Loss of the cylindromatosis tumour suppressor inhibits apoptosis by activating NF-κB
By T. Brummelkamp, Sebastian M. B. Nijman, A. Dirac, René Bernards. Nature, 2003
982 citations recorded by the source corpus.
Subfields: Cancer Research, Immunology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/365a45c0c2d13ce083ea2df7f3e6d5e570c90dc5
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
- Weimin He
- Shizuo Akira
- Ivan Dikic
- Sebastian M. B. Nijman
- A. Dirac
- D. Komander
- John J. Rossi
- T. Brummelkamp
In Immunology
In Molecular Biology
- D. Komander
- Weimin He
- Jason A. Papin
- John J. Rossi
- Bernhard O. Palsson
- Ivan Dikic
- D. Iliopoulos
- René Bernards
Citations in the corpus
- STAT3 activation of miR-21 and miR-181b-1, via PTEN and CYLD, are part of the epigenetic switch linking inflammation to cancer (2010, background): “CYLD is a deubiquitinating enzyme that negatively regulates NF-kB activity (Brummelkamp et al., 2003; Trompouki et al., 2003).”
- A cytoplasmic NF-κB interacting long noncoding RNA blocks IκB phosphorylation and suppresses breast cancer metastasis. (2015, background): “A number of negative regulators for NF-kB pathway, for example deubiquitinase (DUB) A20 (Cake et al., 2003) and CYLD (Brummelkamp et al., 2003), ubiquitin ligase SOCS-1 (Ruland, 2011), and a group of miRNAs (Boldin and Baltimore, 2012), etc, have been shown to be tumor suppressors.”
- A genomic and functional inventory of deubiquitinating enzymes. (2005, background): “CYLD TRAF2/6, NEMO NF-κB and JNK signaling Familial tumor suppressor (cylindromatosis) Brummelkamp et al. (2003); Kovalenko et al.”
- To be, or not to be: NF-κB is the answer – role of Rel/NF-κB in the regulation of apoptosis (2003, background): “Interestingly, CYLD was recently shown to interact directly with TRAF2 and IKKg/NEMO and to function as a TRAF2 deubiquitinating enzyme to negatively regulate IKKmediated activation of NF-kB downstream of CD40, XEDAR and EDAR (Brummelkamp et al., 2003; Kovalenko et al., 2003; Trompouki et al., 2003)”
- The deubiquitinating enzyme USP1 regulates the Fanconi anemia pathway. (2005, methodology): “After selection withthe DUB gene family RNA interference library, previously puromycin, the cells were synchronized using a double-generated in our laboratory (Brummelkamp et al., 2003). thymidine block.”
- Ubiquitylation and cell signaling (2005, background): “Another DUB, the tumor suppressor cylindromatosis (CYLD), removes UbLys63 chains from TRAF2, TRAF6 and NEMO, also leading to the downregulation of NF-kB signaling (Brummelkamp et al, 2003).”
- Involvement of linear polyubiquitylation of NEMO in NF-κB activation (2009, background): “Analysis of the de-ubiquitylation of linear chains by various deubiquitylating enzymes, including those involved in NF-κB signalling, such as CYLD and A20 (Ref”
- Reconstruction of cellular signalling networks and analysis of their properties (2005, background): “, and the interactions between de-ubiquitylating enzymes and the IKK complex that is involved in NF-κB signallin”
- Unlocking the potential of the human genome with RNA interference (2004, background): “Using a library directed against the family of de-ubiquinating enzymes, the tumour suppressor CYLD (encoded by the familial cylindromatosis susceptibility gene) was identified as a suppressor of NF-κB activit”
- CYLD is a deubiquitinating enzyme that negatively regulates NF-κB activation by TNFR family members (2003, background): “Our results indicate that increased or prolonged activation of NF-κB caused by a loss of CYLD is important in the generation and growth of cylindromas, possibly because of the inhibition of apoptosi”