Regulation of cell differentiation in C2C12 myoblasts by the Id3 helix-loop-helix protein.

2.50
Hdl Handle:
http://hdl.handle.net/10541/95838
Title:
Regulation of cell differentiation in C2C12 myoblasts by the Id3 helix-loop-helix protein.
Authors:
Atherton, Graham T; Travers, Helen; Deed, Richard W; Norton, John D
Abstract:
To investigate the biological functions of the helix-loop-helix Id3 protein, we have examined the effects of ectopic modulation of Id3 expression on in vitro induced differentiation of mouse C2C12 myoblast cells. Transient and stable C2C12 transfectants expressing either inducible or constitutive levels of exogenous Id3 were impaired in their ability to differentiate in response to removal of mitogenic serum growth factors. Stable Id3 transfectants displayed an enhanced proliferative capacity associated with a delay in exit from the cell cycle in response to differentiation induction. Antisense blockade of Id3 potentiated differentiation and exit from S phase of the cell cycle. These observations suggest that Id3 functions as a negative regulator of differentiation by integrating mitogenic growth factor signaling into the gene regulatory program maintaining cell cycle progression.
Affiliation:
CRC Department of Gene Regulation, Paterson Institute for Cancer Research, Christie Hospital National Health Service Trust, Manchester, United Kingdom.
Citation:
Regulation of cell differentiation in C2C12 myoblasts by the Id3 helix-loop-helix protein. 1996, 7 (8):1059-66 Cell Growth Differ.
Journal:
Cell Growth & Differentiation
Issue Date:
Aug-1996
URI:
http://hdl.handle.net/10541/95838
PubMed ID:
8853902
Type:
Article
Language:
en
ISSN:
1044-9523
Appears in Collections:
All Paterson Institute for Cancer Research

Full metadata record

DC FieldValue Language
dc.contributor.authorAtherton, Graham Ten
dc.contributor.authorTravers, Helenen
dc.contributor.authorDeed, Richard Wen
dc.contributor.authorNorton, John Den
dc.date.accessioned2010-04-07T10:14:48Z-
dc.date.available2010-04-07T10:14:48Z-
dc.date.issued1996-08-
dc.identifier.citationRegulation of cell differentiation in C2C12 myoblasts by the Id3 helix-loop-helix protein. 1996, 7 (8):1059-66 Cell Growth Differ.en
dc.identifier.issn1044-9523-
dc.identifier.pmid8853902-
dc.identifier.urihttp://hdl.handle.net/10541/95838-
dc.description.abstractTo investigate the biological functions of the helix-loop-helix Id3 protein, we have examined the effects of ectopic modulation of Id3 expression on in vitro induced differentiation of mouse C2C12 myoblast cells. Transient and stable C2C12 transfectants expressing either inducible or constitutive levels of exogenous Id3 were impaired in their ability to differentiate in response to removal of mitogenic serum growth factors. Stable Id3 transfectants displayed an enhanced proliferative capacity associated with a delay in exit from the cell cycle in response to differentiation induction. Antisense blockade of Id3 potentiated differentiation and exit from S phase of the cell cycle. These observations suggest that Id3 functions as a negative regulator of differentiation by integrating mitogenic growth factor signaling into the gene regulatory program maintaining cell cycle progression.en
dc.language.isoenen
dc.subjectCancer Proteinsen
dc.subject.meshAnimals-
dc.subject.meshCOS Cells-
dc.subject.meshCell Differentiation-
dc.subject.meshCell Division-
dc.subject.meshCells, Cultured-
dc.subject.meshGene Expression Regulation-
dc.subject.meshHelix-Loop-Helix Motifs-
dc.subject.meshInhibitor of Differentiation Proteins-
dc.subject.meshMice-
dc.subject.meshMuscle Fibers, Skeletal-
dc.subject.meshMuscle, Skeletal-
dc.subject.meshNeoplasm Proteins-
dc.subject.meshOligonucleotides, Antisense-
dc.subject.meshStem Cells-
dc.subject.meshTranscription Factors-
dc.subject.meshTransfection-
dc.titleRegulation of cell differentiation in C2C12 myoblasts by the Id3 helix-loop-helix protein.en
dc.typeArticleen
dc.contributor.departmentCRC Department of Gene Regulation, Paterson Institute for Cancer Research, Christie Hospital National Health Service Trust, Manchester, United Kingdom.en
dc.identifier.journalCell Growth & Differentiationen

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