Sentence examples for mouse lenses lacking from inspiring English sources

Cells from human posterior subcapsular cataracts had morphological and molecular characteristics similar to the cells at the posterior of mouse lenses lacking Trp53.

These data can also be linked to previous studies showing that mouse lenses lacking the bone morphogenetic protein receptor Acvr1 have increased epithelial and cortical fiber cell death.

This process did not appear to have proceeded normally in lenses lacking alphaA and alphaB.

Deletion of Trp53 in the lens rescued cell death in lenses lacking Acvr1 and prevented a small percentage of fiber cells from withdrawing from the cell cycle.

Adult lens epithelial cells in the mole did not show the cuboidal structure characteristic of mouse lenses, and also lacked mitochondria, indicating that the normal epithelial phenotype observed in other mammals is lost during mole lens development – mole epithelial cells showed a partial lens fibre phenotype.

Hoang, T. V. et al. Comparative transcriptome analysis of epithelial and fiber cells in newborn mouse lenses with RNA sequencing.

Analysis of MsrA knockout mouse lenses revealed oxidation of αB-crystallin/sHSP at methionine 68 [27].

Further analysis of the MsrA knockout mouse lenses revealed oxidation of cyt c at met 80 [26].

These observations suggest that onco-Dbl expression in mouse lenses induces events associated with EMT.

Immunohistochemical analyses of fixed mouse lenses extend these findings.

In targeted gene deletion studies in mice, αA+/- heterozygous mouse lenses do not show lens opacification, whereas αA-/ homozygous lenses develop cataracts at an early age [ 24].