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HIGH QUALITY DNA
TESTING YOU CAN TRUST
OUR PANELS
The tests in our DNA health testing panels are selected based on the scientific evidence available for disorders in the breed. Our scientists stay up to date with the latest developments and discoveries in the field to ensure that our testing panels are as up-to-date as possible.
DID YOU KNOW?
Our ISO-accredited testing services are relied upon by UK police forces for assessing the suitability of canine recruits for police duties.
TESTIMONIALS
approx. 2 weeks
Typical turnaround
5
Conditions screened
Simple cheek swab
At-home sampling
UK laboratory
Tested in-house
Progressive Retinal Atrophy (cord1/rcd4)PRA-cord1/rcd4
Progressive Retinal Atrophy (PRA) is a group of eye disorders which cause progressive degeneration of the retina through thinning and decreased blood flow. Depending on the variant the rod (dim light) or cone (bright light) photoreceptor cells of the eye may also be affected and age of onset and speed of progression can vary. Affected dogs typically have initial vision loss in low light, then peripheral vision loss, and eventually total blindness.
How it's inherited
Recessive
What your result means
Clear (N/N): no copies; not expected to develop PRA-cord1/crd4, nor pass it on.
Carrier (N/PRA): one copy. Healthy, but can pass it on. Breeding two carriers risks affected puppies.
Affected (PRA/PRA): two copies; expected to develop PRA-cord1/crd4. Discuss with your vet.
Mucopolysaccharidosis Type IIIAMPSIIIA
Mucopolysaccharidosis IIIA (MPSIIIA) is an inherited disorder affecting Wire-Haired Dachshunds and New Zealand Huntaway dogs. It causes certain substances to build up inside cells, which can lead to progressive damage. Affected dogs may have poor growth, joint problems, lameness and vision problems caused by clouding of the cornea. MPSIIIA is inherited as an autosomal recessive condition caused by a mutation in the SGSH gene.
Please note this is the Dachshund variant and not applicable to breeds affected by the other disease-causing variant.
How it's inherited
Recessive
What your result means
Clear (N/N): no copies; not expected to develop MPSIIIA, nor pass it on.
Carrier (N/MPSIIIA): one copy. Healthy, but can pass it on. Breeding two carriers risks affected puppies.
Affected (MPSIIIA/MPSIIIA): two copies; expected to develop MPSIIIA. Discuss with your vet.
Neuronal Ceroid Lipofuscinosis 1NCL1
Neuronal Ceroid Lipofuscinosis 1 (NCL1), also known as Batten disease, is an inherited neurological disorder affecting Standard Dachshunds and is caused by a variant in the PPT1 gene. Affected dogs develop progressive neurological problems, including vision loss, behavioural changes, tremors, poor coordination, weakness and seizures, and the disease is ultimately fatal. NCL1 is inherited as an autosomal recessive condition.
How it's inherited
Recessive
What your result means
Clear (N/N): no copies; not expected to develop NCL1, nor pass it on.
Carrier (N/NCL): one copy. Healthy, but can pass it on. Breeding two carriers risks affected puppies.
Affected (NCL/NCL): two copies; expected to develop NCL1. Discuss with your vet.
Neuronal Ceroid Lipofuscinosis 2NCL2
Neuronal Ceroid Lipofuscinosis 2 (NCL2), also known as Batten disease, is an inherited neurological disorder affecting Miniature Long-Haired Dachshunds and is caused by a variant in the TPP1 gene. Affected dogs develop progressive neurological problems, including vision loss, behavioural changes, tremors, poor coordination, weakness and seizures, and the disease is ultimately fatal. NCL2 is inherited as an autosomal recessive condition.
How it's inherited
Recessive
What your result means
Clear (N/N): no copies; not expected to develop NCL2, nor pass it on.
Carrier (N/NCL): one copy. Healthy, but can pass it on. Breeding two carriers risks affected puppies.
Affected (NCL/NCL): two copies; expected to develop NCL2. Discuss with your vet.
Osteogenesis ImperfectaOI
Osteogenesis Imperfecta (OI), also known as brittle bone disease, is an inherited disorder affecting Dachshunds and is caused by a variant in the SERPINH1 gene, which is important for normal collagen formation. Affected dogs have fragile bones that can fracture easily and may develop bone deformities, joint problems, pain and brittle teeth. OI is inherited as an autosomal recessive condition.
