
Thermo Fisher Scientific MADD Polyclonal Antibody
Human MADD 단백질을 인식하는 Rabbit Polyclonal Antibody로, IHC(P) 및 ICC/IF 실험에 적합합니다. 항원 친화 크로마토그래피로 정제되었으며, 고순도 0.7 mg/mL 농도로 제공됩니다. 연구용으로 TNFR1 신호전달 및 MAP kinase 경로 연구에 활용 가능합니다.
- 판매단위
- pk
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Applications
Immunohistochemistry (Paraffin) (IHC (P))
- Tested Dilution: 1:1,000–1:2,500
Immunocytochemistry (ICC/IF)
- Tested Dilution: 0.25–2 µg/mL
Product Specifications
| 항목 | 내용 |
|---|---|
| Species Reactivity | Human |
| Host / Isotype | Rabbit / IgG |
| Class | Polyclonal |
| Type | Antibody |
| Immunogen | Recombinant protein corresponding to Human MADD. Recombinant protein control fragment (Product #RP-97304) |
| Conjugate | Unconjugated |
| Form | Liquid |
| Concentration | 0.7 mg/mL |
| Purification | Antigen affinity chromatography |
| Storage Buffer | PBS, pH 7.2, with 40% glycerol |
| Contains | 0.02% sodium azide |
| Storage Conditions | Store at 4°C short term. For long term storage, store at -20°C, avoiding freeze/thaw cycles. |
| Shipping Conditions | Wet ice |
| RRID | AB_2790585 |
Product Specific Information
Immunogen sequence:
YSQQINEVLD QLANLNGRDL SIWSSGSRHM KKQTFVVHAG TDTNGDIFFM EVCDDCVVLR SNIGTVYERW WYEKLINMTY CPKTKVLCLW RRNGSETQ
Target Information
Tumor necrosis factor receptor 1 (TNFR1) contains a death receptor domain that mediates interactions involved in downstream signaling of TNF.
A novel protein, MADD (Mitogen Activated Protein (MAP)-kinase Activating Death Domain Protein) associates with the death domain of TNFR1 through its own C-terminal death domain, which is critical for TNFR1 signal generation.
Overexpression of MADD activates MAP kinases ERK and JNK and induces phosphorylation of cytosolic phospholipase A2, linking TNF signaling to MAP kinase activation and arachidonic acid release.
MADD shows 98% homology with DENN (Differentially Expressed in Neoplasmic vs. Normal cells) and 93% sequence conservation with Rab3 GDP/GTP exchange protein.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
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