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Anti-CRABP2 Antibody (PE)

  • Product Information
  • Description
Catalog: C-FC-3214A
Product Type: FCM Antibody
Size: 25 Tests/100 Tests
Concentration: 10 μl/Test, 0.1 mg/ml
Reactivity: Human
Specificity: Human CRABP2
Analysis mode: FCM
Host: Mouse
Clonality: Monoclonal
Isotype: IgG1
Alternate names: cellular retinoic acid binding protein 2
Form: Liquid
Shipping: This antibody is shipped as liquid solution at ambient temperature. Upon receipt, store it immediately at the temperature recommended below.
Storage: This antibody can be stored at 2℃-8℃ for twelve months without detectable loss of activity. Protected from prolonged exposure to light. Do not freeze ! Sodium azide is toxic to cells and should be disposed of properly. Flush with large volumes of water during disposal.
Purification method: Protein A
Conjugation: PE
Immunogen: Recombinant Human CRABP2 protein
Buffer: Aqueous solution containing 0.5% BSA and 0.09% sodium azide

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 thecalycin 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.

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