Please note this is the Dachshund variant and not applicable to breeds affected by the other disease-causing variant.
How it's inherited
Recessive
What your result means
Clear (N/N): no copies; not expected to develop OI, nor pass it on.
Carrier (N/OI): one copy. Healthy, but can pass it on. Breeding two carriers risks affected puppies.
Affected (OI/OI): two copies; expected to develop OI. Discuss with your vet.
Progressive Retinal Atrophy (cord1/rcd4)PRA-cord1/rcd4
- Gene
- RPGRIP1
- Variant
- p.(I49Kfs*26)
- Inheritance
- autosomal recessive
- OMIA
- OMIA001432 9615
Molecular mechanism
Progressive retinal atrophy (PRA) encompasses a genetically heterogeneous group of inherited retinal degenerative disorders characterised by the progressive loss of photoreceptor function, ultimately resulting in irreversible blindness. Although the clinical presentation is broadly similar across affected breeds, with initial degeneration of rod photoreceptors causing night blindness followed by cone degeneration and progressive loss of daylight vision, numerous genetically distinct forms of PRA have been identified (Miyadera et al., 2012; Mowat et al., 2024). Advances in canine molecular genetics have demonstrated that variants in multiple genes involved in photoreceptor development, maintenance and function can produce clinically similar retinal phenotypes. Consequently, breed-specific genetic testing is required, as different forms of PRA are associated with different causative variants.
PRA-RPGRIP1 (CORD1/RCD4): Progressive retinal atrophy associated with RPGRIP1 is inherited as an autosomal recessive condition. In Miniature Long-Haired Dachshunds, Mellersh et al., (2006) identified a 44-bp insertion in the RPGRIP1 gene that results in a frameshift and premature protein truncation. Although additional genetic factors may influence disease severity, this variant remains the primary genetic marker used for testing (Miyadera et al., 2012).
The expanding number of recognised PRA-associated variants highlights the marked genetic heterogeneity underlying inherited retinal degeneration in dogs. While many of these variants are breed-specific, others are shared across multiple breeds through historical founder events. Genetic testing enables accurate identification of affected and carrier dogs, supporting informed breeding decisions aimed at reducing disease prevalence while preserving genetic diversity. As additional causative variants continue to be identified, molecular testing will remain an important tool for improving the diagnosis, management and long-term control of progressive retinal atrophy in canine populations (Lewis \u0026amp; Mellersh, 2019; Mowat et al., 2024).
References
Aguirre, G.D., Lohi, H., Kaukonen, M., Murgiano, L. : Formal commentary. PLoS Genet 16:e1009059, 2020. Pubmed reference: 33151924. DOI: 10.1371/journal.pgen.1009059.
Clark, J.A., Anderson, H., Donner, J., Pearce-Kelling, S., Ekenstedt, K.J. : Global frequency analyses of canine progressive rod-cone degeneration-progressive retinal atrophy and Collie eye anomaly using commercial genetic testing data. Genes (Basel) 14:2093, 2023. Pubmed reference: 38003037. DOI: 10.3390/genes14112093.
Downs, L.M., Wallin-Håkansson, B., Boursnell, M., Marklund, S., Hedhammar, Å., Truvé, K., Hübinette, L., Lindblad-Toh, K., Bergström, T., Mellersh, C.S. : A frameshift mutation in golden retriever dogs with progressive retinal atrophy endorses SLC4A3 as a candidate gene for human retinal degenerations. PLoS One 6:e21452, 2011. Pubmed reference: 21738669. DOI: 10.1371/journal.pone.0021452.
Downs, L.M., Bell, J.S., Freeman, J., Hartley, C., Hayward, L.J., Mellersh, C.S. : Late-onset progressive retinal atrophy in the Gordon and Irish Setter breeds is associated with a frameshift mutation in C2orf71. Anim Genet 44:169-77, 2013. Pubmed reference: 22686255. DOI: 10.1111/j.1365-2052.2012.02379.x.
Downs, L.M., Mellersh, C.S. : An intronic SINE insertion in FAM161A that causes exon-skipping is associated with progressive retinal atrophy in Tibetan Spaniels and Tibetan Terriers. PLoS One 9:e93990, 2014. Pubmed reference: 24705771. DOI: 10.1371/journal.pone.0093990.
