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BCR — JUN

Text-mined interactions from Literome

Poe et al., J Biol Chem 2000 : Although augmented calcium responses in CD22-deficient mice should facilitate enhanced c-Jun N-terminal kinase (JNK) activation, BCR ligation did not induce JNK activation in CD22-deficient B cells
Perrotti et al., Mol Cell Biol 2000 : FUS proteolysis is induced by c-Jun , is suppressed by BCR-ABL or Jun kinase 1, and does not depend on c-Jun transactivation potential, ubiquitination, or its interaction with Jun kinase 1
Wu et al., J Immunol 2001 (Severe Combined Immunodeficiency) : Thus, CD72 and BCR activated the extracellular signal regulated kinase ( ERK ) and the c-Jun N-terminal kinase (JNK) but not p38 mitogen activated protein kinase
Inabe et al., FEBS Lett 2002 (Agammaglobulinemia) : Recent studies have shown that Btk plays an important role in BCR mediated c-Jun NH ( 2 ) -terminal kinase ( JNK ) 1 activation ; however, the mechanism by which Btk participates in the JNK1 response remains elusive
Gupta et al., Cancer Res 2008 : Microarray analysis to identify transformation impacting genes regulated by NF-kappaB 's oncogenic v-Rel and c-Rel proteins uncovered that Rel protein expression leads to transcriptional repression of key B-cell receptor (BCR) components and signaling molecules like B-cell linker (BLNK), the B-cell adaptor for phosphoinositide 3-kinase ( BCAP ) and immunoglobulin lambda light chain ( Ig lambda ), and is accompanied by a block in BCR mediated activation of extracellular signal regulated kinase, Akt, and c-Jun-NH ( 2 ) -kinase in response to anti-IgM
Mancini et al., Traffic 2009 (Leukemia, Myelogenous, Chronic, BCR-ABL Positive) : In particular, constitutive tyrosine kinase ( TK ) activity of p210 BCR-ABL blocks c-Jun N-terminal kinase (JNK) phosphorylation leading to 14-3-3 sigma phosphorylation at a critical residue ( Ser ( 186 ) ) for c-ABL binding in response to DNA damage
Kobayashi et al., Leukemia 2009 (Leukemia, Myeloid, Chronic-Phase) : BCR-ABL directly inhibited c-Jun expression, as c-Jun downregulation in primary CML neutrophils and in the CML blast cell lines, KCL22 and K562, was reversed by the tyrosine kinase inhibitor imatinib