| Reactivity | HuSpecies Glossary |
| Applications | Bioactivity |
| Format | Carrier-Free |
| Details of Functionality | Measured by its ability to enhance neurite outgrowth of E16-E18 rat embryonic cortical neurons. Recombinant Human TAFA5/FAM19A5, immobilized at 6-24 μg/mL on a 96-well plate, is able to significantly enhance neurite outgrowth. |
| Source | E. coli-derived human TAFA5/FAM19A5 protein Gln26-Ser125 |
| Accession # | |
| N-terminal Sequence | Gln26 |
| Protein/Peptide Type | Recombinant Proteins |
| Gene | FAM19A5 |
| Purity | >95%, by SDS-PAGE under reducing conditions and visualized by silver stain |
| Endotoxin Note | <0.01 EU per 1 μg of the protein by the LAL method. |
| Dilutions |
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| Theoretical MW | 10.9 kDa. Disclaimer note: The observed molecular weight of the protein may vary from the listed predicted molecular weight due to post translational modifications, post translation cleavages, relative charges, and other experimental factors. |
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| SDS-PAGE | 11 kDa, reducing conditions |
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| Publications |
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| Storage | Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
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| Buffer | Lyophilized from a 0.2 μm filtered solution in PBS. |
| Purity | >95%, by SDS-PAGE under reducing conditions and visualized by silver stain |
| Reconstitution Instructions | Reconstitute at 300 μg/mL in sterile PBS. |
TAFA5 (also FAM19A5) is a 14 kDa type I transmembrane protein and member of the FAM19/TAFA family of chemokine-like proteins (1). Human TAFA5 is 132 amino acids (aa) in length (SwissProt #: Q7Z5A7). It contains a 15 aa extracellular domain, a 23 aa transmembrane sequence, and a 95 aa cytoplasmic region. Alternate splicing produces two additional isoforms. Isoform 2, a secreted form, has a 31 aa substitution for residues 1-38 in isoform 1. Isoform 3 has an eight aa substitution for residues 1-87 in isoform1. Human TAFA5 is 100% aa identical to mouse TAFA5 (1). Within the TAFA family, TAFA5 is the most distinct member, while TAFAs 2, 3, and 4 are the most closely related members (1). Real-time PCR analysis indicates that TAFA5 mRNA expression is restricted to the central nervous system (CNS), with the highest level in the basal ganglia and cerebellum (1). The biological functions of TAFA family members are not yet known, but there are a few tentative hypotheses. First, TAFAs may modulate immune responses in the CNS by functioning as brain-specific chemokines, and may act with other chemokines to optimize the recruitment and activity of immune cells in the CNS (1). Second, TAFAs may represent a novel class of neurokines that act as regulators of immune nervous cells (1, 2). Finally, TAFAs may control axonal sprouting following brain injury (1).
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