Associated Papers
Discriminating activating, deactivating and resistance variants in protein kinases.
Singh G et al.
Genome Medicine, 2025
Gain-of-function IKBKB mutation causes human combined immune deficiency.
Cardinez C et al.
The Journal of Experimental Medicine, 2018
High-throughput sequencing of nodal marginal zone lymphomas identifies recurrent BRAF mutations.
Pillonel V et al.
Leukemia, 2018
29556019 (PubMed )
Supplement: 41375_2018_82_MOESM10_ESM.xlsx › .
Novel GPR34 and CCR6 mutation and distinct genetic profiles in MALT lymphomas of different sites.
Moody S et al.
Haematologica, 2018
29674500 (PubMed )
Supplement: 2018.191601.MOODY_SUPPL.pdf
Synergistic cooperation and crosstalk between MYD88L265P and mutations that dysregulate CD79B and surface IgM.
Wang JQ et al.
The Journal of Experimental Medicine, 2017
Gain-of-Function Mutations in the Toll-Like Receptor Pathway: TPL2-Mediated ERK1/ERK2 MAPK Activation, a Path to Tumorigenesis in Lymphoid Neoplasms?
Rousseau S et al.
Frontiers in Cell and Developmental Biology, 2016
IκB kinase β (IKBKB) mutations in lymphomas that constitutively activate canonical nuclear factor κB (NFκB) signaling.
Kai X et al.
The Journal of Biological Chemistry, 2014
Consequences of the recurrent MYD88(L265P) somatic mutation for B cell tolerance.
Wang JQ et al.
The Journal of Experimental Medicine, 2014
Novel Lys63-linked ubiquitination of IKKβ induces STAT3 signaling.
Gallo LH et al.
Cell Cycle (georgetown, Tex.), 2014
The coding genome of splenic marginal zone lymphoma: activation of NOTCH2 and other pathways regulating marginal zone development.
Rossi D et al.
The Journal of Experimental Medicine, 2012
22891273 (PubMed )
Supplement: supp_jem.20120904_JEM_20120904_TableS7.xlsx › Table_VIIs
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