ArticleMolecular biology of the cell2019
Multiple sources of signal amplification within the B-cell Ras/MAPK pathway.
Article in Molecular biology of the cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- A chemigenetic endogenous Ras activity biosensor for live-cell pharmacology.Nature chemical biology · 2026Article
- Article
- The Evolving Role of Bruton's Tyrosine Kinase Inhibitors in B Cell Lymphomas.International journal of molecular sciences · 2024Review
- Bimodality in Ras signaling originates from processivity of the Ras activator SOS without deterministic bistability.Science advances · 2024Article
- Genetically encodable biosensors for Ras activity.RSC chemical biology · 2024Review
- Cordyceps sinensis relieves non-small cell lung cancer by inhibiting the MAPK pathway.Chinese medicine · 2024Article
- In Vivo Treatment with Insulin-like Growth Factor 1 Reduces CCR5 Expression on Vaccine-Induced Activated CD4Vaccines · 2023Article
- KRAS and RAS-MAPK Pathway Deregulation in Mature B Cell Lymphoproliferative Disorders.Cancers · 2022Review
- Case report: The cardio-facio-cutaneous syndrome due to a novel germline mutation inFrontiers in pediatrics · 2022Article
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Authors and funding
2 authors.
Funding
Abstract
The Ras-Map kinase (MAPK) cascade underlies functional decisions in a wide range of cell types and organisms. In B-cells, positive feedback-driven Ras activation is the proposed source of the digital (all or none) MAPK responses following antigen stimulation. However, an inability to measure endogenous Ras activity in living cells has hampered our ability to test this model directly. Here we leverage biosensors of endogenous Ras and ERK activity to revisit this question. We find that B-cell receptor (BCR) ligation drives switch-like Ras activation and that lower BCR signaling output is required for the maintenance versus the initiation of Ras activation. Surprisingly, digital ERK responses persist in the absence of positive feedback-mediated Ras activation, and digital ERK is observed at a threshold level of Ras activation. These data suggest an independent analogue-to-digital switch downstream of Ras activation and reveal that multiple sources of signal amplification exist within the Ras-ERK module of the BCR pathway.
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