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Notch1, Fc Fusion, Avi-Tag Recombinant
Notch1, Fc Fusion, Avi-Tag Recombinant
Artikelnummer
BPS101895-2
Verpackungseinheit
500 µg
Hersteller
BPS Bioscience
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Encompassing Amino Acids: 19-526
Application: Useful for SDS-PAGE.
Background: The Notch signaling pathway controls cell fate decisions in vertebrates and invertebrates' tissues and is involved in embryonic development, tissue homeostasis, and regulation of the immune and angiogenic systems. Notch signaling is triggered through the binding of a transmembrane ligand, present in opposing cells, to one of the four existing Notch transmembrane receptors (Notch1/Notch2/Notch3/Notch4). This results in proteolytic cleavage of the Notch receptor, releasing the constitutively active intracellular domain of the Notch receptor (NICD). NICD translocate to the nucleus and associates with the transcription factor CSL (CBF1/RBPJκ/Suppressor of Hairless/Lag-1) and coactivator Mastermind to turn on the transcription of Notch-responsive genes. Dysfunction of Notch signaling has severe consequences, including developmental pathologies or cancer (such as T cell acute lymphoblastic leukemia, T-ALL, and urothelial bladder cancer). The use of Notch inhibitors, mainly gamma-secretase inhibitors, as a cancer therapy option and in the regeneration of tissues is ongoing. Further studies will allow us to have a deeper understanding of Notch signaling and will benefit future therapeutic approaches.
Description: Recombinant human Notch1, encompassing amino acids 19-526 (extracellular domain). This construct contains a human IgG1 Fc domain fused at the C-terminal, followed by an Avi-tag™. This protein was affinity purified.
Format: Aqueous buffer solution.
Formulation: 8 mM phosphate, pH 7.4, 110 mM NaCl, 2.2 mM KCl, and 20% glycerol
Genbank: NM_017617.5
Purity: ≥90%
Storage Stability: At least 6 months at -80°C.
Tags: C-terminal Fc-Avi-Tag
Uniprot: P46531
Warnings: Avoid freeze/thaw cycles
Biosafety Level: Not applicable (BSL-1)
Encompassing Amino Acids: 19-526
Application: Useful for SDS-PAGE.
Background: The Notch signaling pathway controls cell fate decisions in vertebrates and invertebrates' tissues and is involved in embryonic development, tissue homeostasis, and regulation of the immune and angiogenic systems. Notch signaling is triggered through the binding of a transmembrane ligand, present in opposing cells, to one of the four existing Notch transmembrane receptors (Notch1/Notch2/Notch3/Notch4). This results in proteolytic cleavage of the Notch receptor, releasing the constitutively active intracellular domain of the Notch receptor (NICD). NICD translocate to the nucleus and associates with the transcription factor CSL (CBF1/RBPJκ/Suppressor of Hairless/Lag-1) and coactivator Mastermind to turn on the transcription of Notch-responsive genes. Dysfunction of Notch signaling has severe consequences, including developmental pathologies or cancer (such as T cell acute lymphoblastic leukemia, T-ALL, and urothelial bladder cancer). The use of Notch inhibitors, mainly gamma-secretase inhibitors, as a cancer therapy option and in the regeneration of tissues is ongoing. Further studies will allow us to have a deeper understanding of Notch signaling and will benefit future therapeutic approaches.
Description: Recombinant human Notch1, encompassing amino acids 19-526 (extracellular domain). This construct contains a human IgG1 Fc domain fused at the C-terminal, followed by an Avi-tag™. This protein was affinity purified.
Format: Aqueous buffer solution.
Formulation: 8 mM phosphate, pH 7.4, 110 mM NaCl, 2.2 mM KCl, and 20% glycerol
Genbank: NM_017617.5
Purity: ≥90%
Storage Stability: At least 6 months at -80°C.
Tags: C-terminal Fc-Avi-Tag
Uniprot: P46531
Warnings: Avoid freeze/thaw cycles
Biosafety Level: Not applicable (BSL-1)
| Artikelnummer | BPS101895-2 |
|---|---|
| Hersteller | BPS Bioscience |
| Hersteller Artikelnummer | 101895-2 |
| Verpackungseinheit | 500 µg |
| Mengeneinheit | STK |
| Wirt | Human |
| Produktinformation (PDF) | Download |
| MSDS (PDF) |
|
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Gernot Ensinger, M.Sc.
Laurent Haze
