ReviewJournal of leukocyte biology2011
LAB/NTAL/Lat2: a force to be reckoned with in all leukocytes?
Review in Journal of leukocyte biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 18 citations in OpenAlex.
- Temporal phosphoproteomics reveals key regulators of procoagulant COAT platelet generation.Blood vessels, thrombosis & hemostasis · 2026Article
- In-depth analysis of retinal RNA transcriptome sequencing in a rat model of hypertensive retinopathy.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026Article
- Prognostic implications of autophagy and pyroptosis related genes in oral squamous cell carcinoma: research on bioinformatics and experiments.Frontiers in oncology · 2025Article
- Article
- Untangling the Role of TREM2 in Conjugation with Microglia in Neuronal Dysfunction: A Hypothesis on a Novel Pathway in the Pathophysiology of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2023Review
- NTAL is associated with treatment outcome, cell proliferation and differentiation in acute promyelocytic leukemia.Scientific reports · 2020Article
- TREM2-Ligand Interactions in Health and Disease.Journal of molecular biology · 2017Review
- Triggering receptor expressed on myeloid cells and 5'adenosine monophosphate-activated protein kinase in the inflammatory response: a potential therapeutic target.Expert review of clinical immunology · 2016Review
- Tespa1 negatively regulates FcεRI-mediated signaling and the mast cell-mediated allergic response.The Journal of experimental medicine · 2014Article
- The AML1/ETO target gene LAT2 interferes with differentiation of normal hematopoietic precursor cells.Leukemia research · 2014Article
- Multiple regulatory roles of the mouse transmembrane adaptor protein NTAL in gene transcription and mast cell physiology.PloS one · 2014Article
- LAB/NTAL facilitates fungal/PAMP-induced IL-12 and IFN-γ production by repressing β-catenin activation in dendritic cells.PLoS pathogens · 2013Article
- Emerging roles for protein S-palmitoylation in immunity from chemical proteomics.Current opinion in chemical biology · 2013Review
- Linker for activation of T-cell family member2 (LAT2) a lipid raft adaptor protein for AKT signaling, is an early mediator of alkylphospholipid anti-leukemic activity.Molecular & cellular proteomics : MCP · 2012Article
- Survey of activated FLT3 signaling in leukemia.PloS one · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
LAB/NTAL/Lat2 is a transmembrane adaptor protein closely related to LAT. It is expressed in various myeloid and lymphoid cells, many of which also express LAT. Phosphorylation of LAB occurs following engagement of various ITAM- and non-ITAM-linked receptors and can play positive and negative roles following receptor engagement. LAT binds PLCγ directly, resulting in efficient Ca²+ flux and degranulation. However, LAB does not contain a PLCγ-binding motif and only binds PLCγ indirectly, possibly via Grb2, thereby resulting in suboptimal signaling. As LAT can signal more efficiently than LAB, competition between the 2 for space/substrates in the lipid rafts can attenuate signaling. This competition model requires coexpression of LAT; however, LAB is repressive, even in cells lacking substantial LAT expression such as macrophages and mature B cells. The reported interaction between LAB and the ubiquitin E3-ligase c-Cbl suggests 1 possible mechanism for LAT-independent inhibition by LAB, but such a model requires further investigation. Given the wide-reaching expression pattern of LAB, LAB has the ability to modulate signaling in virtually every type of leukocyte. Regardless of its ultimate mode of action, the potent regulatory capability of LAB proves this protein to be a complex adaptor that warrants continued, substantial scrutiny by biochemists and immunologists alike.
Indexed as
Identifiers
What OpenQuestion holds
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.