Downs, L.M., Wallin-Håkansson, B., Bergström, T., Mellersh, C.S. : A novel mutation in TTC8 is associated with progressive retinal atrophy in the golden retriever. Canine Genet Epidemiol 1:4, 2014. Pubmed reference: 26401321. DOI: 10.1186/2052-6687-1-4.
Goldstein, O., Mezey, JG., Boyko, AR., Gao, C., Wang, W., Bustamante, CD., Anguish, LJ., Jordan, JA., Pearce-Kelling, SE., Aguirre, GD., Acland, GM. : An ADAM9 mutation in canine cone-rod dystrophy 3 establishes homology with human cone-rod dystrophy 9. Mol Vis 16:1549-69, 2010. Pubmed reference: 20806078.
Karlskov-Mortensen, P., Proschowsky, H.F., Gao, F., Fredholm, M. : Identification of the mutation causing progressive retinal atrophy in Old Danish Pointing Dog. Anim Genet 49:237-241, 2018. Pubmed reference: 29624701. DOI: 10.1111/age.12659.
Kaukonen, M., Quintero, I.B., Mukarram, A.K., Hytönen, M.K., Holopainen, S., Wickström, K., Kyöstilä, K., Arumilli, M., Jalomäki, S., Daub, C.O., Kere, J., Lohi, H. : A putative silencer variant in a spontaneous canine model of retinitis pigmentosa. PLoS Genet 16:e1008659, 2020. Pubmed reference: 32150541. DOI: 10.1371/journal.pgen.1008659.
Kropatsch, R., Petrasch-Parwez, E., Seelow, D., Schlichting, A., Gerding, WM., Akkad, DA., Epplen, JT., Dekomien, G. : Generalized progressive retinal atrophy in the Irish Glen of Imaal Terrier is associated with a deletion in the ADAM9 gene. Mol Cell Probes 24:357-63, 2010. Pubmed reference: 20691256. DOI: 10.1016/j.mcp.2010.07.007.
Lewis, T.W., Mellersh, C.S. : Changes in mutation frequency of eight Mendelian inherited disorders in eight pedigree dog populations following introduction of a commercial DNA test. PLoS One 14:e0209864, 2019. Pubmed reference: 30650096. DOI: 10.1371/journal.pone.0209864.
Mellersh, CS., Boursnell, ME., Pettitt, L., Ryder, EJ., Holmes, NG., Grafham, D., Forman, OP., Sampson, J., Barnett, KC., Blanton, S., Binns, MM., Vaudin, M. : Canine RPGRIP1 mutation establishes cone-rod dystrophy in miniature longhaired dachshunds as a homologue of human Leber congenital amaurosis. Genomics 88:293-301, 2006. Pubmed reference: 16806805. DOI: 10.1016/j.ygeno.2006.05.004.
Mowat, F.M., Iwabe, S., Aguirre, G.D., Petersen-Jones, S.M. : Consensus guidelines for nomenclature of companion animal inherited retinal disorders. Vet Ophthalmol 28:663-667, 2024. Pubmed reference: 38334230. DOI: 10.1111/vop.13185.
Miyadera, K., Acland, G.M., Aguirre, G.D. : Genetic and phenotypic variations of inherited retinal diseases in dogs: the power of within- and across-breed studies. Mamm Genome 23:40-61, 2012. Pubmed reference: 22065099. DOI: 10.1007/s00335-011-9361-3.
Murgiano, L., Becker, D., Torjman, D., Niggel, J.K., Milano, A., Cullen, C., Feng, R., Wang, F., Jagannathan, V., Pearce-Kelling, S., Katz, M.L., Leeb, T., Aguirre, G.D. : Complex structural PPT1 variant associated with non-syndromic canine retinal degeneration. G3 (Bethesda) 9:425-437, 2019. Pubmed reference: 30541930. DOI: 10.1534/g3.118.200859.
Petersen-Jones, S.M., Entz, D.D., Sargan, D.R. : CGMP phosphodiesterase-alpha mutation causes progressive retinal atrophy in the Cardigan Welsh corgi dog Investigative Ophthalmology \u0026amp; Visual Science 40:1637-1644, 1999. Pubmed reference: 10393029.
Suber, M.L., Pittler, S.J., Qin, N., Wright, G.C., Holcombe, V., Lee, R.H., Craft, C.M., Lolley, R.N., Baehr, W., Hurwitz, R.L. : Irish Setter Dogs Affected with Rod/Cone Dysplasia Contain a Nonsense Mutation in the Rod cGMP Phosphodiesterase beta- Subunit Gene Proceedings of the National Academy of Sciences of the United States of America 90:3968-3972, 1993. Pubmed reference: 8387203.
