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Atf3 expression is upregulated during <t>chondrocyte</t> differentiation in vitro . Atf3 mRNA expression during chondrogenic differentiation of mouse embryonic limb bud cells in micromass culture was examined by microarray (A) and real-time PCR (B) analyses (different cell isolations were used for the experiments in A and B). Microarray data sets represent averages from three independent experiments. Real-time data were normalized to Gapdh levels and present average and SEM from four independent experiments. Both approaches show similar expression patterns with a strong increase in Atf3 expression during micromass differentiation.
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Atf3 expression is upregulated during chondrocyte differentiation in vitro . Atf3 mRNA expression during chondrogenic differentiation of mouse embryonic limb bud cells in micromass culture was examined by microarray (A) and real-time PCR (B) analyses (different cell isolations were used for the experiments in A and B). Microarray data sets represent averages from three independent experiments. Real-time data were normalized to Gapdh levels and present average and SEM from four independent experiments. Both approaches show similar expression patterns with a strong increase in Atf3 expression during micromass differentiation.

Journal: BMC Molecular Biology

Article Title: The transcription factor ATF3 is upregulated during chondrocyte differentiation and represses cyclin D1 and A gene transcription

doi: 10.1186/1471-2199-7-30

Figure Lengend Snippet: Atf3 expression is upregulated during chondrocyte differentiation in vitro . Atf3 mRNA expression during chondrogenic differentiation of mouse embryonic limb bud cells in micromass culture was examined by microarray (A) and real-time PCR (B) analyses (different cell isolations were used for the experiments in A and B). Microarray data sets represent averages from three independent experiments. Real-time data were normalized to Gapdh levels and present average and SEM from four independent experiments. Both approaches show similar expression patterns with a strong increase in Atf3 expression during micromass differentiation.

Article Snippet: Micromass cultures from E11.5 mouse limb buds and isolation of primary murine chondrocytes from E15.5 long bones were performed as recently described [ , ].

Techniques: Expressing, In Vitro, Microarray, Real-time Polymerase Chain Reaction

Atf3 expression is upregulated during chondrocyte differentiation in vivo . Tibia isolated from embryonic day 15.5. mice were microdissected into the resting/proliferating, prehypertrophic and hypertrophic areas, and RNA was isolated directly out of cartilage. Expression of type II collagen II ( Col2a1 ), type X collagen ( Col10a1 ) and Atf3 was examined by real-time PCR analyses and normalized to Gapdh expression. All data represent averages and SEM from four independent experiments (*: p < 0.05). Col2a1 was strongly expressed in the resting/proliferating area and declined subsequently (A). Col10a1 was virtually undetectable in the resting/proliferating area and strongly induced in the prehypertrophic and hypertrophic areas (B). Atf3 was already expressed in the resting/proliferating area, but expression was significantly increased in the more mature zones of the growth plate.

Journal: BMC Molecular Biology

Article Title: The transcription factor ATF3 is upregulated during chondrocyte differentiation and represses cyclin D1 and A gene transcription

doi: 10.1186/1471-2199-7-30

Figure Lengend Snippet: Atf3 expression is upregulated during chondrocyte differentiation in vivo . Tibia isolated from embryonic day 15.5. mice were microdissected into the resting/proliferating, prehypertrophic and hypertrophic areas, and RNA was isolated directly out of cartilage. Expression of type II collagen II ( Col2a1 ), type X collagen ( Col10a1 ) and Atf3 was examined by real-time PCR analyses and normalized to Gapdh expression. All data represent averages and SEM from four independent experiments (*: p < 0.05). Col2a1 was strongly expressed in the resting/proliferating area and declined subsequently (A). Col10a1 was virtually undetectable in the resting/proliferating area and strongly induced in the prehypertrophic and hypertrophic areas (B). Atf3 was already expressed in the resting/proliferating area, but expression was significantly increased in the more mature zones of the growth plate.

Article Snippet: Micromass cultures from E11.5 mouse limb buds and isolation of primary murine chondrocytes from E15.5 long bones were performed as recently described [ , ].

Techniques: Expressing, In Vivo, Isolation, Real-time Polymerase Chain Reaction

Inhibition of actin polymerization induces Atf3 expression through transcriptional mechanisms . A) Primary chondrocytes were cultured for 24 hours with DMSO (control) or 1 μM cytochalasin D before harvest and RNA isolation. Real-time PCR demonstrated marked induction of Atf3 mRNA levels by cytochalasin D. Data represent averages and SEM from three independent experiments, normalized to Gapdh (*: p < 0.05). B) Primary chondrocytes were transfected with an Atf3 promoter plasmid and pRLCMV, followed by incubation for 24 hours with DMSO (control) or 1 μM cytochalasin D. Cells were then harvested, firefly luciferase activity was measured and normalized to Renilla luciferase activity. Data represent averages and SEM from three independent experiments, performed in quadruplicate each (*: p < 0.05). Cytochalasin D induced Atf3 promoter activity.

Journal: BMC Molecular Biology

Article Title: The transcription factor ATF3 is upregulated during chondrocyte differentiation and represses cyclin D1 and A gene transcription

doi: 10.1186/1471-2199-7-30

Figure Lengend Snippet: Inhibition of actin polymerization induces Atf3 expression through transcriptional mechanisms . A) Primary chondrocytes were cultured for 24 hours with DMSO (control) or 1 μM cytochalasin D before harvest and RNA isolation. Real-time PCR demonstrated marked induction of Atf3 mRNA levels by cytochalasin D. Data represent averages and SEM from three independent experiments, normalized to Gapdh (*: p < 0.05). B) Primary chondrocytes were transfected with an Atf3 promoter plasmid and pRLCMV, followed by incubation for 24 hours with DMSO (control) or 1 μM cytochalasin D. Cells were then harvested, firefly luciferase activity was measured and normalized to Renilla luciferase activity. Data represent averages and SEM from three independent experiments, performed in quadruplicate each (*: p < 0.05). Cytochalasin D induced Atf3 promoter activity.

