CD40 regulates the processing of NF‐κB2 p100 to p52

By H. Coope, P. Atkinson, B. Huhse, M. Belich, J. Janzen, M. J. Holman, G. Klaus, Leland H. Johnston, Steven C. Ley. 2002

437 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology

View Paper: https://www.semanticscholar.org/paper/e59f43c4bf86c0f5656c74af1a111b75d5a6b6a3

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. M. Karin
2. J. Hong
3. M. Park
4. Sivakumar Vallabhapurapu
5. C. Scheidereit
6. D. Krappmann
7. G. Natoli
8. Serafino Pantano

In Immunology

1. J. Hong
2. M. Park
3. M. Karin
4. Sivakumar Vallabhapurapu
5. G. Natoli
6. D. Vignali
7. S. Ghosh
8. N. Perkins

Citations in the corpus

• Mutations of multiple genes cause deregulation of NF-kB in diffuse large B-cell lymphoma (2009, neutral): “ABC-DLBCL Non-GC/NC-DLBCL Biallelic deletion Mutation plus deletion Biallelic mutation Heterozygous mutation Monoallelic deletion Normal Mutated Deleted Normal Nonsense mutations (12) Frameshift deletions (7) Frameshift insertions (5) Splice site mutations (2)”
• The IκB Kinase Complex and NF-κB Actas Master Regulators of Lipopolysaccharide-Induced Gene Expressionand Control Subordinate Activation ofAP-1 (2004, background): “Aside from this canonical IB degradation pathway, a “novel” pathway, which is activated by a subset of NF-B stimuli, e.g., B-cell activating factor (BAFF), lymphotoxin (LT), CD40 ligand, and lipopolysaccharide (LPS) and enhances the processing of p100 and the generation of p52 containing DNA binding”
• Modulation of NF-κB Activity by Exchange of Dimers (2003, background): “R triggering (ClauN-terminal segment of about 300 amino acids, the Reldio et al., 2002; Coope et al., 2002; Dejardin et al., 2002), homology-domain (RHD), that is responsible for DNA and it has much slower activation kinetics than the cabinding, dimerization, nuclear translocation, interaction…”
• Nonredundant and complementary functions of TRAF2 and TRAF3 in a ubiquitination cascade that activates NIK-dependent alternative NF-κB signaling (2008, background): “This alternative pathway is activated by lymphorganogenic cytokines, such as lymphotoxin-α-β heterotrimers, and B cell survival and maturation factors, such as CD40 ligand (CD40L) and BAF”
• Frequent engagement of the classical and alternative NF-kappaB pathways by diverse genetic abnormalities in multiple myeloma. (2007, background): “We first investigated the molecular basis for outlier expression of NIK, a kinase capable of activating both the alternative and classical NF-kB pathways (Claudio et al., 2002; Coope et al., 2002; O’Mahony et al., 2000; Ramakrishnan et al., 2004; Woronicz et al., 1997; Yin et al., 2001).”