Hhat^{Tg(TFAP2A-cre)1Will}
Transgenic Allele Detail

Summary

• Symbol: Hhat^{Tg(TFAP2A-cre)1Will}
• Name: hedgehog acyltransferase; transgene insertion 1, Trevor Williams
• MGI ID: MGI:3038358
• Synonyms: Ap2-Cre, AP-2CRE, Creface^T, Tg(TFAP2A-cre)1Will
• Gene: Hhat Location: Chr1:192195133-192453546 bp, - strand Genetic Position: Chr1, 97.55 cM
• Alliance: Hhat^{Tg(TFAP2A-cre)1Will} page

Transgene origin

• Strain of Origin: Not Specified

Transgene description

• Transgene Type: Transgenic (Null/knockout, Recombinase)
• Mutation: Insertion
• Hhat^{Tg(TFAP2A-cre)1Will} expression driven by 1 gene
  Transgene expression driven by:
  

  Organism

  Driver Gene

  Homolog in Mouse

  Note

  human

  TFAP2A (7020)

  Tfap2a

  (MGI:104671)

• Mutation details: This transgenic construct consisted of 200 bp of human TFAP2A (TCFAP2A) promoter sequence (encoding a specific enhancer element) followed by NLS-cre, an SV40 polyA signal, and a 1.8 kb TFAP2A genomic fragment extending from within exon 5 through a portion of exon 6. The human intron 5 sequence includes the frontonasal prominence- and limb-specific enhancer. Expression of cre recombinase was detected in the embryonic face and limb mesenchyme. New research has determined that the transgene inserted into intron 9 of the Hhat locus. This insertion creates a non-functional allele. (J:88829, J:190013)

Recombinase activity

Activity:	Tissue activity of this recombinase allele
Driver:	TFAP2A (human) Summary of all recombinase alleles driven by TFAP2A. Comparative matrix view of recombinase activities Alliance human TFAP2A gene page

Disease models

Expression

In Structures Affected by this Mutation:

30 anatomical structure(s)

Find Mice (IMSR)

• Mouse strains and cell lines available from the International Mouse Strain Resource (IMSR)
• Carrying this Mutation: Mouse Strains: 1 strain available Cell Lines: 0 lines available
• Carrying any Hhat Mutation: 26 strains or lines available

References

• Original: J:88829 Nelson DK, et al., Frontonasal process-specific disruption of AP-2alpha results in postnatal midfacial hypoplasia, vascular anomalies, and nasal cavity defects. Dev Biol. 2004 Mar 1;267(1):72-92
• All: 12 reference(s)