Biochimica et biophysica actaDec 15, 2007

How the End Part of Human CTLA4 mRNA Controls Its Stability and Protein Production

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Updated Mar 20, 2026

Abstract

The 3' UTR of CTLA4 regulates firefly luciferase reporter gene expression.

The 3' UTR of CTLA4 may affect the stability of CTLA4 mRNA.
Changes in the 3' UTR could influence the translation efficiency of CTLA4 in vitro.
Disruption of T cell activation balance may lead to immune system defects or over-activation.
CTLA-4 is critical for downregulating T cell responses.
Genetic linkages have been observed between autoimmune diseases and the CTLA4 locus.

Simplified

T cell activation results from the integration of signals generated through the T cell antigen receptor-CD3 complex with those from additional positive and negative regulatory pathways mainly mediated by the engagement of costimulatory receptors on T cells. Disruption of this balance leads to a defective immune response or alternative over-activation of the immune system. CTLA-4 plays a critical role in downregulating T cell responses. Autoimmune diseases have shown genetic linkage to the CTLA4 locus. In this report we demonstrate that the 3' UTR of CTLA4 regulates firefly luciferase reporter gene expression, can confer instability to CTLA4 mRNA and can influence its translation efficiency in vitro.

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How the End Part of Human CTLA4 mRNA Controls Its Stability and Protein Production

Abstract

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