Svensson, M., Olsén, L., Winkler, P.A., Petersen-Jones, S.M., Bergström, T., Garncarz, Y., Narfström, K. : Progressive retinal atrophy in the Polski Owczarek Nizinny dog: a clinical and genetic study. Vet Ophthalmol 19:195-205, 2016. Pubmed reference: 26009980. DOI: 10.1111/vop.12284.
Wiik, A.C., Ropstad, E.O., Ekesten, B., Karlstam, L., Wade, C.M., Lingaas, F. : Progressive retinal atrophy in Shetland sheepdog is associated with a mutation in the CNGA1 gene. Anim Genet 46:515-21, 2015. Pubmed reference: 26202106. DOI: 10.1111/age.12323.
Winkler, P.A., Ekenstedt, K.J., Occelli, L.M., Frattaroli, A.V., Bartoe, J.T., Venta, P.J., Petersen-Jones, S.M. : A large animal model for CNGB1 autosomal recessive retinitis pigmentosa. PLoS One 8:e72229, 2013. Pubmed reference: 23977260. DOI: 10.1371/journal.pone.0072229.
Zangerl, B., Goldstein, O., Philp, AR., Lindauer, SJ., Pearce-Kelling, SE., Mullins, RF., Graphodatsky, AS., Ripoll, D., Felix, JS., Stone, EM., Acland, GM., Aguirre, GD. : Identical mutation in a novel retinal gene causes progressive rod-cone degeneration in dogs and retinitis pigmentosa in humans. Genomics 88:551-563, 2006. Pubmed reference: 16938425. DOI: 10.1016/j.ygeno.2006.07.007.
Mucopolysaccharidosis Type IIIAMPSIIIA
- Gene
- SGSH
- Variant
- 3-bp deletion, 737-739delCCA
- Inheritance
- autosomal recessive
- OMIA
- OMIA001309 9615
Molecular mechanism
Mucopolysaccharidosis IIIA (MPSIIIA) is an inherited lysosomal storage disease caused by defective metabolism of glycosaminoglycans, which accumulate within lysosomes in affected tissues. The condition is inherited as an autosomal recessive trait and has been reported in Wire-Haired Dachshunds and New Zealand Huntaway dogs. In Wire-Haired Dachshunds, Aronovich et al., (2000) identified a 3-bp deletion (737-739delCCA) resulting in the loss of threonine at position 246 on the SGSH gene. The accumulation of glycosaminoglycans within lysosomes results in progressive dysfunction of affected tissues. Clinical signs reported in dogs with mucopolysaccharidosis include growth retardation, joint abnormalities, progressive lameness and visual impairment associated with corneal clouding (Shull et al., 1982).
Please note this is the Dachshund variant (SGSH insertion) and not applicable to New Zealand Huntaway dogs (SGSH deletion) or other breeds affected by IDUA variants.
References
Aronovich, E.L., Carmichael, K.P., Morizono, H., Koutlas, I.G., Deanching, M., Hoganson, G., Fischer, A., Whitley, C.B. : Canine heparan sulfate sulfamidase and the molecular pathology underlying Sanfilippo syndrome type A in Dachshunds Genomics 68:80-84, 2000. Pubmed reference: 10950929. DOI: 10.1006/geno.2000.6275.
Shull, R.M., Munger, R.J., Spellacy, E., Hall, C.W., Constantopoulos, G., Neufeld, E.F. : Canine alpha-L-iduronidase deficiency. A model of mucopolysaccharidosis I. Am J Pathol 109:244-8, 1982. Pubmed reference: 6215865.
Neuronal Ceroid Lipofuscinosis 1NCL1
- Gene
- PPT1
- Variant
- c.736-737insC
- Inheritance
- autosomal recessive
- OMIA
- OMIA001504 9615
Molecular mechanism
Neuronal Ceroid Lipofuscinosis (NCL), also known as Batten disease, is a group of inherited lysosomal storage disorders characterised by progressive neurodegeneration caused by the accumulation of autofluorescent storage material within nerve cells.
Affected dogs develop progressive neurological disease beginning in early life. Clinical signs include vision loss, behavioural changes, tremors, ataxia, weakness, cognitive decline, and seizures, with the disease progressing rapidly and ultimately proving fatal (Awano et al., 2006; Sanders et al., 2010; Sanders et al., 2011).
