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Literature summary for 1.14.18.2 extracted from
- Pancreatic {beta}-cell failure in obese mice with human-like CMP-Neu5Ac hydroxylase deficiency (2011), FASEB J., 25, 1887-1893.
Organism
| Organism | UniProt | Comment | Textmining |
|---|---|---|---|
| Mus musculus | - |
- |
- |
Source Tissue
| Source Tissue | Comment | Organism | Textmining |
|---|
Synonyms
| Synonyms | Comment | Organism |
|---|---|---|
| CMAH | - |
Mus musculus |
| CMP-Neu5Ac hydroxylase | - |
Mus musculus |
General Information
| General Information | Comment | Organism |
|---|---|---|
| malfunction | mice bearing a human-like deletion of the Cmah gene exhibit fasting hyperglycemia and glucose intolerance following a high-fat diet. This phenotype is caused by compromised pancreatic beta-cell function associated with a 65% decrease in islet size and area and 50% decrease in islet number. Obese Cmah-null mice also show an 40% reduction in response to insulin secretagogues in vivo | Mus musculus |
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Release 2023.1 (January 2023)
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