DSPE-PEG5000-TH
DSPE-PEG5000-TH is a PEG compound which composed of DSPE and a pH-responsive cell penetrating peptide (TH). TH is activated in an acidic environment (such as the tumor microenvironment) and can selectively carry small molecules, oligonucleotides, proteins, etc. into tumor cells.
商品は「研究用試薬」です。人や動物の医療用・臨床診断用・食品用の製品ではありません。
研究用途以外に使用した場合、当社は一切の責任を負いかねます。
-
保管条件:
Please store the product under the recommended conditions in the Certificate of Analysis.
生物活性
製品説明
化学情報
-
SMILES
[Mal-Cys-AGYLLGHINLHHLAHL-Aib-HHIL-NH2]C(CCOCCOC(NCCOP(OC[C@](COC(CCCCCCCCCCCCCCCCC)=O)([H])OC(CCCCCCCCCCCCCCCCC)=O)(O)=O)=O)=O.[n]
-
輸送条件
Room temperature in continental US; may vary elsewhere.
-
保管条件
Please store the product under the recommended conditions in the Certificate of Analysis.
プロトコル
-
Multiplex immunofluorescence IHC
Multiplex immunofluorescence IHC detects multiple protein biomarkers in one tissue section by sequential antibody staining, HRP-mediated tyramide fluorophore deposition, heat-mediated antibody stripping, nuclear counterstaining, multispectral imaging, spectral unmixing, and digital cell phenotyping; TSA deposits fluorophore near the antigen so the fluorescence signal remains after primary and secondary antibodies are removed, enabling repeated staining cycles, including with antibodies from the same host species. Classic FFPE tumor immune-profiling applications use panels such as CD3, CD8, CD68/CD163, FOXP3, PD-1, PD-L1, pancytokeratin, Ki67, and DAPI to identify tumor cells, immune-cell subsets, checkpoint-marker expression, co-expression phenotypes, cell density, and spatial relationships in the tumor microenvironment.
-
Multiplex immunohistochemistry
Multiplex immunohistochemistry (mIHC), also known as tyramide dignal amplification (TSA), is an enzymatic detection method that uses horseradish peroxidase (HRP) to perform high-density in-situ labeling of target proteins or nucleic acids.
-
Research Protocol for Cancer Immunology
Cancer immunology studies how the immune system recognizes, suppresses, edits, or fails to eliminate malignant cells through tumor antigen release, antigen presentation, T-cell priming, immune trafficking, tumor-cell killing, and feedback inhibition in the tumor microenvironment. The cancer-immunity cycle links tumor antigenicity, dendritic-cell priming, CD8+ T-cell infiltration, cytotoxic function, and immune-checkpoint regulation to tumor rejection or immune escape. Immune-checkpoint pathways such as PD-1/PD-L1 and CTLA-4 suppress antitumor T-cell activity and can be therapeutically blocked, but many tumors remain resistant because of poor antigen presentation, weak T-cell infiltration, suppressive myeloid cells, regulatory T cells, and tumor-intrinsic immune-exclusion programs. Unresolved questions include which immune-cell states predict response, how tumor-intrinsic pathways exclude immune cells, how myeloid suppression limits checkpoint blockade, and which combination strategies
純度とドキュメンテーション
参考文献
Calculators
濃度 (開始) × 体積 (開始) = 濃度 (終了) × 体積 (終了)