The NCL1 variant, identified in Standard Dachshunds, was first described by Sanders et al., (2010). It is caused by a single nucleotide insertion, PPT1:c.736_737insC, in exon 8 of the PPT1 gene on canine chromosome 15 (CFA15). The frameshift introduces a premature stop codon, producing a truncated protein with severely reduced enzyme activity.
The NCL2 variant, identified in Miniature Long-Haired Dachshunds, was first reported by Awano et al., (2006). It is caused by a single nucleotide deletion, TPP1:c.325delC, in exon 4 of the TPP1 gene on canine chromosome 21 (CFA21). This frameshift mutation results in a premature stop codon and loss of normal tripeptidyl peptidase 1 enzyme function.
Both forms are inherited as autosomal recessive conditions. Genetic testing can identify clear, carrier, and affected dogs, allowing breeders to avoid producing affected puppies.
References
Awano, T., Katz, ML., O\u0026#39;Brien, DP., Sohar, I., Lobel, P., Coates, JR., Khan, S., Johnson, GC., Giger, U., Johnson, GS. : A frame shift mutation in canine TPP1 (the ortholog of human CLN2) in a juvenile Dachshund with neuronal ceroid lipofuscinosis. Mol Genet Metab 89:254-60, 2006. Pubmed reference: 16621647. DOI: 10.1016/j.ymgme.2006.02.016.
Sanders, D.N., Kanazono, S., Coates, J.R., Johnson, G.S., Johnson, G.C., Narfstrom, K., O\u0026#39;Brien, D.P., Katz, M.L. : COGNITIVE DECLINE IN A DOG MODEL FOR AN INHERITED NEURODEGENERATIVE DISEASE USING T-MAZE PERFORMANCE. J Vet Behav 5:154, 2010. Pubmed reference: 20672015. DOI: 10.1016/j.jveb.2009.12.020.
Sanders, D.N., Kanazono, S., Wininger, F.A., Whiting, R.E., Flournoy, C.A., Coates, J.R., Castaner, L.J., O\u0026#39;Brien, D.P., Katz, M.L. : A reversal learning task detects cognitive deficits in a Dachshund model of late-infantile neuronal ceroid lipofuscinosis. Genes Brain Behav 10:798-804, 2011. Pubmed reference: 21745338. DOI: 10.1111/j.1601-183X.2011.00718.x.
Neuronal Ceroid Lipofuscinosis 2NCL2
- Gene
- TPP1
- Variant
- c.325delC
- Inheritance
- autosomal recessive
- OMIA
- OMIA001472 9615
Molecular mechanism
Neuronal Ceroid Lipofuscinosis (NCL), also known as Batten disease, is a group of inherited lysosomal storage disorders characterised by progressive neurodegeneration caused by the accumulation of autofluorescent storage material within nerve cells.
Affected dogs develop progressive neurological disease beginning in early life. Clinical signs include vision loss, behavioural changes, tremors, ataxia, weakness, cognitive decline, and seizures, with the disease progressing rapidly and ultimately proving fatal (Awano et al., 2006; Sanders et al., 2010; Sanders et al., 2011).
The NCL1 variant, identified in Standard Dachshunds, was first described by Sanders et al., (2010). It is caused by a single nucleotide insertion, PPT1:c.736_737insC, in exon 8 of the PPT1 gene on canine chromosome 15 (CFA15). The frameshift introduces a premature stop codon, producing a truncated protein with severely reduced enzyme activity.
The NCL2 variant, identified in Miniature Long-Haired Dachshunds, was first reported by Awano et al., (2006). It is caused by a single nucleotide deletion, TPP1:c.325delC, in exon 4 of the TPP1 gene on canine chromosome 21 (CFA21). This frameshift mutation results in a premature stop codon and loss of normal tripeptidyl peptidase 1 enzyme function.
Both forms are inherited as autosomal recessive conditions. Genetic testing can identify clear, carrier, and affected dogs, allowing breeders to avoid producing affected puppies.
References
Awano, T., Katz, ML., O\u0026#39;Brien, DP., Sohar, I., Lobel, P., Coates, JR., Khan, S., Johnson, GC., Giger, U., Johnson, GS. : A frame shift mutation in canine TPP1 (the ortholog of human CLN2) in a juvenile Dachshund with neuronal ceroid lipofuscinosis. Mol Genet Metab 89:254-60, 2006. Pubmed reference: 16621647. DOI: 10.1016/j.ymgme.2006.02.016.
