ArticleTH open : companion journal to thrombosis and haemostasis2018
TULA-2 Deficiency Enhances Platelet Functional Responses to CLEC-2 Agonists.
Article in TH open : companion journal to thrombosis and haemostasis, 2018. 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, 13 citations in OpenAlex.
- Phosphorylation at Y317 on Syk negatively regulates both ITAM- and hemITAM-mediated signaling and function in platelets.Blood advances · 2025Article
- Phosphorylation of (Ser 291) in the linker insert of Syk negatively regulates ITAM signaling in platelets.Platelets · 2024Article
- C-type lectin-like receptor 2: roles and drug target.Thrombosis journal · 2024Review
- TULA Proteins in Men, Mice, Hens, and Lice: Welcome to the Family.International journal of molecular sciences · 2023Review
- TULA-Family Regulators of Platelet Activation.International journal of molecular sciences · 2022Review
- D121 Located within the DRY Motif of P2Y12 Is Essential for P2Y12-Mediated Platelet Function.International journal of molecular sciences · 2022Article
- Clustering extent-dependent differential signaling by CLEC-2 receptors in platelets.Research and practice in thrombosis and haemostasis · 2022Article
- A role for the Sts phosphatases in negatively regulating IFNγ-mediated production of nitric oxide in monocytes.Immunity, inflammation and disease · 2020Article
- Phosphorylation of protein kinase Cδ Tyr311 positively regulates thromboxane generation in platelets.The Journal of biological chemistryArticle
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Platelet activation is essential for hemostasis. Central to platelet activation are the signals transmitted through surface receptors such as glycoprotein VI, the protease-activated receptors, and C-type lectin-like receptor 2 (CLEC-2). CLEC-2 is a HemITAM (hem-immunoreceptor tyrosine activation motif)-bearing receptor that binds podoplanin and signals through spleen tyrosine kinase (Syk). T-cell ubiquitin ligand-2 (TULA-2) is a protein tyrosine phosphatase that is highly expressed in platelets and targets phosphorylated Y352 of Syk. We wanted to determine whether TULA-2 regulates Syk phosphorylation and activity downstream of CLEC-2. To that end, we used TULA-2 knockout mice and wild-type (WT) littermate controls. We found that TULA-2 deficiency enhances the aggregation and secretion response following stimulation with an excitatory CLEC-2 antibody or the CLEC-2 agonist rhodocytin. Consistently, Syk phosphorylation of Y346 is enhanced, as well as phosphorylation of the downstream signaling molecule PLCγ2, in TULA-2 knockout platelets treated with either CLEC-2 antibody or rhodocytin, compared with WT control platelets. Furthermore, the kinetics of Syk phosphorylation, as well as that of PLCγ2 and SLP-76, is enhanced in TULA-2 knockout platelets treated with 2.5-μg/mL CLEC-2 antibody compared with WT platelets. Similarly, thromboxane production was enhanced, in both amount and kinetics, in TULA-2
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