Tumor Necrosis Factor Receptor Superfamily, Member 12A (TNFRSF12A) Antikörper (PE)

Antigen: Tumor Necrosis Factor Receptor Superfamily, Member 12A (TNFRSF12A)

Synonyme: FN14, CD266, TWEAKR

Klonalität: Monoklonal (ITEM-1)

Wirt: Maus

Reaktivität: Human

Konjugat: PE

Applikation: Durchflusszytometrie (FACS), Western Blot (WB), Immunhistochemie (Gefrierschnitte) (IHC (fro)), Apoptose-Induktion (AI)

Produktnummer: ABIN158805

Produktbeschreibung

Weitere Bezeichnung: Fn14/TWEAK Receptor

Immunogen: Human Fn14 transfected P815

Isotyp: IgG1, kappa chain

Klon: ITEM-1

Beschreibung: TWEAK receptor is also known as fibroblast growth factor inducible 14 kDa protein (Fn14) or CD266. It is a 14 kD transmembrane protein that is expressed on a variety of tissue types. This receptor binds TWEAK and interacts with the cytoplasmic proteins TRAF1, 2, and 3. The TWEAK receptor is rapidly induced during liver regeneration and m play a role in hepatocyte growth. TWEAK receptor engagement can induce cell death and may play a role in inflammation. The ITEM-1 antibody is useful for flow cytometric analysis, induction of tumor cells apoptosis or necrotic cell death, enhancing endothelial cell proliferation, and immunohistochemistry on frozen tissues. Distribution: Widely expressed, high constitutive expression in heart placenta, lung, muscle, kidney, pancreas, and HUVEC Function: Binds to TWEAK (CD255), thought to play a role in cell death and inflammation Synonyms: Fibroblast growth factor-inducible 14 kDa protein (Fn14), TNFRS12a Structure: Transmembrane TNF superfamily receptor, contains no death domain, 14 kD

Anwendungen

Applikationshinweise: Additional reported applications (for the relevant formats) include: Western blotting, immunohistochemistry of acetone-fixed frozen sections, Blocking of TWEAK-induced RANTES production in vitro , and in vitro induction of caspase-dependent cell death. The LEAF(TM) purified antibody (Endotoxin <0.1 EU/µg, Azide-Free, 0.2 µm sterile-filtered) is recommended for functional assays (ABIN158807). Each lot of this antibody is quality control tested by immunofluorescent staining with flow cytometric analysis. For immunofluorescent staining, the suggested use of this reagent is < 1.0 µg per 10 cells in 100 µl volume. It is recommended that the reagent be titrated for optimal performance in each application.

Reinigung: The antibody was purified by affinity chromatography, and conjugated with PE under optimal conditions. The solution is free of unconjugated PE and unconjugated antibody.

Buffer: Phosphate-buffered solution, pH 7.2, containing 0.09% sodium azide.

Lagerung: The antibody solution should be stored undiluted at 4°C and protected from prolonged exposure to light. Do not freeze.

Beschränkungen: Nur für Forschungszwecke einsetzbar

Bilder

Human Fn14 transfected cells stained with ITEM-1 PE

Publikationen

Publikationen: Lynch, Wang, Lund et al.: "TWEAK induces angiogenesis and proliferation of endothelial cells." in: The Journal of biological chemistry, Vol. 274, Issue 13, pp. 8455-9, 1999 (PubMed).

Meighan-Mantha, Hsu, Guo et al.: "The mitogen-inducible Fn14 gene encodes a type I transmembrane protein that modulates fibroblast adhesion and migration." in: The Journal of biological chemistry, Vol. 274, Issue 46, pp. 33166-76, 2000 (PubMed).

Feng, Guo, Factor et al.: "The Fn14 immediate-early response gene is induced during liver regeneration and highly expressed in both human and murine hepatocellular carcinomas." in: The American journal of pathology, Vol. 156, Issue 4, pp. 1253-61, 2000 (PubMed).

Nakayama, Ishidoh, Kojima et al.: "Fibroblast growth factor-inducible 14 mediates multiple pathways of TWEAK-induced cell death." in: Journal of immunology (Baltimore, Md. : 1950), Vol. 170, Issue 1, pp. 341-8, 2002 (PubMed).

Jin, Nakao, Nakayama et al.: "Induction of RANTES by TWEAK/Fn14 interaction in human keratinocytes." in: The Journal of investigative dermatology, Vol. 122, Issue 5, pp. 1175-9, 2004 (PubMed).

Felli, Pedini, Zeuner et al.: "Multiple members of the TNF superfamily contribute to IFN-gamma-mediated inhibition of erythropoiesis." in: Journal of immunology (Baltimore, Md. : 1950), Vol. 175, Issue 3, pp. 1464-72, 2005 (PubMed).