ArticleFrontiers in immunology2023
The critical role of Rap1-GAPs Rasa3 and Sipa1 in T cells for pulmonary transit and egress from the lymph nodes.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- RAS P21 Protein Activator 3 finetunes Type I immunity by limiting HCK-mediated STAT4 phosphorylation.Nature communications · 2026Article
- Genome-wide methylation profiling identifies signatures of pain, fatigue and health scores in women with systemic lupus erythematosus.Rheumatology (Oxford, England) · 2026Article
- Graph in Graph (GiG): A novel graph AI framework for integrating and interpreting medical and omics data.bioRxiv : the preprint server for biology · 2026Article
- A Rasa3-Gαi signaling axis orchestrates B lymphocyte trafficking into and through lymphoid organs.Cell reports · 2026Article
- Ras-proximate-1 (RAP1): a prognosis and therapeutic target in the metastatic spread of breast cancer.Clinical & experimental metastasis · 2025Review
- Interleukin-33-activated basophils promote asthma by regulating Th2 cell entry into lung tissue.The Journal of experimental medicine · 2024Article
- Mind the GAP: RASA2 and RASA3 GTPase-activating proteins as gatekeepers of T cell activation and adhesion.Trends in immunology · 2023Review
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Authors and funding
7 authors.
Funding
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Abstract
Rap1-GTPase activates integrins and plays an indispensable role in lymphocyte trafficking, but the importance of Rap1 inactivation in this process remains unknown. Here we identified the Rap1-inactivating proteins Rasa3 and Sipa1 as critical regulators of lymphocyte trafficking. The loss of Rasa3 and Sipa1 in T cells induced spontaneous Rap1 activation and adhesion. As a consequence, T cells deficient in Rasa3 and Sipa1 were trapped in the lung due to firm attachment to capillary beds, while administration of LFA1 antibodies or loss of talin1 or Rap1 rescued lung sequestration. Unexpectedly, mutant T cells exhibited normal extravasation into lymph nodes, fast interstitial migration, even greater chemotactic responses to chemokines and sphingosine-1-phosphate, and entrance into lymphatic sinuses but severely delayed exit: mutant T cells retained high motility in lymphatic sinuses and frequently returned to the lymph node parenchyma, resulting in defective egress. These results reveal the critical trafficking processes that require Rap1 inactivation.
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