Recombinant Mouse Slit1 (aa 1126-1531) Protein, CF Summary
Ser1126-Ala1531, with a C-terminal 6-His tag
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CF stands for Carrier Free (CF). We typically add Bovine Serum Albumin (BSA) as a carrier protein to our recombinant proteins. Adding a carrier protein enhances protein stability, increases shelf-life, and allows the recombinant protein to be stored at a more dilute concentration. The carrier free version does not contain BSA.
In general, we advise purchasing the recombinant protein with BSA for use in cell or tissue culture, or as an ELISA standard. In contrast, the carrier free protein is recommended for applications, in which the presence of BSA could interfere.
|Formulation||Lyophilized from a 0.2 μm filtered solution in PBS.|
|Reconstitution||Reconstitute at 500 μg/mL in PBS.|
|Shipping||The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature recommended below.|
|Stability & Storage:||
2μg/lane of Recombinant Mouse Slit1 was resolved with SDS-PAGE under reducing (R) and non-reducing (NR) conditions and visualized by Coomassie® Blue staining, showing bands at 60 - 68 kDa.
Slit1 is a member of the Slit family of large secreted axon guidance molecules that are ligands for Robo receptors (1, 2). Like other mammalian family members, the 1531 amino acid (aa), ~200 kDa Slit1 contains a 33 aa signal sequence followed by 23 leucine-rich repeats (LRR, aa 34-900) and 9 EGF-like sequences (aa 930-1451) (2). Mammalian Slits also contain a laminin-G domain between EGF6 and EGF7 (aa 1163-1336), and a C-terminal cysteine-rich domain (cysteine knot; aa 1456-1531) (2). Heparin sulfates are required for interaction of Robo with Slit LRR domains (2, 3). The C-terminal fragment (aa 1126-1531) of mouse Slit 1 shares 96% and 99% aa identity with human and rat respectively. Slit1 and Slit2 (or in some cases Slit3) are expressed in complementary locations during development of the optic and olfactory tracts and the forebrain, and appear to work together to mediate Robo guidance of retinal, olfactory, hippocampal and motor axons (1, 4-9). Deletion of either Slit1 or Slit2 has less effect than deletion of both, which allows axons to wander from tracts and inappropriately cross or recross the midline (4, 5, 7-9). In the injured spinal cord, presence of Slit1 along with Slit3 and Netrin-1 may be responsible for failure of axons to regenerate in the adult CNS (10). Slit1 also promotes dendrite growth and branching of cortical neurons indicating it may exert important influence on the final morphology of cortical neurons (11). Although Slit1 has mainly been found in the fetal and adult brain, it is also detected in the heart and kidney. The C-terminal cysteine knot, which may mediate interaction with other proteins, is absent in the rat brain splicing variant, Slit1 alpha (12).
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