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ITN1688

ITN1688
  • Catalog: ITN1688
  • Gene/Protein: TSC22D3 DSIPI GILZ
  • Product Description: Immunotag™ T22D3 Polyclonal Antibody
385.0000
Price in reward points: 385

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Immunotag™ T22D3 Polyclonal Antibody
Antibody Specification
Datasheet
Target Protein T22D3
Clonality Polyclonal
Storage/Stability -20°C/1 year
Application WB,ELISA
Recommended Dilution WB 1:500-2000 ELISA 1:5000-20000
Concentration 1 mg/ml
Reactive Species Human
Host Species Rabbit
Immunogen Synthesized peptide derived from part region of human protein
Specificity T22D3 Polyclonal Antibody detects endogenous levels of protein.
Purification The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen
Form Liquid in PBS containing 50% glycerol, and 0.02% sodium azide.
Gene Name TSC22D3 DSIPI GILZ
Accession No. Q99576 Q9Z2S7 Q9EQZ1
Description TSC22 domain family member 3(TSC22D3) Homo sapiens This gene encodes the anti-inflammatory protein glucocorticoid (GC)-induced leucine zipper. Expression of this gene stimulated by glucocorticoids and interleukin 10 and it appears to play a key role in the anti-inflammatory and immunosuppressive effects of this steroid. This protein has also been shown to inhibit pro-inflammatory molecules including nuclear factor κB. Alternate splicing results in multiple transcript variants. [provided by RefSeq, Jan 2016],
Protein Expression Adipose tissue,Brain,Colon,Embryonic carcinoma,Epithelium,Fetal brain,Fetal
Subcellular Localization nucleus,cytoplasm,cytosol,
Protein Function domain:The leucine-zipper is involved in homodimerization.,function:Plays a role as a mediator of e2f1-induced apoptosis in the absence of tp53/p53.,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.,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.,induction:Up-regulated in the mitochondria by E2F1 after addition of 4-hydroxytamoxifen (at protein level).,similarity:Belongs to the TSC-22/Dip/Bun family.,similarity:Contains 1 GRAM domain.,subcellular location:Colocalizes with COX4I1.,subunit:Can form homodimers, however it is likely to function as a monomer. Interacts with AP1 (By similarity). Interacts with NFKB1.,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 haemopoietic 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.,tissue specificity:Expressed in lung and in primary lung squamous cell carcinoma (LSCC).,
Usage For Research Use Only! Not for diagnostic or therapeutic procedures.
Material Safety Data Sheet
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