BAFF controls B cell metabolic fitness through a PKCβ- and Akt-dependent mechanism Journal Article
| Authors: | Patke, A.; Mecklenbräuker, I.; Erdjument-Bromage, H.; Tempst, P.; Tarakhovsky, A. |
| Article Title: | BAFF controls B cell metabolic fitness through a PKCβ- and Akt-dependent mechanism |
| Abstract: | 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. JEM © The Rockefeller University Press. |
| Keywords: | signal transduction; protein kinase b; controlled study; unclassified drug; nonhuman; cell proliferation; protein analysis; animal cell; mouse; animals; mice; cell death; cell survival; cells, cultured; gene expression; animal experiment; in vivo study; in vitro study; b lymphocyte; b-lymphocytes; nucleotide sequence; proto-oncogene proteins c-akt; autoimmunity; protein kinase c; immune deficiency; tumor necrosis factor; protein kinase c beta; b cell activating factor of the tumor necrosis factor family; b-cell activating factor |
| Journal Title: | Journal of Experimental Medicine |
| Volume: | 203 |
| Issue: | 11 |
| ISSN: | 0022-1007 |
| Publisher: | Rockefeller University Press |
| Date Published: | 2006-10-30 |
| Start Page: | 2551 |
| End Page: | 2562 |
| Language: | English |
| DOI: | 10.1084/jem.20060990 |
| PUBMED: | 17060474 |
| PROVIDER: | scopus |
| PMCID: | PMC2118121 |
| DOI/URL: | |
| Notes: | --- - "Cited By (since 1996): 56" - "Export Date: 4 June 2012" - "CODEN: JEMEA" - "Source: Scopus" |
