- impaired glucose tolerance / IMPC
- decreased startle reflex / IMPC
- decreased prepulse inhibition / IMPC
- decreased exploration in new environment / IMPC
- small spleen / IMPC
- enhanced contextual conditioning behavior / IMPC
- increased monocyte cell number / IMPC
- abnormal freezing behavior / IMPC
- increased circulating alkaline phosphatase level / IMPC
- increased freezing behavior / IMPC
- increased fasting circulating glucose level / IMPC
- decreased bone mineral content / IMPC
- decreased locomotor activity / IMPC
- abnormal spleen morphology / IMPC
STOCK Cacna2d1tm1Aschw/AschwAdlpnH
| Status | Available to order |
| EMMA ID | EM:08421 |
| Citation information | RRID:IMSR_EM:08421 Research Resource Identifiers (RRID) are persistent unique ID numbers assigned to help researchers cite key resources (e.g. antibodies, model organisms and software projects) in the biomedical literature to improve transparency and reproducibility in research. See https://www.rrids.org/ for more information. |
| International strain name | STOCK Cacna2d1tm1Aschw/AschwAdlpnH |
| Alternative name | C57BL6N |
| Strain type | Targeted Mutant Strains : Knock-out |
| Allele/Transgene symbol | Cacna2d1tm1Aschw |
| Gene/Transgene symbol | Cacna2d1 |
Information from provider
| Provider | Arnold Schwartz |
| Provider affiliation | Internal Medicine, University of Cincinnati |
| Genetic information | Cacna2d1 knockout. |
| Phenotypic information | Homozygous:In these mice, exon 2 of the targeted calcium channel 21 (Cacna2d1) allele is replaced with a neomycin resistance (neo) cassette abolishing Cacna2d1 gene function. Mice homozygous for this mutation exhibit a smooth muscle deficiency and increased urination. Homozygous males are impotent. Cacna2d1 KO mice lack gabapentin (GPB) binding sites, show decreased basal myocardial contractility and relaxation, and decreased L-type calcium currents in cardiomyocytes. Homozygous males have reduced mechanosensory responses and delayed development of neuropathic mechanical hypersensitivity following sensory nerve injury.Heterozygous:none detected |
| Breeding history | Mice were obtained from Prof. A. Schwartz, rederived at Harwell MGU and backcrossed twice by us. Number of generations backcrossed is unknown, but the mice were black coated when we obtained them. |
| References |
|
| Homozygous fertile | females only |
| Homozygous viable | yes |
| Homozygous matings required | no |
| Immunocompromised | no |
Information from EMMA
| Archiving centre | Mary Lyon Centre at MRC Harwell, Oxford, United Kingdom |
Disease and phenotype information
Orphanet associated rare diseases, based on orthologous gene matching
- Familial short QT syndrome / Orphanet_51083
IMPC phenotypes (gene matching)
MGI phenotypes (gene matching)
Literature references
- Targeted disruption of the voltage-dependent calcium channel alpha2/delta-1-subunit.;Fuller-Bicer Geraldine A, Varadi Gyula, Koch Sheryl E, Ishii Masakazu, Bodi Ilona, Kadeer Nijiat, Muth James N, Mikala Gabor, Petrashevskaya Natalia N, Jordan Michael A, Zhang Sui-Po, Qin Ning, Flores Christopher M, Isaacsohn Idit, Varadi Maria, Mori Yasuo, Jones W Keith, Schwartz Arnold, ;2009;American journal of physiology. Heart and circulatory physiology;297;H117-24; 19429829
- α2δ-1 gene deletion affects somatosensory neuron function and delays mechanical hypersensitivity in response to peripheral nerve damage.;Patel Ryan, Bauer Claudia S, Nieto-Rostro Manuela, Margas Wojciech, Ferron Laurent, Chaggar Kanchan, Crews Kasumi, Ramirez Juan D, Bennett David L H, Schwartz Arnold, Dickenson Anthony H, Dolphin Annette C, ;2013;The Journal of neuroscience : the official journal of the Society for Neuroscience;33;16412-26; 24133248
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