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  2. Diabetes with additional phenotypes suggestive of a monogenic aetiology
  3. ACE
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Diabetes with additional phenotypes suggestive of a monogenic aetiology

Gene: ACE

No list
ACE (angiotensin I converting enzyme)
EnsemblGeneIds (GRCh38): ENSG00000159640
EnsemblGeneIds (GRCh37): ENSG00000159640
OMIM: 106180, Gene2Phenotype
ACE is in 9 panels

2 reviews

Ellen McDonagh (Genomics England Curator)

Gene should be removed from the panel.
Created: 19 Oct 2015, 8:15 a.m.
Created: 19 Oct 2015, 8:15 a.m.

Panel version: 0

Sian Ellard (University of Exeter Medical School)

remove from panel - no evidence to suggest a monogenic cause of diabetes
Created: 18 Oct 2015, 8:13 a.m.
Created: 18 Oct 2015, 8:13 a.m.

Panel version: 0

Details

Sources
  • Expert Review Removed
  • Radboud University Medical Center, Nijmegen
Phenotypes
  • {Myocardial infarction, susceptibility to}
  • {Alzheimer disease, susceptibility to}, 104300
  • {Microvascular complications of diabetes 3}, 612624
  • [Angiotensin I-converting enzyme, benign serum increase]
  • {SARS, progression of}
  • Renal tubular
Tags
curated_removed
OMIM
106180
Clinvar variants
Variants in ACE
Penetrance
Complete
Panels with this gene

History Filter Activity

26 Feb 2021, Gel status: 0

Added Tag

Arina Puzriakova (Genomics England Curator)

Tag curated_removed tag was added to gene: ACE.

25 Jul 2016, Gel status: 0

panel promoted to version 1

Ellen McDonagh (Genomics England Curator)

25th July 2016: Panel revised acccording to expert review, further evidence sources and comparison with the Familial Diabetes version 1 panel. Promoted to version 1.

22 Jul 2016, Gel status: 0

Gene classified by Genomics England curator

Ellen McDonagh (Genomics England Curator)

This gene has been removed from the panel.

7 Jun 2016, Gel status: 0

Gene classified by Genomics England curator

Chris Boustred (Genomics England)

This gene has been removed from the panel.

17 Jul 2015, Gel status: 1

Added New Source

Ellen McDonagh (Genomics England Curator)

ACE was added to Diabetes with additional phenotypes suggestive of a monogenic aetiologypanel. Sources: Radboud University Medical Center, Nijmegen