Sentence examples for mouse epidermis resulted from inspiring English sources

Consistent with those observations, loss of Lrig1 in mouse epidermis resulted in hyperproliferation in the IFE.

In summary, with the exception of modest increases in epidermal proliferation in 4OHT-treated IKOα mice, the acute single ablation of C/EBPα or C/EBPβ in adult mouse epidermis results in a phenotype similar to the germline knockout phenotype [25], [26], indicating developmental compensatory events do not have a major role in masking the postnatal germline knockout phenotype.

Taken together, our data suggest that the overexpression of a Cldn tail truncation mutant in the suprabasal compartment of the mouse epidermis results in its delayed maturation, a propensity for injury, diminished repair and skin barrier deficiency reminiscent of the intrinsic aging process of human skin.

Accordingly, the targeted ablation of ARNT in mouse epidermis results in profound defects in desquamation and epidermal barrier function, particularly decreased filaggrin and SPRR2A expression [ 18].

Activation of Myc in the basal layer of mouse epidermis results in increased proliferation (Arnold and Watt, 2001; Waikel et al., 2001), whereas, in cultured human epidermal keratinocytes, LRIG1 overexpression decreases Myc levels and reduces proliferation (Jensen and Watt, 2006).

If the modifications contribute to the mechanism of Myc-induced exit from the epidermal stem cell compartment [11], [23], then TSA treatment of wild-type mouse epidermis should result in a similar phenotype to Myc activation.

Overexpression of either Dsg2 or Dsg3 in suprabasal layers of mouse epidermis also results in keratinocyte hyperproliferation (Merritt et al, 2002; Brennan et al, 2007).

When serum- and normal tissue sediment-absorbed antisera prepared against mouse epidermal urea-extracted proteins were further absorbed with carcinoma urea antigens, antisera specific for epidermis resulted.

Depletion of DSC3 in mice resulted in embryonic lethality before implantation [39], while conditional depletion of DSC3 in mouse epidermis led to epidermal blistering [40].

Topical application of RAL and HAF resulted in a significant increase of pro-HB-EGF and HB-EGF protein levels in mouse epidermis as well as a slight increase in erbB1 protein expression.

These data are consistent with results from a recent RNA-seq analysis of the developing mouse epidermis [ 53] and from p63 isoform-specific knockout experiments that demonstrated the major functional role of ΔNp63 in the epidermis [ 54, 55].