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|Recombinant Mouse CRABP2 protein (Catalog#50535-M07E)|
|0.2 μm filtered solution in PBS with 5% trehalose|
|Produced in rabbits immunized with purified, recombinant Mouse CRABP2 (rM CRABP2; Catalog#50535-M07E; P22935; Pro 2-Glu 138). CRABP2 specific IgG was purified by Mouse CRABP2 affinity chromatography.|
|WB, ELISA, IHC-P|
WB: 1-2 μg/mL
ELISA: 0.1-0.2 μg/mL
This antibody can be used at 0.1-0.2 μg/mL with the appropriate secondary reagents to detect Mouse CRABP2. The detection limit for Mouse CRABP2 is approximately 0.00975 ng/well.
IHC-P: 0.1-2 μg/mL
|This antibody can be stored at 2℃-8℃ for one month without detectable loss of activity. Antibody products are stable for twelve months from date of receipt when stored at -20℃ to -80℃. Preservative-Free.|
Sodium azide is recommended to avoid contamination (final concentration 0.05%-0.1%). It is toxic to cells and should be disposed of properly. Avoid repeated freeze-thaw cycles.
Mouse cellular retinoic acid-binding protein 2, also known as Cellular retinoic acid-binding protein II, CRABP-II and CRABP2, is a protein which belongs to the calycin superfamily and Fatty-acid binding protein (FABP) family. Cellular retinoic acid binding proteins (CRABP) are low molecular weight proteins whose precise function remains unknown. The predicted amino acid sequences of human CRABP1 and CRABP2 demonstrated a 99.3% and 93.5% identity to mouse CRABP1 and CRABP2, respectively. CRABP2 forms a beta-barrel structure that accommodates hydrophobic ligands in its interior. Expression of CRABP2, but not CRABP1 mRNA, was markedly increased (greater than 15-fold) by retinoic acid treatment of fibroblasts cultured from human skin, whereas no significant induction of CRABP2 mRNA was observed in human lung fibroblasts. CRABP2 transports retinoic acid to the nucleus. It regulates the access of retinoic acid to the nuclear retinoic acid receptors. CRABP2 is necessary for elastin induction by All-trans retinoic acid (ATRA) in MRC-5 cells. It is expressed at low levels in emphysema fibroblasts. This alteration in the retinoic acid signalling pathway in lung fibroblasts may contribute to the defect of alveolar repair in human pulmonary emphysema.