PKC-θ is required for TCR-induced NF-κB activation in mature but not immature T lymphocytes

By Zuoming Sun, C. Arendt, W. Ellmeier, E. Schaeffer, M. Sunshine, L. Gandhi, J. Annes, D. Petrzilka, A. Kupfer, P. Schwartzberg and 1 more. Nature, 2000

915 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology

View Paper: https://www.semanticscholar.org/paper/8de5789775cd7019618419dd8378d5f049265941

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Citations in the corpus

NF-κB and the immune response (2006, background): “Although there has been some controversy, available data suggest that PKCy is largely essential for activation of NF-kB via T-cell stimulation (Sun et al., 2000; Pfeifhofer et al., 2003) and can mediate the activation of IKK (Lin et al., 2000).”
The Immunological Synapse (2014, background): “The third major family of transcription factors activated by the TCR is the PKCθ/IκB/inhibitor of κB kinase pathway leading to phosphorylation and degradation of IκB, the regulatory subunit of the nuclear factor-κB (NF-κB) transcription factor [ 34 ].”
IKKβ Is Required for Peripheral B Cell Survival and Proliferation1 (2003, background): “Nonetheless, IKK -deficient T cells display a proliferation defect similar to that exhibited by T cells lacking the protein kinase C isozyme, which is required for NF- B activation in response to ligation of the TCR (29).”
Defective IgG2a/2b Class Switching in PKCα−/− Mice1 (2006, background): “4B), and AP-1 (Fig.”
CARMA1 is a critical lipid raft–associated regulator of TCR-induced NF-κB activation (2002, background): “PKC-t is a critical component because mice deficient for PKC-t show impaired activation of NF-κ”