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Signalling for B cell survival

Journal

CURRENT OPINION IN CELL BIOLOGY
Volume 51, Issue -, Pages 8-14

Publisher

CURRENT BIOLOGY LTD
DOI: 10.1016/j.ceb.2017.10.002

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Funding

  1. Francis Crick Institute [FC001194]
  2. UK Medical Research Council
  3. Wellcome Trust
  4. Cancer Research UK
  5. MRC [MC_U117527252] Funding Source: UKRI
  6. Medical Research Council [MC_U117527252] Funding Source: researchfish
  7. The Francis Crick Institute [10398, BB/L502297/1, 10194] Funding Source: researchfish

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The number of mature B cells is carefully controlled by signalling from receptors that support B cell survival. The best studied of these are the B cell antigen receptor (BCR) and BAFFR. Recent work has shown that signalling from these receptors is closely linked, involves the CD19 co-receptor, and leads to activation of canonical and non-canonical NF-kappa B pathways, ERK1, ERK2 and ERK5 MAP kinases, and PI-3 kinases. Importantly, studies show that investigation of the importance of signalling molecules in cell survival requires the use of inducible gene deletions within mature B cells. This overcomes the limitations of many earlier studies using constitutive gene deletions which were unable to distinguish between requirements for a protein in development versus survival.

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