B cell life depends critically on the cytokine B cell–activating factor of the tumor necrosis factor family (BAFF). Lack of BAFF signaling leads to B cell death and immunodeficiency. Excessive BAFF signaling promotes lupus-like autoimmunity. Despite the great importance of BAFF to B cell biology, its signaling mechanism is not well characterized. We show that BAFF initiates signaling and transcriptional programs, which support B cell survival, metabolic fitness, and readiness for antigen-induced proliferation. We further identify a BAFF-specific protein kinase C β–Akt signaling axis, which provides a connection between BAFF and generic growth factor–induced cellular responses.
BAFF controls B cell metabolic fitness through a PKCβ- and Akt-dependent mechanism
Alina Patke,Ingrid Mecklenbräuker,H. Erdjument‐Bromage,P. Tempst,A. Tarakhovsky
Published 2006 in Journal of Experimental Medicine
ABSTRACT
PUBLICATION RECORD
- Publication year
2006
- Venue
Journal of Experimental Medicine
- Publication date
2006-10-30
- Fields of study
Biology, Medicine
- Identifiers
- External record
- Source metadata
Semantic Scholar, PubMed
CITATION MAP
EXTRACTION MAP
CLAIMS
- No claims are published for this paper.
CONCEPTS
- No concepts are published for this paper.
REFERENCES
Showing 1-72 of 72 references · Page 1 of 1