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Article

Redundancy in B cell developmental pathways: c-Cbl inactivation rescues early B cell development through a B cell linker protein-independent pathway.

Journal of immunology (Baltimore, Md. : 1950) - 15 Jan 2007

Song Haifeng, Zhang Juan, Chiang Y Jeffrey, Siraganian Reuben P, Hodes Richard J

Abstract excerpt

Deficiency in the adaptor protein B cell linker protein (BLNK) results in a substantial but incomplete block in B cell development, suggesting that alternative pathways exist for B lineage differentiation. Another adaptor protein, c-Cbl, plays a negative regulatory role in several BCR-signaling pathways. We therefore investigated the role of c-Cbl during B cell development and addressed the possibility that...

Read the complete abstract on PubMed

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Share to Adaptor Proteins, Signal Transducing
Share to B-Lymphocytes

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Share to Proto-Oncogene Proteins c-cbl

Share to Receptors, Antigen, B-Cell

Source

Identifiers

PMID: 17202354
DOI: 10.4049/jimmunol.178.2.926

Genes

BLNK
BCR

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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Redundancy in B cell developmental pathways: c-Cbl inactivation rescues early B cell development through a B cell linker protein-independent pathway.PMID 17202354Read ↗

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Modulation of Immune Cell Functions by the E3 Ligase Cbl-bSemantic proximity Read ↗

Defects in early B-cell development: comparing the consequences of abnormalities in pre-BCR signaling in the human and the mouse.Semantic proximity Read ↗

Loss of Cbl-PI3K interaction enhances osteoclast survival due to p21-Ras mediated PI3K activation independent of Cbl-b.Semantic proximity Read ↗

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