Chronic activation of the BCR engages multiple intracellular pathways. PI3K is inhibited by idelalisib. Bcl, B-cell lymphoma; Bcl-2, Bcl-2 gene; Bcl-xL, Bcl extra large; BCR, B-cell receptor; BTK, Bruton tyrosine kinase; CARD11, caspase recruiting domaine-11; IgL, immunoglobulin light chain; IKKa, inhibitor of NF-κB kinase; MALT1, mucosa-associated lymphoid tissue translocation protein 1; MAPK, mitogen-activated protein kinase; MAPKK, MAPK kinase; Mcl-1, myeloid cell leukemia differentiation protein-1; NfκB, nuclear factor κB; NFAT, nuclear factor of activated T cells; P, phosphorylation; PKCb, protein kinase C beta; SFK, SRC family kinase; SYK, spleen tyrosine kinase; Y, tyrosine. Figure is reproduced from Figure 2 in Young and Staudt11 with permission.

Chronic activation of the BCR engages multiple intracellular pathways. PI3K is inhibited by idelalisib. Bcl, B-cell lymphoma; Bcl-2, Bcl-2 gene; Bcl-xL, Bcl extra large; BCR, B-cell receptor; BTK, Bruton tyrosine kinase; CARD11, caspase recruiting domaine-11; IgL, immunoglobulin light chain; IKKa, inhibitor of NF-κB kinase; MALT1, mucosa-associated lymphoid tissue translocation protein 1; MAPK, mitogen-activated protein kinase; MAPKK, MAPK kinase; Mcl-1, myeloid cell leukemia differentiation protein-1; NfκB, nuclear factor κB; NFAT, nuclear factor of activated T cells; P, phosphorylation; PKCb, protein kinase C beta; SFK, SRC family kinase; SYK, spleen tyrosine kinase; Y, tyrosine. Figure is reproduced from Figure 2 in Young and Staudt11  with permission.

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