Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Ntal/Lab/Lat2.

Shoko Iwaki1, Bettina M Jensen, Alasdair M Gilfillan

  • 1Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 10, Room 11C206, 10 Center Drive, MSC 1881, Bethesda, MD 20892-1881, USA.

The International Journal of Biochemistry & Cell Biology
|November 23, 2006
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

MMP9 and CCL18 associate with chronic urticaria while type I, IV, and VI collagens change with omalizumab treatment.

Allergy·2024
Same author

Expression of CCR8 and CCX-CKR on Basophils in Chronic Urticaria Is Amplified by IgE-Mediated Activation.

Biomedicines·2023
Same author

Elevated, FcεRI-dependent MRGPRX2 expression on basophils in chronic urticaria.

Skin health and disease·2023
Same author

Correction to: Measuring Histamine and Cytokine Release from Basophils and Mast Cells.

Methods in molecular biology (Clifton, N.J.)·2023
Same author

Mast cell progenitors in chronic urticaria.

Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology·2023
Same author

FcεRI-activated basophils express CCR4, CCR8, CCR9, CCX-CKR and XCR1.

Allergy·2022
Same journal

Corrigendum to "Sodium butyrate down-regulation of indoleamine 2, 3-dioxygenase at the transcriptional and post-transcriptional levels" [Int. J. Biochem. Cell Biol. 42 (2010) 1840-1846].

The international journal of biochemistry & cell biology·2026
Same journal

Whole-brain spatial metabolomics reveals metabolic gradient shifts in a murine glioma model following boron neutron capture therapy (130 characters).

The international journal of biochemistry & cell biology·2026
Same journal

LCN2 modulates Th17/Treg balance in vitro and is associated with an adaptive response to intestinal ischemia-reperfusion injury under Hmox1-deficient conditions.

The international journal of biochemistry & cell biology·2026
Same journal

Chloroquine modulates the redox-sensitive signalling via inhibiting the AMPK-ULK1 under LPS induced state in murine splenic macrophages.

The international journal of biochemistry & cell biology·2026
Same journal

The vicious cycle of hyperglycemia and oxidative stress: Novel mechanistic insights into a pathogenic alliance.

The international journal of biochemistry & cell biology·2026
Same journal

Fibroblast growth factors (FGF) in the pathogenesis and treatment of inflammatory bowel diseases (IBD): An overview.

The international journal of biochemistry & cell biology·2026
See all related articles

Non-T cell activation linker (NTAL), also known as LAT2, is a transmembrane adaptor protein found in hematopoietic cells. Its precise role in cell activation remains unclear despite its involvement in various signaling pathways.

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Non-T cell activation linker (NTAL)/linker for activation of B cells (LAB), now LAT2, is a transmembrane adaptor protein.
  • LAT2 is associated with lipid rafts in hematopoietic cells.
  • Its expression is noted in mast cells, monocytes, B cells, and NK cells.

Purpose of the Study:

  • To investigate the role of LAT2 in hematopoietic cell activation.
  • To understand the signaling pathways involving LAT2.

Main Methods:

  • Studies utilized gene knockout and knockdown approaches.
  • Analysis of receptor aggregation-induced tyrosine phosphorylation of LAT2.
  • Investigation of LAT2's recruitment of signaling molecules.

Related Experiment Videos

Main Results:

  • LAT2 phosphorylation is induced by FcεRI, Kit, FcγRI, and BCR aggregation.
  • Phosphorylated LAT2 recruits Grb2, Gab1, and c-Cbl.
  • LAT2 is expressed in NK cells but not resting T cells.

Conclusions:

  • LAT2 is implicated in the signaling complexes of various immune receptors.
  • LAT2's function as a positive or negative regulator in mast cell activation requires further elucidation.
  • The exact role of LAT2 in hematopoietic cell activation remains enigmatic.