[5][6] CRABP1 is assumed to play an important role in retinoic acid-mediated differentiation and proliferation processes.
[10] The domains for the nuclear localization and the retinoic acid binding are shown in Figure 3.
Knockout mice without CRABP1 showed increased neural stem cell proliferation and thus hippocampus neurogenesis.
Furthermore, learning and memory were improved in knockout mice, as measured by the Morris water maze test and an object recognition task.
[12] Figure 2 illustrates both pathways of retinoic acid binding to CRABP for cell proliferation and apoptotic activity.
Figure 1. An overview of retinoid transfer by CRABP. R = Retinoic acid, RAR = retinoic acid receptor, RXR = Retinoic X receptor, RRE = retinoid response element. CRABP binds to retinoic acid and transports it to the nucleus where binding with RAR or RXR homodimers or heterodimers further regulates RREs to regulate transcription events on DNA.
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Figure 2. Retinoic acid (RA) is processed from vitamin A to bind to fatty acid binding protein (FABP5) along with CRABP to associate with the binding to DNA to mediate pathways. RA binds with CRABP to mediate further action with retinoic acid receptor (RAR) on DNA for pathway mediation as well.
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Figure 3. Image of the domain locations for CRABP1. The nuclear localization signal (NLS) is at position 21-31 and the retinoic acid binding site (RBS) is at position 132-134.
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