Sentence examples for differentiation barrier from inspiring English sources

Consistent with this idea, Hemberger and colleagues found that ES cells in which the maintenance DNA methyltransferase Dnmt1 is mutated lack this differentiation barrier (Ng et al., 2008).

This provides evidence that the nature of the differentiation barrier faced by ES cells is likely to be maintained by the ability of those cells to repress expression of certain genes.

Ectopic expression of normally silent transcription factors has been shown to allow ES cells to overcome this differentiation barrier and adopt the normally inaccessible TE fate (Gu et al., 2011; Ng et al., 2008; Niwa et al., 2005).

In skin, TH exerts profound effects on fetal epidermal differentiation, barrier formation, hair growth, sebum production, wound healing, epidermal oxygen consumption, keratinocyte proliferation, and keratin gene expression  [6 12].

Here we demonstrate that transcriptional silencing by the NuRD complex, which at some genes involves specification of DNA methylation, also contributes to this differentiation barrier by maintaining repression of the TE-specific transcription factor genes Elf5 and Eomes.

Cumulatively, however, such minor effects may engender disease-associated haplotypes that contribute to population-level variation in PRE occupancy (e.g., by AP-1), which is in turn connected to susceptibility through its influence on the expression of genes promoting normal KC differentiation and barrier function (Figure 8B).

The importance of Cldns in epidermal differentiation and barrier function has been confirmed by experiments in which Cldn expression has been perturbed in epidermal cells; for example, Cldn1 knockout mice die shortly after birth due to skin barrier dysfunction [14].

In contrast, genes with decreased expression in sensitized dogs were associated with differentiation and barrier function of the skin.

We have shown previously that uroplakin expression decreases during bladder carcinogenesis [ 19– 21], which is reflected in partial urothelial differentiation and barrier disruption [ 22, 23].

Using the ORESTES (open reading frame ESTs) method, an excellent study investigating human genes involved in epidermal differentiation and barrier function, revealed a list of several potential candidates for the postulated unknown epidermal TAG lipase.

Filaggrin deficiency is responsible for decreased amounts of free amino acids in the stratum corneum (SC), abnormal keratinocyte differentiation, epidermal barrier defects and enhanced percutaneous sensitization, all characteristics of the atopic skin.