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Pancreatic islet expression profiling in diabetes prone C57BLKS/J mice vs C57BL6/J mice.


ABSTRACT: C57BLKS/J mice are susceptible to diabetes, because of islet dysfunction, whereas C57BL6/J mice are not. Differences in gene expression between the two strains may account for this sensitivity. Furthermore these differences may only be evident in the hyperstimulated (diabetic or hyperglycemic) state. To this end profiling islets from these two strains cultured in both low and high glucose may reveal the underlying mechanism. Keywords: Mouse strain comparison under different culture conditions In the study presented here, pancreatic islets from 20 mice grown in low and high glucose conditions were assayed for differences in gene expression. (five C57BLKS/J low glucose, four C57BLKS/J high glucose, six C57BL6/J low glucose, five C57BL6/J high glucose). Technical replicates are achieved by labeling each sample with both Cy3 and Cy5, and combining the values for each hybridization.

ORGANISM(S): Mus musculus

SUBMITTER: Dan Baker 

PROVIDER: E-GEOD-11257 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Pancreatic islet expression profiling in diabetes-prone C57BLKS/J mice reveals transcriptional differences contributed by DBA loci, including Plagl1 and Nnt.

Anderson Abraham A AA   Helmering Joan J   Juan Todd T   Li Chi-Ming CM   McCormick Jocelyn J   Graham Melissa M   Baker Daniel M DM   Damore Michael A MA   Véniant Murielle M MM   Lloyd David J DJ  

PathoGenetics 20090122 1


<h4>Background</h4>C57BLKS/J (BLKS) mice are susceptible to islet exhaustion in insulin-resistant states as compared with C57BL6/J (B6) mice, as observed by the presence of the leptin receptor (Lepr) allele, Leprdb/db. Furthermore, DBA2/J (DBA) mice are also susceptible to beta-cell failure and share 25% of their genome with BLKS; thus the DBA genome may contribute to beta-cell dysfunction in BLKS mice.<h4>Results</h4>Here we show that BLKS mice exhibit elevated insulin secretion, as evidenced b  ...[more]

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