ArticleThe Journal of experimental medicine2002
Differential requirement for LAT and SLP-76 in GPVI versus T cell receptor signaling.
Article in The Journal of experimental medicine, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 31 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
31 citing papers in PubMed, 89 citations in OpenAlex.
- Beyond Hemostasis: Platelets' Multifaceted Functions in Immune Responses.Life (Basel, Switzerland) · 2026Review
- Vav family exchange factors: Potential regulator in atherosclerosis.Biochemistry and biophysics reports · 2024Review
- cAMP- and cGMP-elevating agents inhibit GPIbα-mediated aggregation but not GPIbα-stimulated Syk activation in human platelets.Cell communication and signaling : CCS · 2019Article
- Platelet Signaling and Disease: Targeted Therapy for Thrombosis and Other Related Diseases.Pharmacological reviews · 2018Review
- Heat shock protein 70 regulates platelet integrin activation, granule secretion and aggregation.American journal of physiology. Cell physiology · 2016Article
- Article
- Platelet immunoreceptor tyrosine-based activation motif (ITAM) signaling and vascular integrity.Circulation research · 2014Review
- Peptide LSARLAF induces integrin β3 dependent outside-in signaling in platelets.Thrombosis research · 2012Article
- Integrin signalling and function in immune cells.Immunology · 2012Review
- Crucial role of SLP-76 and ADAP for neutrophil recruitment in mouse kidney ischemia-reperfusion injury.The Journal of experimental medicine · 2012Article
- What is vinculin needed for in platelets?Journal of thrombosis and haemostasis : JTH · 2010Article
- Article
- Cbl-b is a novel physiologic regulator of glycoprotein VI-dependent platelet activation.The Journal of biological chemistry · 2010Article
- Immunopathologies linked to integrin signalling.Seminars in immunopathology · 2010Review
- Coordination of receptor signaling in multiple hematopoietic cell lineages by the adaptor protein SLP-76.Cold Spring Harbor perspectives in biology · 2010Review
- The adapter protein SLP-76 mediates "outside-in" integrin signaling and function in T cells.Molecular and cellular biology · 2009Article
- SLP-76 couples Syk to the osteoclast cytoskeleton.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- The Role of SH2 Domain-containing Leukocyte Phosphoprotein of 76 kDa in the Regulation of Immune Cell Development and Function.Immune network · 2009Article
- Cutting edge: rescue of pre-TCR but not mature TCR signaling in mice expressing membrane-targeted SLP-76.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- Differential roles for the adapters Gads and LAT in platelet activation by GPVI and CLEC-2.Journal of thrombosis and haemostasis : JTH · 2008Article
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 7 institutions in 3 countries.
Funding
Abstract
Mice deficient in the adaptor Src homology 2 domain-containing leukocyte phosphoprotein of 76 kD (SLP-76) exhibit a bleeding disorder and lack T cells. Linker for activation of T cells (LAT)-deficient mice exhibit a similar T cell phenotype, but show no signs of hemorrhage. Both SLP-76 and LAT are important for optimal platelet activation downstream of the collagen receptor, GPVI. In addition, SLP-76 is involved in signaling mediated by integrin alphaIIbbeta3. Because SLP-76 and LAT function coordinately in T cell signal transduction, yet their roles appear to differ in hemostasis, we investigated in detail the functional consequences of SLP-76 and LAT deficiencies in platelets. Previously we have shown that LAT(-/-) platelets exhibit defective responses to the GPVI-specific agonist, collagen-related peptide (CRP). Consistent with this, we find that surface expression of P-selectin in response to high concentrations of GPVI ligands is reduced in both LAT- and SLP-76-deficient platelets. However, platelets from LAT(-/-) mice, but not SLP-76(-/-) mice, aggregate normally in response to high concentrations of collagen and convulxin. Additionally, unlike SLP-76, LAT is not tyrosine phosphorylated after fibrinogen binding to integrin alphaIIbbeta3, and collagen-stimulated platelets deficient in LAT spread normally on fibrinogen-coated surfaces. Together, these findings indicate that while LAT and SLP-76 are equally required for signaling via the T cell antigen receptor (TCR) and pre-TCR, platelet activation downstream of GPVI and alphaIIbbeta3 shows a much greater dependency on SLP-76 than LAT.
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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.