Adapter molecule for TNFRSF1A/TNFR1 that specifically associates with the cytoplasmic domain of activated TNFRSF1A/TNFR1 mediating its interaction with FADD. Overexpression of TRADD leads to two major TNF-induced responses, apoptosis and activation of NF-kappa-B (By similarity). The nuclear form acts as a tumor suppressor by preventing ubiquitination and degradation of isoform p19ARF/ARF of CDKN2A by TRIP12: acts by interacting with TRIP12, leading to disrupt interaction between TRIP12 and isoform p19ARF/ARF of CDKN2A (By similarity). Stimulation of TNF-alpha receptor TNFRSF1A leads to the formation of two distinct signaling complexes. Plasma membrane-bound complex I is composed of TNFRSF1A, TRADD, RIPK1, TRAF2 and BIRC2/c-IAP1 or BIRC3 which interacts with CHUCK/IKK-alpha, IKBKB/IKK-beta and IKBKG/IKK-gamma promoting cell survival. Subsequently, TRADD, RIPK1 and TRAF2 dissociate from TNFRSF1A and form cytoplasmic complex II with FADD and caspase CASP8 promoting cell apoptosis. Within complex I, interacts with TNFRSF1A/TNFR1, TRAF2 and kinase RIPK1. Within complex I, interacts with TRPC4AP; the interaction promotes NF-kappa B activation. UXT1 associates with complex I; the interaction prevents the formation of complex II. Within complex I Interacts with scaffold protein DAB2IP. Interacts with autophagy receptor SQSTM1 (By similarity). Interacts with E3 ligase TRIP12 (By similarity). Interacts with kinase HIPK2. Interacts with keratin KRT14. Interacts with keratin KRT18 (By similarity). Interacts with keratins KRT16 and KRT17 (By similarity). Interacts with FADD (By similarity). Interacts with TOMM70 (By similarity). Shuttles between the cytoplasm and the nucleus. Requires the intact death domain to associate with TNFRSF1A/TNFR1.