Summary | Transgene origin | Transgene description | Expression | Recombinase activity | Phenotypes | Disease models | Find Mice (IMSR) | References

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

Strain of Origin:

Not Specified

Transgene Type:    Transgenic (Null/knockout, Recombinase) Mutation:    Insertion   HhatTg(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)

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

View phenotypes and curated references for all genotypes (concatenated display).

In Structures Affected by this Mutation:

30 anatomical structure(s)

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:	27 strains or lines available

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)