Siva-1 negatively regulates NF-κB activity: effect on T-cell receptor-mediated activation-induced cell death (AICD)

Participation of the Cell Polarity Protein PALS1 to T-Cell Receptor-Mediated NF-κB Activation

BACKGROUND Beside their established function in shaping cell architecture, some cell polarity proteins were proposed to participate to lymphocyte migration, homing, scanning, as well as activation following antigen receptor stimulation. Although PALS1 is a central component of the cell polarity network, its expression and function in lymphocytes remains unknown. Here we investigated whether PAL...

Zebrafish IκB Kinase 1 Negatively Regulates NF-κB Activity

The I B kinase (IKK) activity is critical for processing I B inhibitory proteins and activating the NFB signaling, which is involved in a series of physiological and developmental steps in vertebrates [1–4]. The IKK activity resides in two catalytic subunits, IKK1 and IKK2, and two regulatory subunits, NEMO and ELKS [5–8]. IKK2 is the major cytokine-responsive I B kinase [9–11] because depletio...

SPATA2 promotes CYLD activity and regulates TNF-induced NF-κB signaling and cell death.

K63- and Met1-linked ubiquitylation are crucial posttranslational modifications for TNF receptor signaling. These non-degradative ubiquitylations are counteracted by deubiquitinases (DUBs), such as the enzyme CYLD, resulting in an appropriate signal strength, but the regulation of this process remains incompletely understood. Here, we describe an interaction partner of CYLD, SPATA2, which we id...

A20 Negatively Regulates T Cell Receptor

The TNF receptor 1-associated protein TRADD signals cell death and NF-κB activation

Many diverse activities of tumor necrosis factor (TNF) are signaled through TNF receptor 1 (TNFRl). We have identified a novel 34 kDa protein, designated TRADD, that specifically Interacts with an Intracellular domain of TNFRl known to be essential for mediating programmed cell death. Overexpression of TRADD leads to two major TNF-Induced responses, apoptosis and activation of NF-KB. The C-term...