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

Amplifying Btk's signal.

Pamela L Schwartzberg1

  • 1National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA.

Immunity
|November 15, 2003
PubMed
Summary
This summary is machine-generated.

Bruton's tyrosine kinase (Btk) activates phosphatidylinositol-4-phosphate 5-kinase (PIP5K), creating a positive feedback loop. This loop generates PI(4,5)P2, a key molecule for immune cell signaling pathways.

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

Tuning PI3K: striking the right balance for optimal CD8 T-cell responses.

Journal of immunology (Baltimore, Md. : 1950)·2026
Same author

SARS-CoV-2 infection and vaccination elicit distinct pharyngeal mucosal B cell responses in children.

Nature communications·2026
Same author

A Rasa3-Gαi signaling axis orchestrates B lymphocyte trafficking into and through lymphoid organs.

Cell reports·2026
Same author

A PI3Kδ-Foxo1-FasL signaling amplification loop rewires CD4+ T cell signaling and differentiation.

The Journal of experimental medicine·2026
Same author

Gain of function NOTCH4 variants disrupt angiogenesis in systemic sclerosis.

Annals of the rheumatic diseases·2026
Same author

Optimal CXCR5 expression during Tfh maturation involves the Bhlhe40-Pou2af1 axis.

Cell reports·2025
Same journal

Targeting cholesterol esterification sensitizes liver cancer to CD8<sup>+</sup> T cell attack by impairing metabolic and redox resilience.

Immunity·2026
Same journal

Brain endothelial cells orchestrate a neuroprotective antiviral state in the CNS in response to peripheral viral pattern sensing.

Immunity·2026
Same journal

Extracellular ATP-P2RY2 signaling drives intratumoral prostaglandin E2 accumulation and adaptive resistance to immunotherapy in solid tumors.

Immunity·2026
Same journal

B cell-derived type I interferon sustains T cell functionality upon strong TCR stimulation during chronic infection.

Immunity·2026
Same journal

Lactate binds and inhibits the innate immune sensor STING to promote tumor immune evasion.

Immunity·2026
Same journal

Antibody binding geometry and affinity control inhibitory hFcγRIIB receptor signaling.

Immunity·2026
See all related articles

Area of Science:

  • Immunology and Cell Signaling

Background:

  • The Tec kinase Bruton's tyrosine kinase (Btk) is crucial for regulating antigen receptor signaling.
  • Btk controls the activation of phospholipase C-gamma (PLC-gamma), a key enzyme in immune cell activation.

Purpose of the Study:

  • To investigate the role of Btk in activating phosphatidylinositol-4-phosphate 5-kinase (PIP5K).
  • To elucidate the mechanisms by which Btk influences phosphoinositide metabolism and signaling.

Main Methods:

  • Experimental data from Carpenter and colleagues (Saito et al.) were analyzed.
  • Focus on the interaction between Btk and PIP5K activity.

Main Results:

  • Btk was found to activate PIP5K, indicating a novel regulatory pathway.
  • This activation stimulates a positive feedback loop, enhancing the production of PI(4,5)P2.

Related Experiment Videos

  • PI(4,5)P2 serves as a substrate for both phosphoinositide 3-kinase (PI3K) and PLC-gamma.
  • Conclusions:

    • Btk plays a dual role in antigen receptor signaling by activating both PLC-gamma and PIP5K.
    • The Btk-PIP5K interaction establishes a positive feedback mechanism for PI(4,5)P2 generation.
    • This finding deepens the understanding of Btk's function in immune cell activation and phosphoinositide signaling networks.