Target intelligence / Profile preview

FAS-associated death domain protein (FADD)

Target
FADD
Molecular classification
Death domain-containing adaptor protein, Apoptosis signaling molecule, Receptor-associated signaling adaptor, Nuclear factor-interacting adaptor, Other (not classified as receptor, enzyme, transporter, transcription factor, ion channel, or histone modifier)
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Overview

FAS-associated death domain protein (FADD) is a 23 kDa adaptor protein consisting of two main domains: a C-terminal death domain and an N-terminal death effector domain. It functions by bridging death receptors such as Fas (CD95) with initiator caspases (notably procaspase-8 and -10), forming the death-inducing signaling complex (DISC) that triggers apoptosis. FADD also regulates necroptosis, autophagic cell death, cell proliferation, and immune system responses. It is encoded by the FADD gene on chromosome 11q13.3, and its expression and function are crucial for proper cell death signaling, immune homeostasis, and genome surveillance. Dysregulation or mutation of FADD is implicated in cancer, autoimmunity, and infectious diseases.

Other names
MORT1Fas-associated protein with death domainFADD
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Mechanism of action

Promote or inhibit death receptor signaling, leading to apoptosis. Induction of cell cycle arrest. Potential inhibition of FADD for drug-resistant cancer therapy (proposed, not established clinically).

03

Biological functions

Apoptosis (programmed cell death) via death-inducing signaling complex (DISC)Necroptosis regulationAutophagic cell death modulationCell cycle regulationCell proliferationImmune response (T and B cell homeostasis, TLR signaling)DNA damage response and genome surveillance
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Disease associations

Cancer, including tumor surveillance and the effect of FADD mutations in malignanciesAutoimmune disease (defects associated with lymphoproliferation and autoantibody production)Inflammation (immune modulation)Infection (roles in immune system signaling and apoptosis)Neurodegenerative processes, indirectly through apoptosisCardiovascular disease (not reported prominently in primary sources)Other (embryonic development, hematopoietic abnormalities)
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Safety considerations

Inhibition or mutation of FADD can result in severe autoimmune complications, lymphadenopathy, and splenomegalyPotential embryonic lethality if FADD function is disruptedRisk of impaired immune response or unchecked proliferation of lymphoid cellsFADD-targeting therapies may cause excessive apoptosis or necroptosis, leading to tissue damage
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Interacting drugs

Paclitaxel (Taxol), reported to interfere with FADD-related cell cycle pathways and proposed as a drug in ovarian cancer

3 more in the full profile.

07

Biomarkers

FADD expression and post-translational modifications (e.g., phosphorylation at Ser-194) are used as biomarkers to monitor apoptosis and immune cell activityFADD mutations in malignancies can inform cancer prognosis and response to therapyFADD presence and localization may indicate propensity for cell death or cell survival in disease tissues

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