ArticleThe Journal of biological chemistry2012
Genetic evidence for critical roles of P38α protein in regulating mast cell differentiation and chemotaxis through distinct mechanisms.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- PRL2 Phosphatase Promotes Oncogenic KIT Signaling in Leukemia Cells through Modulating CBL Phosphorylation.Molecular cancer research : MCR · 2024Article
- ATP/IL-33-Co-Sensing by Mast Cells (MCs) Requires Activated c-Kit to Ensure Effective Cytokine Responses.Cells · 2023Article
- CREB Is Activated by the SCF/KIT Axis in a Partially ERK-Dependent Manner and Orchestrates Survival and the Induction of Immediate Early Genes in Human Skin Mast Cells.International journal of molecular sciences · 2023Article
- Early development and functional properties of tryptase/chymase double-positive mast cells from human pluripotent stem cells.Journal of molecular cell biology · 2021Article
- IL-3 is essential for ICOS-L stabilization on mast cells, and sustains the IL-33-induced RORγtImmunology · 2021Article
- The underestimated role of the microphthalmia-associated transcription factor (MiTF) in normal and pathological haematopoiesis.Cell & bioscience · 2021Review
- p38α regulates cytokine-induced IFNγ secretion via the Mnk1/eIF4E pathway in Th1 cells.Immunology and cell biology · 2017Article
- The transcriptional program, functional heterogeneity, and clinical targeting of mast cells.The Journal of experimental medicine · 2017Review
- TAK1 and IKK2, novel mediators of SCF-induced signaling and potential targets for c-Kit-driven diseases.Oncotarget · 2015Article
- Article
- p38α protein negatively regulates T helper type 2 responses by orchestrating multiple T cell receptor-associated signals.The Journal of biological chemistry · 2012Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Mast cells mediate a range of immune responses. However, the mechanisms that contribute to their development remain poorly understood. Here, using a P38α conditional knockout system, we provide evidence to suggest that P38α plays critical roles in regulating mast cell differentiation and migration via distinct mechanisms. Induced deletion of P38α in bone marrow cells retards the maturation of mast cells in part by inhibiting the activation of cAMP response element-binding protein and expression of microphthalmia-associated transcription factor, which encourages the generation of basophils over mast cells. In fully differentiated mast cells, absence of P38α inhibits stem cell factor-induced activation of Akt and ERK, which is associated with reduced chemotaxis. In vivo, conditional deletion of P38α results in reduced numbers of mast cells in certain tissues and a failure to reconstitute these cells in W(sh) mice transplanted with P38α(-/-) Lin(-)c-kit(+)Sca-1(+) (LKS(+)) cells. Our findings suggest that P38α plays a dual role in mast cell development by regulating IL-3-induced differentiation of mast cell progenitor cells as well as by regulating stem cell factor-induced migration of fully differentiated mast cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.