| First Author | Han A | Year | 2003 |
| Journal | Immunity | Volume | 19 |
| Issue | 4 | Pages | 621-32 |
| PubMed ID | 14563325 | Mgi Jnum | J:86182 |
| Mgi Id | MGI:2678969 | Doi | 10.1016/s1074-7613(03)00275-9 |
| Citation | Han A, et al. (2003) Bam32 links the B cell receptor to ERK and JNK and mediates B cell proliferation but not survival. Immunity 19(4):621-32 |
| abstractText | Bam32 is an adaptor protein recruited to the plasma membrane upon B cell receptor (BCR) crosslinking in a phosphoinositol 3-kinase (PI3K)-dependent manner; however, its physiologic function is unclear. To determine its physiologic function, we produced Bam32-deficient mice. Bam32(-/-) B cells develop normally but have impaired T-independent antibody responses in vivo and diminished responses to BCR crosslinking in vitro. Biochemical analysis revealed that Bam32 acts in a novel pathway leading from the BCR to MAPK/ERK Kinases (MEK1/2), MAPK/ERK Kinase Kinase-1 (MEKK1), extracellular signal-regulated kinase (ERK), and c-jun NH2-terminal kinase (JNK), but not p38 mitogen-activated protein kinase (p38). This pathway appears to be initiated by hematopoietic progenitor kinase-1 (HPK1), which interacts directly with Bam32, and differs from all previously characterized BCR signaling pathways in that it is required for normal BCR-mediated proliferation but not for B cell survival. |
