Interaction of myogenic factors and the retinoblastoma protein mediates muscle cell commitment and differentiation

Gu, Wei; Schneider, Jay W.; Condorelli, Gianluigi; Kaushal, Sunjay; Mahdavi, Vijak; Nadal‐Ginard, Bernardo

doi:10.1016/0092-8674(93)90110-c

Cited by 701 publications

(538 citation statements)

References 84 publications

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“…Muscle cells lacking Rb can growth arrest, but they show delayed upregulation of late differentiation markers and are capable of re-entering the cell cycle when stimulated with mitogens. Rb can cooperate with the transcription factor MyoD to induce transcription of muscle target genes, and MyoD was shown to bind to Rb (Gu et al, 1993), although the physiological significance of these interactions is unclear. An alternative model suggests that Rb may promote differentiation indirectly by sequestering inhibitors of MyoD (Nguyen and McCance, 2005).…”

Section: The Role Of Rb In Differentiationmentioning

confidence: 99%

Retinoblastoma family genes

2006

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Section: The Role Of Rb In Differentiationmentioning

confidence: 99%

Retinoblastoma family genes

2006

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“…The importance of RB and associated pathways in myogenic di erentiation was demonstrated by the discoveries that: pRB binds directly with MyoD and other myogenic basic HLH members; pRB is required for MyoD to inhibit cell growth; and that inactivation of pRB disrupts normal myogenesis, and even permits terminally di erentiated cells to reenter the cell cycle (Gu et al, 1993;Thorburn et al, 1993;Novitch et al, 1996). In addition, forced expression of the E2F family member E2F-1 interferes with myogenic di erentiation , and constitutive expression of cyclin D1 blocks MyoD-dependent transactivation of muscle-speci®c promoters via a CDK-dependent mechanism (Rao et al, 1994;Skapek et al, 1995).…”

Section: Digging Deeper ± Prb and P53 At The Crossroadsmentioning

confidence: 99%

Rhabdomyosarcoma – working out the pathways

1999

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Rhabdomyosarcomas constitute a collection of childhood malignancies thought to arise as a consequence of regulatory disruption of skeletal muscle progenitor cell growth and di erentiation. Our understanding of the pathogenesis of this neoplasm has recently bene®ted from the study of normal and malignant myogenic cells in vitro, facilitating the identi®cation of diagnostic cytogenetic markers and the elucidation of mechanisms by which myogenesis is regulated. It is now appreciated that the delicate balance between proliferation and di erentiation, mutually exclusive yet intimately associated processes, is normally controlled in large part through the action of a multitude of growth factors, whose signals are interpreted by members of the MyoD family of helix ± loop ± helix proteins, and key regulatory cell cycle factors. The latter have proven to be frequent targets of mutational events that subvert myogenesis and promote the development of rhabdomyosarcoma. Although signi®cant progress has been made in the treatment of rhabdomyosarcoma, patients presenting with metastatic disease or certain high risk features are still faced with a dismal prognosis. Only now are genetically engineered mouse models becoming available that are certain to provide fresh insights into the molecular/genetic pathways by which rhabdomyosarcomas arise and progress, and to suggest novel avenues of therapeutic opportunity.

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“…As interaction of Rb with other proteins has been demonstrated in a number of contexts (Chellappan et al, 1991;Dowdy et al, 1993;Gu et al, 1993;Hagemeier et al, 1993;Whyte et al, 1988), we hypothesized that a speci®c interaction might occur in F5-5 cultures upon activin treatment. F5-5 cells were cultured with or without activin and immunoprecipitated with rabbit anti-Rb antibodies or rabbit anti-CDK4 antibodies as control.…”

Section: Ectopic Expression Of Goosecoid (Gsc) In the Erythroblast Cementioning

confidence: 99%