Although early expression of ntla, gsc and sox32 at 30% epiboly is downregulated or absent in MZ eomesa; foxh1 morphants, it is possible expression may recover at later stages; therefore, we analysed expression at shield stage (6 hpf; Additional file 12: Figure S6).
In standard (1-dimensional) possible worlds semantics, the semantic value of an expression is an intension, a function that assigns an extension to the expression "at" every possible world.
By performing a series of immunolabeling tests we found evidence in favor of a possible expression of HCN2 by RBCs, clustered at the tips of their short dendrites, in register with rod synaptic ribbons.
Even when this is possible, expression constructs may still fail to yield soluble protein, commonly expressing insolubly or at unusable yields.
But the range of possible expression remained a surprise.
This explains, at least partially, the diversity of findings on GP expression in McArdle muscle cell cultures and the lack of reports on possible expression of other isoforms.
To detect possible differential expression at the cellular level, we applied non-radioisotopic RNA in situ hybridisation in a subset of normal (n = 10) and cancerous (invasive ductal type, n = 10) breast tissue samples derived from the initial evaluation TMA.
Although Tal1 expression was downregulated in the Tal2 ko brains at E11.5 (Fig. 5J), and Tal1 inactivation alone did not affect GABAergic neurogenesis in the midbrain (Fig. 1K O) (Achim et al., 2012), it is possible that its expression at an earlier stage or at an undetectable level accounts for the survival of the few GABAergic cells observed in the Tal2 ko mutants.
In light of recent studies demonstrating a role for Arf in ribosome biogenesis [29] and in post-transcriptional control of VEGF expression [30], we assessed possible changes in VEGF expression at the protein level upon loss of Arf.
It is possible that transient Cdh1 expression at an age they did not assay (e.g., E17 – P4) may be eliminated by lack of CHRNB2 in the retina, and that this transient defect in the adherens junction leads to subsequent compensatory overexpression of CRB1.
