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TSC22D3 Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, IHC-P, IF, E |
|---|---|
| Primary Accession | Q99576 |
| Other Accession | NP_932174, 37622903 |
| Reactivity | Human, Mouse |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | IgG |
| Calculated MW | Predicted: 22 kDa Observed: 23 kDa |
| Application Notes | TSC22D3 antibody can be used for detection of TSC22D3 by Western blot at 1 - 2 µg/mL. |
| Gene ID | 1831 |
|---|---|
| Target/Specificity | TSC22D3; |
| Reconstitution & Storage | TSC22D3 antibody can be stored at 4℃ for three months and -20℃, stable for up to one year. |
| Precautions | TSC22D3 Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | TSC22D3 (HGNC:3051) |
|---|---|
| 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 (PubMed:15031210). In macrophages, plays a role in the anti- inflammatory and immunosuppressive effects of glucocorticoids and IL10 (PubMed:12393603). In T-cells, inhibits anti-CD3-induced NFKB1 nuclear translocation and thereby NFKB1 DNA-binding activities (PubMed:11468175). In vitro, suppresses AP-1 transcription factor complex DNA-binding activities (By similarity). |
| Cellular Location | [Isoform 1]: Cytoplasm {ECO:0000250|UniProtKB:Q9Z2S7}. Nucleus {ECO:0000250|UniProtKB:Q9Z2S7} Note=Localization depends on differentiation status of myoblasts (By similarity). In undifferentiated myoblasts; localizes to the cytoplasm, but in differentiating myoblast; localizes to the nucleus (By similarity). {ECO:0000250|UniProtKB:Q9Z2S7} |
| Tissue Location | Ubiquitously expressed, including in the fetal brain and liver (PubMed:26752201). Expressed in brain, lung, spleen and skeletal muscle (PubMed:11313722, PubMed:12393603). Lower levels detected in heart and kidney (PubMed:11313722, PubMed:12393603). Not detected in the pancreas (PubMed:11313722). In non-lymphoid tissues, in the absence of inflammation, the major source of constitutive expression is the macrophage lineage (PubMed:12393603). Also expressed in cells from different hemopoietic cell lineages, including bone marrow cells, CD34+ stem cells, mature B- and T-cells, monocytes and granulocytes (PubMed:11313722). 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 (PubMed:12393603) |
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Provided below are standard protocols that you may find useful for product applications.
Background
TSC22D3 Antibody: The TSC22 domain family member 3 protein (TSC22D3) is a leucine zipper protein that functions as a transcriptional regulator. The expression of TSC22D3 is stimulated by glucocorticoids and IL-10 and is thought to play a key role in the anti-inflammatory and immunosuppressive effects of these molecules. TSC22D3 can physically interact with and inhibit the activities of key inflammatory signaling mediators such NF-κB and AP-1. TSC22D3 functions as a transcriptional co-activator for various nuclear receptors and NF-κB. It has also been shown to be involved in the differentiation of mesenchymal stem cells towards osteoblasts and bone formation.
References
Riccardi C, Cifone MG, and Migliorati G. Glucocorticoid hormone-induced modulation of gene expression and regulation of T-cell death: role of GITR and GILZ, two dexamethasone-induced genes. Cell Death Differ. 1999; 6:1182-9.
Berrebi D, Bruscoli S, Cohen N, et al. Synthesis of glucocorticoid-induced leucine zipper (GILZ) by macrophages: an anti-inflammatory and immunosuppressive mechanism shared by glucocorticoids and IL-10. Blood 2003; 101:729-38
Ayroldi E, Migliorati G, Bruscoli S, et al. Modulation of T-cell activation by the glucocorticoid-induced leucine zipper factor via inhibition of nuclear factor kappaB. Blood 2001; 98:743-53.
Mittelstadt PR and Ashwell JD. Inhibition of AP-1 by the glucocorticoid-inducible protein GILZ. J. Biol. Chem. 2001; 276:29603-10.
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