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B-Cell Receptor Signaling and Beyond: The Role of Igα (CD79a)/Igβ (CD79b) in Normal and Malignant B Cells
A. Tkachenko, K. Kupcova, O. Havranek
Language English Country Switzerland
Document type Journal Article, Review
Grant support
AZV NV18-03-00117
Czech Health Research Council
PRIMUS/17/MED/9, UNCE/MED/016, Cooperatio
Charles University in Prague
Programme EXCELES, reg. No. LX22NPO5102
European Union - Next Generation EU
Ukraine Bridge Funding Award
European Hematology Association
NLK
Free Medical Journals
from 2000
Freely Accessible Science Journals
from 2000
PubMed Central
from 2007
Europe PubMed Central
from 2007
ProQuest Central
from 2000-03-01
Open Access Digital Library
from 2000-01-01
Open Access Digital Library
from 2007-01-01
Health & Medicine (ProQuest)
from 2000-03-01
ROAD: Directory of Open Access Scholarly Resources
from 2000
PubMed
38203179
DOI
10.3390/ijms25010010
Knihovny.cz E-resources
- MeSH
- Cell Membrane MeSH
- Cognition MeSH
- Mutation MeSH
- Receptors, Antigen, B-Cell * genetics MeSH
- Signal Transduction * MeSH
- Publication type
- Journal Article MeSH
- Review MeSH
B-cell receptor (BCR) is a B cell hallmark surface complex regulating multiple cellular processes in normal as well as malignant B cells. Igα (CD79a)/Igβ (CD79b) are essential components of BCR that are indispensable for its functionality, signal initiation, and signal transduction. CD79a/CD79b-mediated BCR signaling is required for the survival of normal as well as malignant B cells via a wide signaling network. Recent studies identified the great complexity of this signaling network and revealed the emerging role of CD79a/CD79b in signal integration. In this review, we have focused on functional features of CD79a/CD79b, summarized signaling consequences of CD79a/CD79b post-translational modifications, and highlighted specifics of CD79a/CD79b interactions within BCR and related signaling cascades. We have reviewed the complex role of CD79a/CD79b in multiple aspects of normal B cell biology and how is the normal BCR signaling affected by lymphoid neoplasms associated CD79A/CD79B mutations. We have also summarized important unresolved questions and highlighted issues that remain to be explored for better understanding of CD79a/CD79b-mediated signal transduction and the eventual identification of additional therapeutically targetable BCR signaling vulnerabilities.
References provided by Crossref.org
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