Targeting the non‐ATP‐binding pocket of the MAP kinase p38γ mediates a novel mechanism of cytotoxicity in cutaneous T‐cell lymphoma (CTCL)
Author:
Affiliation:
1. Beckman Research Institute of City of Hope Duarte CA USA
Publisher
Wiley
Subject
Cell Biology,Genetics,Molecular Biology,Biochemistry,Structural Biology,Biophysics
Link
https://onlinelibrary.wiley.com/doi/pdf/10.1002/1873-3468.14186
Reference64 articles.
1. Activation and signaling of the p38 MAP kinase pathway
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3. Phosphorylation of NFATc4 by p38 Mitogen-Activated Protein Kinases
4. Alternative p38 activation pathway mediated by T cell receptor–proximal tyrosine kinases
5. Alternative ZAP70-p38 signals prime a classical p38 pathway through LAT and SOS to support regulatory T cell differentiation
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1. Kinases Inhibitors as New Therapeutic Opportunities in Cutaneous T-Cell Lymphoma;Kinases and Phosphatases;2024-08-28
2. The interplay of p38 MAPK signaling and mitochondrial metabolism, a dynamic target in cancer and pathological contexts;Biochemical Pharmacology;2024-07
3. Pirfenidone ameliorates alcohol-induced promotion of breast cancer in mice;Frontiers in Oncology;2024-03-25
4. Architecture of the MKK6-p38α complex defines the basis of MAPK specificity and activation;Science;2023-09-15
5. p38γ MAPK Inflammatory and Metabolic Signaling in Physiology and Disease;Cells;2023-06-21
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