Article Snippet: Micromass cultures from E11.5 mouse limb buds and isolation of primary murine chondrocytes from E15.5 long bones were performed as recently described [ , ].

Techniques: Inhibition, Expressing, Cell Culture, Control, Isolation, Real-time Polymerase Chain Reaction, Transfection, Plasmid Preparation, Incubation, Luciferase, Activity Assay

ATF3 suppresses Sox9-dependent transcription and stimulates Runx2-dependent transcription . Primary chondrocytes were cotransfected with SOX9 (A) or RUNX2 (B) reporter plasmids, pcDNA3 (control) or an ATF3 expression vector, and pRLCMV. 24 hours after transfection, cells were harvested, firefly luciferase activity was measured and normalized to Renilla luciferase activity. Data represent averages and SEM from three independent experiments, performed in quadruplicate each (*: p < 0.05). ATF3 overexpression suppressed SOX9-dependent transcription and stimulated RUNX2-dependent transcription.

Journal: BMC Molecular Biology

Article Title: The transcription factor ATF3 is upregulated during chondrocyte differentiation and represses cyclin D1 and A gene transcription

doi: 10.1186/1471-2199-7-30

Figure Lengend Snippet: ATF3 suppresses Sox9-dependent transcription and stimulates Runx2-dependent transcription . Primary chondrocytes were cotransfected with SOX9 (A) or RUNX2 (B) reporter plasmids, pcDNA3 (control) or an ATF3 expression vector, and pRLCMV. 24 hours after transfection, cells were harvested, firefly luciferase activity was measured and normalized to Renilla luciferase activity. Data represent averages and SEM from three independent experiments, performed in quadruplicate each (*: p < 0.05). ATF3 overexpression suppressed SOX9-dependent transcription and stimulated RUNX2-dependent transcription.

Article Snippet: Micromass cultures from E11.5 mouse limb buds and isolation of primary murine chondrocytes from E15.5 long bones were performed as recently described [ , ].

Techniques: Control, Expressing, Plasmid Preparation, Transfection, Luciferase, Activity Assay, Over Expression

ATF3 suppresses CRE-dependent transcription . Primary chondrocytes were cotransfected with a CRE reporter (A), a cyclin D1 promoter (-1745CD1LUC, B) or cyclin A promoter plasmids (p707cycAluc and p707cycAlucMut; C), pcDNA3 (control) or an ATF3 expression vector, and pRLCMV. 24 hours after transfection, cells were harvested, firefly luciferase activity was measured and normalized to Renilla luciferase activity. Data represent averages and SEM from three independent experiments, performed in quadruplicate each (*: p < 0.05). ATF3 overexpression suppressed the CRE reporter, cyclin D1 and cyclin A wild type promoters significantly, whereas the mutant cyclin A construct showed no response to ATF3 overexpression.

Journal: BMC Molecular Biology

Article Title: The transcription factor ATF3 is upregulated during chondrocyte differentiation and represses cyclin D1 and A gene transcription

doi: 10.1186/1471-2199-7-30

Figure Lengend Snippet: ATF3 suppresses CRE-dependent transcription . Primary chondrocytes were cotransfected with a CRE reporter (A), a cyclin D1 promoter (-1745CD1LUC, B) or cyclin A promoter plasmids (p707cycAluc and p707cycAlucMut; C), pcDNA3 (control) or an ATF3 expression vector, and pRLCMV. 24 hours after transfection, cells were harvested, firefly luciferase activity was measured and normalized to Renilla luciferase activity. Data represent averages and SEM from three independent experiments, performed in quadruplicate each (*: p < 0.05). ATF3 overexpression suppressed the CRE reporter, cyclin D1 and cyclin A wild type promoters significantly, whereas the mutant cyclin A construct showed no response to ATF3 overexpression.

Article Snippet: Micromass cultures from E11.5 mouse limb buds and isolation of primary murine chondrocytes from E15.5 long bones were performed as recently described [ , ].

Techniques: Control, Expressing, Plasmid Preparation, Transfection, Luciferase, Activity Assay, Over Expression, Mutagenesis, Construct

Model for ATF3 action in chondrocyte differentiation . We suggest that induction of ATF3 by differentiation stimuli antagonizes the CRE-dependent expression of cyclin D1 and cyclin A, which are induced by mitogenic stimuli through ATF2 and CREB. Reduced cyclin-dependent kinase activity and hypophosphorylation of pocket proteins in response to ATF3 upregulation then results both in cell cycle exit and in increased activity of Runx2, promoting chondrocyte differentiation.

Journal: BMC Molecular Biology

Article Title: The transcription factor ATF3 is upregulated during chondrocyte differentiation and represses cyclin D1 and A gene transcription

doi: 10.1186/1471-2199-7-30

Figure Lengend Snippet: Model for ATF3 action in chondrocyte differentiation . We suggest that induction of ATF3 by differentiation stimuli antagonizes the CRE-dependent expression of cyclin D1 and cyclin A, which are induced by mitogenic stimuli through ATF2 and CREB. Reduced cyclin-dependent kinase activity and hypophosphorylation of pocket proteins in response to ATF3 upregulation then results both in cell cycle exit and in increased activity of Runx2, promoting chondrocyte differentiation.

Article Snippet: Micromass cultures from E11.5 mouse limb buds and isolation of primary murine chondrocytes from E15.5 long bones were performed as recently described [ , ].

Techniques: Expressing, Activity Assay