DLL1 Proteins, Antibodies, cDNA Clones, ELISA Kits Research Reagents

All DLL1 reagents are produced in house and quality controlled, including 13 DLL1 Antibody, 2 DLL1 ELISA, 39 DLL1 Gene, 5 DLL1 Lysate, 5 DLL1 Protein, 3 DLL1 qPCR. All DLL1 reagents are ready to use.

DLL1 Protein (5)

    DLL1 Antibody (13)

      DLL1 ELISA キット(すぐに使用できます)& ELISA抗体ペアセット(すぐに使用できません)(2)

      DLL1 cDNA Clone (39)

      NM_005618.3

      クローニングベクター cDNA 製品

      In lentiviral vector

      NM_007865.3

      クローニングベクター cDNA 製品

      In lentiviral vector

      NM_032063.1

      クローニングベクター cDNA 製品

      In lentiviral vector

      DLL1 Lysate (5)

        DLL1 の背景知識

        Delta-like protein 1(DLL1), also known as Delta1, a single-pass type I membrane protein which contains one DSL domain and eight EGF-like domains, acts as a ligand for Notch receptors, and positively regulates T-cell development. DLL1 is proteolytically processed in a similar manner to the Notch receptor, and it has been speculated to participate in bidirectional signaling. The proteolytic processing of DLL1 helps achieve an asymmetry in Notch signaling in initially equivalent myogenic cells and helps sustain the balance between differentiation and self-renewal. Interactions between DLL1 and Notch in trans activate the Notch pathway, whereas DLL1 binding to Notch in cis inhibits Notch signaling. DLL1 undergoes proteolytic processing in its extracellular domain by ADAM1. It had been demonstrated that DLL1 represents a substrate for several other members of the ADAM family. In co-transfected cells, DLL1 is constitutively cleaved by ADAM12, and the N-terminal fragment of DLL1 is released to medium. ADAM12-mediated cleavage of DLL1 is cell density-dependent, takes place in cis orientation, and does not require the presence of the cytoplasmic domain of ADAM12. Full-length DLL1, but not its N- or C-terminal proteolytic fragment, co-immunoprecipitates with ADAM12. By using a Notch reporter construct, we show that DLL1 processing by ADAM12 increases Notch signaling in a cell-autonomous manner. Furthermore, ADAM9 and ADAM17 have the ability to process DLL1. In contrast, ADAM15 does not cleave DLL1, although the two proteins still co-immunoprecipitate with each other. During fetal development, DLL1 is an essential Notch ligand in the vascular endothelium of large arteries to activate Notch1 and maintain arterial identity. DLL1-Notch signaling was required for VEGF receptor expression in fetal arteries.

        DLL1 の参考文献

        • Dyczynska E, et al. (2007) Proteolytic processing of delta-like 1 by ADAM proteases. J Biol Chem. 282(1): 436-44.
        • Sun D, et al. (2008) The role of Delta-like 1 shedding in muscle cell self-renewal and differentiation. J Cell Sci. 121(Pt 22): 3815-23.
        • Srensen I, et al. (2009) DLL1-mediated Notch activation regulates endothelial identity in mouse fetal arteries. Blood. 113(22): 5680-8.

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