SA1 (ST86) genome
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| CBTW01.dat.gz | Other | |||
| CBTW01.fasta.gz | Fasta.gz | |||
| CBTW01.master.dat | Other | |||
| CBTW01.dat.gz | Other |
Items per page: 5 1 - 4 of 4 |
Similar Datasets
Project description:Vertebrates have two cohesin complexes that consist of Smc1, Smc3, Rad21/Scc1 and either SA1 or SA2, but their functional specificity is unclear. Mouse embryos lacking SA1 show developmental delay and die before birth. Comparison of the genome wide distribution of cohesin in wild-type and SA1-null cells reveals that SA1 is largely responsible for cohesin accumulation at promoters and at sites bound by the insulator protein CTCF. As a consequence, ablation of SA1 alters transcription of genes involved in biological processes related to Cornelia de Lange syndrome (CdLS), a genetic disorder linked to dysfunction of cohesin. We show that the presence of cohesin-SA1 at the promoter of myc and of protocadherin genes positively regulates their expression, a task that cannot be assumed by cohesin-SA2. Cohesin binding pattern along some gene clusters is also affected by the lack of SA1, leading to dysregulation of the genes within. We hypothesize that impaired cohesin-SA1 function in gene expression underlies the molecular etiology of CdLS. Examination of genome wide distribution of cohesin subunits in wildtype and SA1-null cells
2012-03-15 | E-GEOD-32319 | biostudies-arrayexpress
Project description:Vertebrates have two cohesin complexes that consist of Smc1, Smc3, Rad21/Scc1 and either SA1 or SA2, but their functional specificity is unclear. Mouse embryos lacking SA1 show developmental delay and die before birth. Comparison of the genome wide distribution of cohesin in wild-type and SA1-null cells reveals that SA1 is largely responsible for cohesin accumulation at promoters and at sites bound by the insulator protein CTCF. As a consequence, ablation of SA1 alters transcription of genes involved in biological processes related to Cornelia de Lange syndrome (CdLS), a genetic disorder linked to dysfunction of cohesin. We show that the presence of cohesin-SA1 at the promoter of myc and of protocadherin genes positively regulates their expression, a task that cannot be assumed by cohesin-SA2. Cohesin binding pattern along some gene clusters is also affected by the lack of SA1, leading to dysregulation of the genes within. We hypothesize that impaired cohesin-SA1 function in gene expression underlies the molecular etiology of CdLS.
2012-03-15 | GSE32319 | GEO
Project description:Vertebrates have two cohesin complexes that consist of Smc1, Smc3, Rad21/Scc1 and either SA1 or SA2, but their functional specificity is unclear. Mouse embryos lacking SA1 show developmental delay and die before birth. Comparison of the genome wide distribution of cohesin in wild-type and SA1-null cells reveals that SA1 is largely responsible for cohesin accumulation at promoters and at sites bound by the insulator protein CTCF. As a consequence, ablation of SA1 alters transcription of genes involved in biological processes related to Cornelia de Lange syndrome (CdLS), a genetic disorder linked to dysfunction of cohesin. We show that the presence of cohesin-SA1 at the promoter of myc and of protocadherin genes positively regulates their expression, a task that cannot be assumed by cohesin-SA2. Cohesin binding pattern along some gene clusters is also affected by the lack of SA1, leading to dysregulation of the genes within. We hypothesize that impaired cohesin-SA1 function in gene expression underlies the molecular etiology of CdLS.
2012-03-15 | GSE32234 | GEO
Project description:Liao2011 - Genome-scale metabolic
reconstruction of Klebsiella pneumoniae (iYL1228)
This model is described in the article:
An experimentally validated
genome-scale metabolic reconstruction of Klebsiella pneumoniae
MGH 78578, iYL1228.
Liao YC, Huang TW, Chen FC,
Charusanti P, Hong JS, Chang HY, Tsai SF, Palsson BO, Hsiung
CA.
J. Bacteriol. 2011 Apr; 193(7):
1710-1717
Abstract:
Klebsiella pneumoniae is a Gram-negative bacterium of the
family Enterobacteriaceae that possesses diverse metabolic
capabilities: many strains are leading causes of
hospital-acquired infections that are often refractory to
multiple antibiotics, yet other strains are metabolically
engineered and used for production of commercially valuable
chemicals. To study its metabolism, we constructed a
genome-scale metabolic model (iYL1228) for strain MGH 78578,
experimentally determined its biomass composition,
experimentally determined its ability to grow on a broad range
of carbon, nitrogen, phosphorus and sulfur sources, and
assessed the ability of the model to accurately simulate growth
versus no growth on these substrates. The model contains 1,228
genes encoding 1,188 enzymes that catalyze 1,970 reactions and
accurately simulates growth on 84% of the substrates tested.
Furthermore, quantitative comparison of growth rates between
the model and experimental data for nine of the substrates also
showed good agreement. The genome-scale metabolic
reconstruction for K. pneumoniae presented here thus provides
an experimentally validated in silico platform for further
studies of this important industrial and biomedical
organism.
This model is hosted on
BioModels Database
and identified by:
MODEL1507180054.
To cite BioModels Database, please use:
BioModels Database:
An enhanced, curated and annotated resource for published
quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2024-10-15 | MODEL1507180054 | BioModels
Project description:Streptococcus agalactiae Genome str. SA1
| PRJNA369807 | ENA
Project description:Vertebrates have two cohesin complexes that consist of Smc1, Smc3, Rad21/Scc1 and either SA1 or SA2, but their functional specificity is unclear. Mouse embryos lacking SA1 show developmental delay and die before birth. Comparison of the genome wide distribution of cohesin in wild-type and SA1-null cells reveals that SA1 is largely responsible for cohesin accumulation at promoters and at sites bound by the insulator protein CTCF. As a consequence, ablation of SA1 alters transcription of genes involved in biological processes related to Cornelia de Lange syndrome (CdLS), a genetic disorder linked to dysfunction of cohesin. We show that the presence of cohesin-SA1 at the promoter of myc and of protocadherin genes positively regulates their expression, a task that cannot be assumed by cohesin-SA2. Cohesin binding pattern along some gene clusters is also affected by the lack of SA1, leading to dysregulation of the genes within. We hypothesize that impaired cohesin-SA1 function in gene expression underlies the molecular etiology of CdLS. Two-condition experiment, SA1 KO vs. WT cells. 3 Biological replicates.
2012-03-15 | E-GEOD-32234 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE35746: Comparative analysis of regulatory elements between Escherichia coli and Klebsiella pneumoniae by genome-wide transcription start site profiling [tiling arrays] GSE35821: Comparative analysis of regulatory elements between Escherichia coli and Klebsiella pneumoniae by genome-wide transcription start site profiling [TSS-Seq] Refer to individual Series
2012-07-29 | E-GEOD-35822 | biostudies-arrayexpress
Project description:Bacillus tuticoriensis (Strain SA1-12) Genome sequencing and assembly
| PRJNA280024 | ENA
Project description:Novosphingobium resinovorum SA1 Genome sequencing
| PRJNA336270 | ENA
Project description:A strain of Klebsiella pneumoniae exposed to native and heat-inactivated serum for different time points
2023-10-16 | MSV000093124 | MassIVE