English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Mice deficient for the RB gene (RB-/-), prior to death at embryonic day 14.5, show increased cell death in all tissues that normally express RB1: the nervous system, liver, lens, and skeletal muscle precursor cells. We have generated transgenic mice (RBlox) that express low levels of pRb, driven by an RB1 minigene. RBlox/RB-/- mutant fetuses die at birth with specific skeletal muscle defects, including increased cell death prior to myoblast fusion, shorter myotubes with fewer myofibrils, reduced muscle fibers, accumulation of elongated nuclei that actively synthesized DNA within the myotubes, and reduction in expression of the late muscle-specific genes MCK and MRF4. Thus, insufficient pRb results in failure of myogenesis in vivo, manifest in two ways. First, the massive apoptosis of myoblasts implicates a role of pRb in cell survival. Second, surviving myotubes failed to develop normally and accumulated large polyploid nuclei, implicating pRb in permanent withdrawal from the cell cycle. These results demonstrate a role for pRb during terminal differentiation of skeletal muscles in vivo and place pRb at a nodal point that controls cell proliferation, differentiation, and death.

pRb controls proliferation, differentiation, and death of skeletal muscle cells and other lineages during embryogenesis.