androl Urol
November 2024
Department of Urology, Second People's Hospital of China Three Gorges University, Yichang, China.
Background And Objective: Prostate cancer is a major cause of cancer-related morbidity and mortality in men globally. The pathogenesis involves complex interactions between genetic mutations and environmental factors, activating multiple signaling pathways, especially Wnt/β-catenin, PI3K/Akt, and NF-κB pathways. Tumor suppressor genes and are key inhibitors of these pathways, crucial in suppressing tumor growth and metastasis.
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