Human DLK-1/Pref-1, soluble
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| Cat-Nr. | 400-020S |
| Size | 5 µg |
| Price | 99 € |
| Source | E. coli |
| Label | His-Tag |
| Formulation | lyophilized |
| Purity Confirmation | > 98% by SDS-PAGE |
| Length [aa] | 282 |
| Molecular Weight | 30.2 kDa |
| N Terminal Sequence | AECFP |
| Species Reactivity | Human |
| Buffer | PBS |
| Reconstitution | Centrifuge vial prior to opening. Human sDLK1/Pref1 should be reconstituted in water to a concentration of 0.1 mg/ml. This solution can be diluted in water or other buffer solutions or stored at -20°C. |
| Stability and Storage | The lyophilized human sDLK1/Pref1, though stable at room temperature, is best stored desiccated below 0°C. Reconstituted human sDLK1/Pref1 should be stored in working aliquots at -20°C. |
| Synonyms | Protein delta homolog 1, pG2, Fetal antigen 1, FA1, ZOG |
| Description | Delta-like 1 (DLK1), also known as Pref-1 and FA1, is a transmembrane protein pertaining to the epidermal growth factor superfamily. DLK1 affects several differentiation processes, including adipogenesis, muscular and neuronal differentiation, bone differentiation, and haematopoiesis. Several reports support that DLK1 may operate as a non-canonical ligand of the NOTCH pathway. Since the NOTCH signaling pathway is essential for vascular development and physiology by controlling angiogenesis in pre- and post-natal life, it was reasoned that DLK1 could contribute to regulate this process in adult endothelial cells through the interaction with NOTCH receptors. It was found that overexpression of DLK1 inhibits migration and angiotube formation in mammalian vascular endothelial cells and disrupts normal embryonic vascularization in zebrafish. Genetic ablation of DLK1 in mice is associated with increased angiogenesis in vitro and with focal areas of retinal hyper-vascularization. Specific knockdown of the orthologous Dlk1 of zebrafish results in ectopic angiogenesis. Moreover, in a tumor angiogenesis model in zebrafish, suppression of Dlk1 promotes vessel migration towards the tumor cell mass. It was also found that the NOTCH signaling pathway is targeted by DLK1 in the context of angiogenesis and that DLK1 antagonizes NOTCH-dependent signaling in endothelial cells, while, in contrast, this signaling is enhanced in Dlk1-null mice. Collectively, these results revealed a previously unknown role for DLK1 in the vasculature as a regulator of NOTCH-mediated angiogenesis. |
| Protein Sequence | AECFPACNPQNGFCEDDNVCRCQPGWQGPLCDQCVTSPGCLHGLCGEPGQCICTDGWDGELCDRDVRACSSAPCANNGTCVSLDDGLYECSCAPGYSGKDCQKKDGPCVINGSPCQHGGTCVDDEGRASHASCLCPPGFSGNFCEIVANSCTPNPCENDGVCTDIGGDFRCRCPAGFIDKTCSRPVTNCASSPCQNGGTCLQHTQVSYECLCKPEFTGLTCVKKRALSPQQVTRLPSGYGLAYRLTPGVHELPVQQPEHRILKVSMKELNKKTPLEHHHHHH |
| Uniprot ID | P80370 |
| Protein RefSeq | NP_003827.3 |
| mRNA RefSeq | NM_003836.5 |
Figures
SDS-PAGE analysis of recombinant human soluble DLK-1/Pref-1. Sample was loaded in 15% SDS-polyacrylamide gel under reducing condition and stained with Coomassie blue.
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