Sentence examples for differentiation attributes from inspiring English sources

Collectively, these observations strongly support the notion that the retention of RARRES3 expression and the production of signaling mediators and precursors through its PLA1/2 activity are associated with BC tumors preserving some of their differentiation attributes.

First, RARRES3 blocks adhesion to the lung parenchyma and, second, the phospholipase activity of RARRES3 stimulates differentiation attributes, thus blunting metastasis-initiating functions at the lung required for the ER− BC cells to establish a lesion.

However, it is unknown whether genes that promote the maintenance of differentiation attributes in basal-like ER− BC tumors restrain the malignant phenotype and metastatic dissemination by limiting metastasis-initiating capacity.

Similarly, lung metastatic tumors in mice originated from RARRES3-expressing LM2 cells also showed increased expression of some differentiation attributes, including the differentiation transcription factor GATA3, as well as some PPAR targets (PPARD, PPARG, and ACSL5) significantly correlated with RARRES3 expression in primary tumors (Fig 6F).

Within Amazonia there was a moderate level of significant differentiation attributed to isolation by distance.

RhoH-deficient mice did not develop lymphomas and had no obvious defects in HSC maintenance, but they showed impaired T-cell differentiation attributed to defective T-cell receptor signalling.

The absence of population structure between the Peruvian groups and SAC (and the low levels of population structure between SAC and the HGDP Native American groups) indicates that the difference cannot be explained by population differentiation attributed to genetic drift.

During midgestational mammary development in vivo, several signal transducers and activators of transcription are known to be increased by prolactin; in the HC11 cells, Stat1 (Table 2), Stat3, Stat5a and Stat6 as well as the prolactin-induced protein increased, indicating that the cells retain this mammary epithelial cell-differentiation attribute.

The decreased commitment to early adipocyte progenitors and defects in adipogenic differentiation were attributed to aberrant splicing of mTOR described in Sam68−/− mice [ 35].

This differentiation was attributed to the continuous fixation of target genomic regions within subpopulations and strong isolation between subpopulations during maize breeding practices.

The inactivation of Mst1/2 in the intestine compartment to promote the hyperproliferation of intestinal stem cells and to inhibit intestinal epithelial differentiation is attributed largely to an enhancement of β-catenin action and an activation of Notch signaling.