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In addition, the role of chromatin reassembly factors (CRFs) has been postulated in regulating the viral gene expression [ 46].
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A role for cell cycle inhibitors has been postulated in promoting favorable vascular remodeling and preventing pathologic intimal hyperplasia by regulating G1 to S phase progression in vascular smooth muscle cells (reviewed in [26]).
A major role of genes regulating neurotransmitters, leading mainly to dopamine (DA) dysfunction, has been postulated in the disease etiology (reviewed in [ 6]).
Also, contradictory results were postulated in these two recent studies.
In C. neoformans, for instance, GPI anchor has been postulated to regulate the secretion of phospholipase B1 in response to environmental conditions and hence determine virulence [ 9].
Primary cilia and polycystins are co-expressed in cells within the osteoblast lineage [8] where they have been postulated to regulate skeletogenesis [4], [9], [25], [26], [27].
VDACs have also been postulated to regulate cell death mechanisms.
MicroRNAs have been postulated to regulate ∼30% of the human genome (Bartel, 2004).
It has been postulated that CDKB1 1 regulates the CDKA 1 activity in dividing cells through controlling the KRP2 protein abundance [ 39].
sAC expression has been postulated to be regulated via tissue-specific alternative splicing [ 34, 35].
Another example is homology group 11, whose mORFs are predicted to encode trehalose-6-phosphate phosphatase (TPPase); trehalose-6-phosphate is postulated to regulate sugar metabolism in plants [ 37].
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