Genomic Organization and Cytokine-Mediated Inducibility of the Human Trim-8/Gerp Gene

• Published in: International journal of immunopathology and pharmacology Vol. 17; no. 2_suppl; pp. 71 - 76
• Main Authors: Toniato, E., Flati, V., Laglia, E., Mincione, G., Martinotti, S.
• Format: Journal Article
• Language: English
• Published: London, England SAGE Publications 01.05.2004
• Subjects: Amino Acid Sequence; Animals; Carrier Proteins - biosynthesis; Carrier Proteins - chemistry; Carrier Proteins - genetics; Cloning, Molecular; Gene Expression Regulation; HeLa Cells; Humans; Interferon-gamma - biosynthesis; Interferon-gamma - genetics; Mice; Molecular Sequence Data; Nerve Tissue Proteins - biosynthesis; Nerve Tissue Proteins - chemistry; Nerve Tissue Proteins - genetics; Zinc Fingers; cytokine; TRIM-8/GERP; genomic; PTK
• ISSN: 0394-6320; 2058-7384
• DOI: 10.1177/03946320040170S212

Cytokine signaling is negatively regulated by a set of SH2 domain-containing proteins, the Suppressors of Cytokine Signaling (SOCS) acting as intracellular modulators. Experimental evidence indicates that SOCS gene expression is induced by cytokines and pro-inflammatory stimuli and is highly controlled both at transcription and translation level. Furthermore, SOCS proteins appear rapidly degraded inside the cells, mostly controlling their stability by interacting with specific molecules such as elongin B and C. It has been shown that SOCS-1/JAB, a member of the SOCS family, interacts with TRIM-8/Gerp, a new ring protein specifically binding SOCS-1 recombinant polypeptide in-vitro and in-vivo. Trim-8/Gerp, transcribes a 3.0-kb mRNA, spans 551 AA and is highly conserved during evolution. In addition, it can be induced by IFN-γ in epithelial and lymphoid cells and is expressed mostly ubiquitously in murine and human tissues. Here in this report we present the genomic organization of this new SOCS-1 interactor, and we add new tools for extending investigation of the complex mechanism that undergoes negatively regulation of cytokine signaling.