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CHUK — MALT1
Pathways - manually collected, often from reviews:
-
NCI Pathway Database BCR signaling pathway:
IKK complex complex (CHUK-IKBKB-IKBKG)
→
CARD11/BCL10/MALT1/TAK1 complex (CARD11-BCL10-MALT1-MAP3K7)
(modification, collaborate)
-
NCI Pathway Database BCR signaling pathway:
CARD11/BCL10/MALT1/TAK1 complex (CARD11-BCL10-MALT1-MAP3K7)
→
IKK alpha (CHUK)
(modification, activates)
-
Reactome Reaction:
CHUK
→
MALT1
(reaction)
Wang et al., Nature 2001, Zhou et al., Nature 2004, Shinohara et al., J Exp Med 2005, Häcker et al., Science's STKE : signal transduction knowledge environment 2006, Shinohara et al., Immunol Rev 2009, Zhang et al., Chin Med Sci J 2010
-
Reactome Reaction:
CHUK
→
MALT1
(indirect_complex)
Shinohara et al., J Exp Med 2005, Sommer et al., Immunity 2005, Shinohara et al., Immunol Rev 2009
-
WikiPathways T-Cell antigen Receptor (TCR) pathway during Staphylococcus aureus infection:
Complex of MALT1-CARD11-BCL10
→
Complex of IKBKG-IKBKB-CHUK
(activation)
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Ruland et al., Immunity 2003
(Lymphoma, B-Cell, Marginal Zone) :
Malt1 operates downstream of Bcl10,
controls the catalytic activity of the canonical
IKK complex , and regulates the signaling of Jnk and p38 MAP kinases
Patke et al., Curr Opin Immunol 2004
:
BCR signaling leads to
activation of the
inhibitor of NF-kappa B kinase (IKK) complex via Carma1, Bcl10 and
MALT1 , whereas BAFF-R engagement promotes processing of NF-kappa B2 protein p100, which is dependent on NF-kappa B-inducing kinase (NIK) and IKK alpha
Sun et al., Mol Cell 2004
(Lymphoma, B-Cell, Marginal Zone) :
RNAi mediated silencing of
MALT1 , TAK1, TRAF6, and TRAF2
suppressed TCR dependent
IKK activation and interleukin-2 production in T cells ... Strikingly, only these oligomeric forms of BCL10 and
MALT1 can
activate IKK in vitro
Lynch et al., Mol Interv 2004
:
Overexpression of MALT1, as observed in a subset of lymphoma patients, leads to the potent activation of NF-kappaB, suggesting that
MALT1 might
stimulate ( directly or indirectly ) the kinase complex [
IKK , inhibitor of NF-kappaB (IkappaB) kinase ] responsible for activating cytoplasmic NF-kappaB for translocation into the nucleus
Ho et al., Blood 2005
(Lymphoma, B-Cell...) :
API2-MALT1 and exogenous MALT1 increased constitutive NF-kappa B activity and
enhanced I kappa B kinase (IKK) activation induced by CD40 stimulation