Mice Available Upon Request
Posted by Wendy Wise on
We maintain a broad range of mouse research models to support many different therapeutic and disease areas of research. Our mouse models are fully licensed and maintained as breeding pairs in our Novi, MI location. These lines are available by request only. If you are interested in placing an order, please contact us at sales@innov-research.com for pricing and order details.
Currently Available Mice Lines
C1 Inhibitor Knockout Mouse/ Innovative Grade C1 Inhibitor C57BL6/SJL Knockout Mouse
Our C1 Inhibitor Knockout Mouse Models were created via targeted gene excision using CRISPR-Cas9 technology licensed from the Broad Institute of MIT and Harvard targeting SERPING1. Mutations were then confirmed using various methods, including PCR genotyping, Sanger sequencing, and Western Blot. C1 Inhibitor is a serine protease inhibitor (serpin) that is involved in the contact and complement systems and could be a therapeutic target for a wide range of conditions including hereditary angioedema (HAE), hemorrhagic & septic shock, transplant rejection, and other inflammatory disorders.
Our C1 Inhibitor Knockout Mouse Models are available as homozygous mice, completely lacking all C1 Inhibitor protein expression.
Mouse Model Details:
C1 Inhibitor Knockout Mouse/ Innovative Grade C1 Inhibitor C57BL6/6J Knockout Mouse
Our C1 Inhibitor Knockout Mouse Models were created via targeted gene excision using CRISPR-Cas9 technology licensed from the Broad Institute of MIT and Harvard targeting SERPING1. Mutations were then confirmed using various methods, including PCR genotyping, Sanger sequencing, and Western Blot. C1 Inhibitor is a serine protease inhibitor (serpin) that is involved in the contact and complement systems and could be a therapeutic target for a wide range of conditions including hereditary angioedema (HAE), hemorrhagic & septic shock, transplant rejection, and other inflammatory disorders.
Our C1 Inhibitor Knockout Mouse Models are available as homozygous mice, completely lacking all C1 Inhibitor protein expression.
Mouse Model Details:
- Strain: C57BL/6J (Black 6 background)
- Chromosome: 2
- Gene: SERPING1
- Genomic Target: Exon 3
- Mutation: 131 base pair deletion
- Phenotype: Absence of C1Inh protein expression in homozygous mice; increased vascular permeability in both homozygous and heterozygous mice
- Protein: Serine (or cysteine) peptidase inhibitor, clade G, member 1
- Synonyms: C1INH, C1 inhibitor, C1nh
Innovative Grade tPA Knockin Mouse
Our Tissue Plasminogen Activator (tPA) knockin mouse model was created by targeted substitution of active-site serine at position 510 (or 478 in mature peptide) using programed nuclease. This serine residue is critical for plasminogen activation and formation of stable complexes between tPA and PAI-1.This research model is useful for a wide range of scientific studies, including research related to cardiovascular and neurological studies. This research model is useful for a wide range of scientific studies, including research related to cardiovascular and neurological studies.
Mouse Model Details:
Innovative Grade Factor IX Knockout Mouse
Our Factor IX Knockout Mouse Model is a research model for human Hemophilia B, created via targeted disruption of the F9 gene using CRISPR-Cas9 technology licensed from the Broad Institute of MIT and Harvard. Mutations were then confirmed using various methods, including PCR genotyping, Sanger sequencing, and RT-PCR. Factor IX deficiency is the genetic cause of Hemophilia B, and this model can be useful for a wide range of research, including studies of gene therapies and pharmaceutical development.
Our Factor IX Mutant Mouse Models are available as male hemizygous mice, as Factor IX deficiency is an X-linked disorder. These mice have a hemophilia B phenotype with prolonged clotting time (confirmed via aPTT) as well as tail clipping-induced mortality in the absence of cauterization.
Mouse Model Details:
Innovative Grade Factor XII Knockout Mouse
Our Factor XII Knockout Mouse Models were created via targeted disruption of the F12 gene using CRISPR-Cas9 technology licensed from the Broad Institute of MIT and Harvard. Mutations were then confirmed using various methods, including PCR genotyping and Sanger sequencing, and the complete absence of Factor XII protein in the plasma of homozygous mice was confirmed by Western Blot. This research model is useful for a wide range of scientific studies, including research related to cardiovascular disease and neurological studies.
Our Factor XII Knockout Mouse Models are available as live homozygous mice. Coagulation Factor XII is also referred to as Hageman Factor.
Mouse Model Details: