|Application ||WB, IHC-P, IF, E|
|Other Accession||NP_932174, 37622903|
|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.|
|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.|
|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). Isoform 1 inhibits myogenic differentiation and mediates anti- myogenic effects of glucocorticoids by binding and regulating MYOD1 and HDAC1 transcriptional activity resulting in reduced expression of MYOG (By similarity).|
|Cellular Location||Isoform 1: Cytoplasm. Nucleus. Note=Localization depends on differentiation status of myoblasts. In undifferentiated myoblasts, isoform 1 localizes to the cytoplasm, but in differentiating myoblasts, isoform 1 is localized to the nucleus (By similarity).|
|Tissue Location||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.|
Thousands of laboratories across the world have published research that depended on the performance of antibodies from Abgent to advance their research. Check out links to articles that cite our products in major peer-reviewed journals, organized by research category.
email@example.com, and receive a free "I Love Antibodies" mug.
Provided below are standard protocols that you may find useful for product applications.
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.
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.
If you have used an Abgent product and would like to share how it has performed, please click on the "Submit Review" button and provide the requested information. Our staff will examine and post your review and contact you if needed.
If you have any additional inquiries please email technical services at firstname.lastname@example.org.