FKBP1a/FKBP12 human

FKBP1A is part of the family of immunophilins, which have in common high affinity for immunosuppressant drugs and a peptidyl-prolyl cis-trans isomerase (PPIase). In the absence of immunosuppressive ligands, FKBP1A is involved in intracellular calcium regulation by associating with 3 types of Ca2+ release channel complexes: skeletal ryanodine receptors, cardiac ryanodine receptors and the inositol 1, 4, 5-triphosphate receptor. FKBP1A also interacts with TGF type I receptor exerting an inhibitory effect on the TGF?-I signaling pathway. FKBP12 plays a role in modulation of ryanodine receptor isoform-1 (ryr-1), a component of the calcium release channel of skeletal muscle sarcoplasmic reticulum. FKBP1A increase the folding of proteins and catalyzes the cis-trans isomerization of proline imidic peptide bonds in oligopeptides.

FKFBP1A (FK506-binding protein 1A) belongs to the FK506-binding protein (FKBP) family. It is widely expressed in nerve systems. This gene is mapped to human chromosome 20p13. FKFBP1A interacts with various cellular molecules and participates in intracellular signaling pathways.

FKFBP1A (FK506-binding protein 1A) is a peptidyl-prolyl cis-trans isomerase. It interacts with the ryanodine receptor (RyR1) and helps in maintaining intracellular Ca²⁺ homeostasis. It is also involved in protein folding, cell cycle and protein trafficking. In neurodegenerative diseases, FKFBP1A is dysregulated and might be associated with the pathogenesis. In human cell lines, it controls the localization and processing of amyloid precursor protein, and thus might be involved in the pathogenesis of Alzheimer′s disease. FKFBP1A is also involved in Huntington′s disease. It plays a role in the structural properties and proteotoxicity of mHTT (mutant huntingtin) aggregates.

1 mg/mL solution in 20 mM Tris-HCl buffer (pH 8.0) containing 100 mM NaCl, 1 mM DTT and 10% glycerol.

Centrifuge the vial prior to opening.

MGSSHHHHHH SSGLVPRGSH MGVQVETISP GDGRTFPKRG QTCVVHYTGM LEDGKKFDSS RDRNKPFKFM LGKQEVIRGW EEGVAQMSVG QRAKLTISPD YAYGATGHPG IIPPHATLVF DVELLKLE