Fmr1 knockout rats HsdSage:SD-Fmr1+/-em1Sage
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- An expansion of CGG trinucleotide repeat in Fmr1 has been implicated in Fragile X syndrome
- Background strain: Sprague Dawley
- Homozygous knockout rats display total loss of protein via Western blot
- Preliminary results suggest Fmr1 knockout rats possess perseverative chewing behavior and decreased juvenile play
- This gene is X-linked
- This model was created in collaboration with Autism Speaks and underwent phenotypic characterization by Dr. Richard Paylor.
Availability: Live colony
Zygosity genotype: Homozygous (Females) / Hemizygous (Males)
This model contains a deletion of the Fragile X mental retardation 1 gene (Fmr1). Mutations in Fmr1 result in Fragile X syndrome, the leading monogenic cause of autism, making this rat useful for the study of both Fragile X syndrome and autism.
The X-linked gene Fmr1 produces the fragile X metal retardation protein, or FMRP. FMRP is essential for normal mental development. An expansion of the trinucleotide CGG repeat in the Fmr1 gene is responsible for fragile X syndrome, a syndrome characterized by autism and mental disability.
The Fmr1 KO rat model was originally created at SAGE Labs, Inc. in St. Louis, MO and distributed out of the Boyertown, PA facility. The line continues to be maintained through the original SAGE Labs animal inventory acquired by Envigo, then Envigo was acquired by Inotiv in 2021.
Diet and Husbandry:
Our rodent models are raised and maintained on Teklad diet, bedding, and enrichment products:
- Diet: Teklad Global Rodent Diet
- Bedding: Teklad Contact Bedding (U.S. only)
- Enrichment: Teklad Enrichment Products (U.S. only)
Model Support Services:
Inotiv offers related model support services to deliver research-ready models to your facility:
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For pricing please contact us using the phone number above
us
- Autism
- Fragile x syndrome
- Neuroscience
- Autism (ASD)
- Fragile X syndrome
- Neuroscience
