Interferon-induced protein 44 (IFI44)

Interferon-induced protein 44 (IFI44) is a cytoplasmic protein upregulated upon type I interferon stimulation and plays key roles in innate immunity, acting as both a regulator and effector in antiviral defense. IFI44 is implicated in cell cycle arrest, inhibition of cell proliferation, immune response modulation, and direct suppression of viral gene expression. It influences key signaling pathways, such as the IFN, JAK/STAT, Caspase-3/Bcl-2/Bax, and ERK pathways, and interacts with proteins like FKBP5 to feedback-regulate interferon responses. IFI44's activity has broad relevance in viral infection, cancer progression, autoimmune disease, and inflammation, making it both a mechanistic biomarker and a potential therapeutic target[2][3][1][4].

Other names

TLDC5MTAP44p44Microtubule-associated protein 44Hepatitis C-associated microtubular aggregate protein (44 kD)

Upregulation by interferons leads to inhibition of cell proliferation and suppression of viral replication[2][3]. Suppression of viral transcription by direct promoter binding (e.g., HIV-1)[2]. Disruption of ERK signaling via GTP binding, causing cell cycle arrest[2][3]. Negative modulation of interferon responses through interaction with FKBP5, reducing IKK activity and phosphorylation of IRF-3/IκBα[2][4].