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Human FAM19A2 Protein (Fc Tag)

TAFA-2,TAFA2

Catalog Number P11169-H01H
Organism Species Human
Host Human Cells
Synonyms TAFA-2,TAFA2
Molecular Weight The recombinant human FAM19A2/Fc is a disulfide-linked homodimer. The reduced monomer comprises 361 amino acids and has a predicted molecular mass of 39.7 kDa. The apparent molecular mass of the protein is approximately 43 kDa in SDS-PAGE under reducing conditions.
predicted N Glu
SDS-PAGE
Purity > 79 % as determined by SDS-PAGE
Protein Construction A DNA sequence encoding the human FAM19A2 (Q8N3H0-1) (Ala31-His131) was expressed, fused with the Fc region of human IgG1 at the N-terminus.
Bio-activity
Research Area Immunology |Inflammation / Inflammatory Mediator |Inflammatory Cytokines & Chemoki and Receptors |Chemokines and Receptors |Other Chemokine-related Ligands and Receptors
Formulation Lyophilized from sterile PBS, pH 7.4
1. Normally 5 % - 8 % trehalose, mannitol and 0.01% Tween80 are added as protectants before lyophilization. Specific concentrations are included in the hardcopy of COA.
Background FAM19A2 belongs to the FAM19/TAFA family. FAM19/TAFA family members are chemokine-like proteins. The biological functions of TAFA family members remain to be determined, 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. Second, TAFAs may represent a novel class of neurokines that act as regulators of immune nervous cells. And third, TAFAs may control axonal sprouting following brain injury. Human FAM19A2 is 97% aa identical to mouse FAM19A2 and is expressed in the central nervous system (CNS), colon, heart, lung, spleen, kidney, and thymus, however its expression in the CNS is 50 to 1000 fold higher than in other tissues. FAM19A2 gene is a member of the TAFA family which is composed of five highly homologous genes that encode small secreted proteins.
Reference
  • Parsa A, et al. (2011) Hypertrophy-associated polymorphisms ascertained in a founder cohort applied to heart failure risk and mortality. Clin Transl Sci. 4(1):17-23.
  • Rose JE, et al. (2010) Personalized smoking cessation: interactions between nicotine dose, dependence and quit-success genotype score. Mol Med. 16(7-8):247-53.
  • Trynka G, et al. (2009) Coeliac disease-associated risk variants in TNFAIP3 and REL implicate altered NF-kappaB signalling. Gut. 58(8):1078-83.