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Light is known to induce nuclear c-Fos expression in the INL of the mouse retina, however this response is reduced in a mouse model of photoreceptor degeneration[34].
We attempted to detect Cav1.4 channel protein in sections of mouse retina; however our antibody is directed against the C-terminus of the human protein, which shares only ∼50% sequence homology with the mouse protein (rendering the antibody only weakly cross-reactive and therefore unsuitable for immunohistochemistry in mouse).
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Interestingly, RBP-J has been shown to be required to maintain Sox9 expression during the gliogenic phase of spinal cord development [20] and Notch signaling is essential for Sox9 expression in the mouse retina [21], however whether Notch signaling directly or indirectly regulates Sox9 expression has not been determined.
We found a higher expression level of Nos2 in the retina of P2Y1R-KO mice as compared with Wt retina, however, we did not study the functional role of iNOS in more detail.
This method is limited, however, to sorting rod photoreceptors from adult mouse retina.
However, to our knowledge there is no data on Aβ accumulation in the mouse retina as a part of a normal ageing process.
In the mouse retina and optic nerve head, we identified numerous astrocytes that expressed GFAP, S100β, Sox2 and Sox9; however, we found no evidence for NIRG-like cells that were positive for Nkx2.2, nestin, and negative for GFAP.
However, it is possible that there is some overlapping, redundant expression around P0 in the developing mouse retina.
However, the postmitotic photoreceptor precursor cells used in these studies are derived from the early postnatal mouse retina.
However, it is not known if Rb, p107 and p130 are expressed redundantly in the developing mouse retina or if intrinsic genetic compensation by p107, p130 or both prevents retinoblastoma in Rb-deficient mice.
What about the retina, however?
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CEO of Professional Science Editing for Scientists @ prosciediting.com