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The connectivity analysis showed that each stimulation condition induced a pattern of functional connectivity.
Serial 5'-deletion mutations of the full-length promoter revealed a pattern of functional activity in transfected cells.
The data on distribution of editing sites among codon positions, codons, and genes as we presented above demonstrate clearly that fixation of editing sites and fixation of mutations at editable sites followed a pattern of functional selection.
A pattern of functional redundancy and specificity among Ssa proteins has previously been observed for both yeast prion propagation and protein folding activities (Sharma et al., 2009; Sharma and Masison, 2011).
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Tedeschi et al. [31] reported a pattern of increased functional connection within the visual network in migraine with aura in comparison with migraine without aura and controls.
These tests and the graphical evaluation describe a pattern of low functional diversity but only in species-rich communities.
With the publication of additional case reports, and the clinical descriptions of large cohorts of individuals with 1p36 deletions, a pattern of characteristic functional deficits, congenital anomalies, and physical features associated with 1p36 deletions emerged.
These events coincided with a bimodal pattern of functional recovery, with, an early recovery independent of neovascularization, and a delayed hVEGF-dependent recovery coincident with neovascularization.
Our findings demonstrate a consistent pattern of functional deficiency and provide further support for a helicase-dependent cellular function of RECQL4 in addition to its Nterminus-dependent role in initiation of replication, a function that may underlie the phenotype of RECQL4-linked disease.
These concerns are underscored by the fact that protein domains are redundantly used to perform diverse biochemical activities [ 12, 13], leading to the expectation that short peptides will simply align to all the proteins carrying their "domains of origin", resulting in a confounded pattern of functional predictions based on a variety of reference proteins carrying that domain [ 14, 15].
From these analyses we uncovered a consistent pattern of functional deficiency, which may serve as an initial step in uncovering the cellular origin of RECQL4 disease phenotypes.
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CEO of Professional Science Editing for Scientists @ prosciediting.com