Function: Protects T-cells from IL2 deprivation-induced apoptosis through the inhibition of FOXO3A transcriptional activity that leads to the down-regulation of the pro-apoptotic factor BCL2L11. In macrophages, plays a role in the anti-inflammatory and immunosuppressive effects of glucocorticoids and IL10. In T-cells, inhibits anti-CD3-induced NFKB1 nuclear translocation. In vitro, suppresses AP1 and NFKB1 DNA-binding activities
By similarity. Ref.15
Subunit structure: Can form homodimers, however it is likely to function as a monomer. Interacts with AP1
By similarity. Interacts with NFKB1. Ref.13 Ref.14
Tissue specificity: Expressed in brain, lung, spleen and skeletal muscle. Lower levels detected in heart and kidney. Not detected in the pancreas. In non-lymphoid tissues, in the absence of inflammation, the major source of constitutive expression is the macrophage lineage. Also expressed in cells from different hemopoietic cell lineages, including bone marrow cells, CD34+ stem cells, mature B- and T-cells, monocytes and granulocytes. Down-regulated in activated macrophages from inflammatory lesions of delayed-type hypersensitivity (DTH) reactions, such as in tuberculosis and in Crohn disease, whereas in Burkitt lymphoma, persists in macrophages involved in the phagocytosis of apoptotic malignant cells. Ref.2 Ref.14
Induction: By glucocorticoids in lymphoid cells and upon IL4, IL10, IL13 or glucocorticoid treatment in monocyte/macrophage cells. Transiently induced by IL2 deprivation in T-cells. Ref.14 Ref.15
Domain: The leucine-zipper is involved in homodimerization
By similarity.
Sequence similarities: Belongs to the TSC-22/Dip/Bun family.
Sequence caution: The sequence AAH18148.3 differs from that shown. Reason: Erroneous initiation. The sequence CAA90644.1 differs from that shown. Reason: Erroneous initiation. The sequence CAB53669.1 differs from that shown. Reason: Frameshift at position 4.
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