Biomedical subjects

F Cole

Publications and source records attributed to F Cole.

9 recordsLinked to original sources

PubMed1992

Monoclonal antibodies identify a possible regulatory domain of MyoD1.

A panel of monoclonal antibodies (mAbs) to murine MyoD1 was generated. One set of mAbs is shown to react with epitope(s) in the cysteine/histidine-rich (C/H) region while another set is shown to react with epitope(s) in the C-terminal portion of MyoD1. One of the mAbs reactive with a C-terminal epitope sensitively detected MyoD1 in whole cell extracts by Western blotting. Time course studies of total protein accumulation during C2C12 myoblast differentiation revealed only subtle changes in the phosphorylation and quantity of MyoD1 protein present in C2C12 cells from induction to 120 hr after induction. These results suggest that modulation of MyoD1 protein or total phosphorylation levels is not tightly associated with the transition of undifferentiated myoblasts to differentiated myocytes. Monoclonal antibodies to the C-terminal epitope produced supershifted bands in gel retardation assays, indicating that these mAbs had no effect on DNA binding. Although the C/H region of MyoD1 does not participate in DNA binding, mAbs reactive with the C/H region neutralized this activity in gel retardation assays. These data suggest that the conserved C/H domain may serve to modulate MyoD1 DNA-binding activity by interacting with another regulator.

Animals↗

PubMed1991

Infection and inhibition of differentiation of human fetal skeletal myoblasts by adenovirus.

The effects of adenovirus type 5 infection on the differentiation of cultured human skeletal myoblasts and of myoblast differentiation on the replication of adenovirus were investigated. Although infection of myoblasts concurrently with differentiation induction was inhibitory, myoblast differentiation was not impeded when infection was carried out 2 hr or later after induction. Similar studies conducted with E1A mutant viruses (dI312, pm975, and dI1500) revealed that complete inhibition was dependent on the product of 13 S E1A transcript expression, although partial inhibition could be induced by the 12 S product. Differentiation of myoblasts results in the generation of multinucleated myotubes and quiescent mononuclear cells. The three cell types (myoblasts, myotubes, mononuclear cells) were differentially permissive to adenovirus infection. The precursor myoblasts and the multinucleated myotubes were found to be permissive for adenovirus infection. The kinetics of their infection was delayed 24-48 hr relative to that of HeLa cells. Quiescent mononuclear cells in the differentiated myoblast cultures were found to be inefficient in supporting the production of adenovirus particles, despite the accumulation of adenovirus DNA and capsid proteins. Host protein synthesis in the three cell types also responded differently to adenovirus infection. In the multinucleated myotubes, host protein synthesis was potently inhibited by adenovirus at late times after infection, whereas it persisted in the proliferating myoblasts and quiescent mononuclear cells.

Adenoviridae Infections↗

PubMed1991