Sanders, D.N., Kanazono, S., Coates, J.R., Johnson, G.S., Johnson, G.C., Narfstrom, K., O\u0026#39;Brien, D.P., Katz, M.L. : COGNITIVE DECLINE IN A DOG MODEL FOR AN INHERITED NEURODEGENERATIVE DISEASE USING T-MAZE PERFORMANCE. J Vet Behav 5:154, 2010. Pubmed reference: 20672015. DOI: 10.1016/j.jveb.2009.12.020.
Sanders, D.N., Kanazono, S., Wininger, F.A., Whiting, R.E., Flournoy, C.A., Coates, J.R., Castaner, L.J., O\u0026#39;Brien, D.P., Katz, M.L. : A reversal learning task detects cognitive deficits in a Dachshund model of late-infantile neuronal ceroid lipofuscinosis. Genes Brain Behav 10:798-804, 2011. Pubmed reference: 21745338. DOI: 10.1111/j.1601-183X.2011.00718.x.
Osteogenesis ImperfectaOI
- Gene
- SERPINH1
- Variant
- c.977T>C, p.Leu326Pro
- Inheritance
- autosomal recessive
- OMIA
- OMIA001400 9615
Molecular mechanism
Osteogenesis Imperfecta (OI), also known as brittle bone disease, is an inherited connective tissue disorder characterised by fragile bones that fracture easily due to defects in collagen formation. Multiple genetic forms of the disease have been identified in dogs. The variant offered by our test is found in Dachshunds and is inherited as an autosomal recessive trait.
Affected dogs typically exhibit reduced bone density, spontaneous fractures, bone deformities, joint laxity, pain, and brittle teeth. Additional clinical signs may include blue-grey sclera, progressive hearing loss, dwarfism, and, in severe cases, stillbirths (Drögemüller et al., 2009; Lindert et al., 2015; Seeliger et al., 2003).
The causative variant was first identified by Drögemüller et al., (2009) following homozygosity mapping to canine chromosome 21 (CFA21) and is a missense variant, c.977T\u0026gt;C,p.Leu326Pro, affecting the SERPINH1 gene, which encodes a collagen-specific molecular chaperone required for normal collagen assembly.
Genetic testing can identify clear, carrier, and affected dogs, enabling informed breeding decisions to prevent affected puppies while maintaining genetic diversity within the breed. Carrier frequencies have been reported at approximately 13% across European Dachshund populations, with higher frequencies observed in some wire-haired lines (Schütz et al., 2012; Eckardt et al., 2013).
Please note this is the Dachshund variant (SERPINH1) and not applicable to breeds affected by COL1A1 or COL1A2 variants.
References
Drögemüller, C., Becker, D., Brunner, A., Haase, B., Kircher, P., Seeliger, F., Fehr, M., Baumann, U., Lindblad-Toh, K., Leeb, T. : A missense mutation in the SERPINH1 gene in Dachshunds with osteogenesis imperfecta. PLoS Genet 5:e1000579, 2009. Pubmed reference: 19629171. DOI: 10.1371/journal.pgen.1000579.
Eckardt, J., Kluth, S., Dierks, C., Philipp, U., Distl, O. : Population screening for the mutation associated with osteogenesis imperfecta in dachshunds. Vet Rec 172:364, 2013. Pubmed reference: 23315765. DOI: 10.1136/vr.101122.
Lindert, U., Weis, M.A., Rai, J., Seeliger, F., Hausser, I., Leeb, T., Eyre, D., Rohrbach, M., Giunta, C. : Molecular consequences of the SERPINH1/HSP47 mutation in the dachshund natural model of osteogenesis imperfecta. J Biol Chem 290:17679-89, 2015. Pubmed reference: 26004778. DOI: 10.1074/jbc.M115.661025.
Schütz, E., Drögemüller, C., Scharfenstein, M., Brenig, B. : [Osteogenesis imperfecta in the Dachshund]. Kleintierpraxis 57:57-62, 2012.
Seeliger, F., Leeb, T., Peters, M., Brugmann, M., Fehr, M., Hewicker-Trautwein, M. : Osteogenesis imperfecta in two litters of dachshunds. Vet Pathol 40:530-9, 2003. Pubmed reference: 12949410. DOI: 10.1354/vp.40-5-530.
