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Parentage Verification Horse – Icelandic Horse

Este producto incluye la verificación de la filiación y el perfil de ADN de la descendencia. Si el perfil de ADN de los progenitores (esperados) no está disponible, es necesario solicitar un perfil de ADN por separado.

Se establece un perfil de ADN utilizando marcadores de ADN. El perfil de cada muestra se almacena en una base de datos y se puede representar como un código de barras, que es único para cada individuo. Este perfil de ADN sirve para la verificación de la filiación, lo que implica una comparación de la información genética presente en una descendencia con la de los padres potenciales. Para una verificación precisa de la filiación, toda la información genética de la descendencia debe ser rastreable hasta la combinación de la madre y el padre. En la mayoría de los casos, la fiabilidad de este análisis supera el 99,5 por ciento.

CombiBreed Karelian Bear Dog

Este pack está diseñado para proporcionarle información vital sobre la salud genética, los rasgos y la diversidad de su perro, e incluye pruebas de ADN para numerosas enfermedades y / o rasgos importantes. Además, también calculamos el Coeficiente de Endogamia (COI) y el porcentaje de Heterocigosidad del ADN de tu perro. El COI muestra el grado de endogamia de su perro, mientras que el porcentaje de heterocigosidad es una medida de la diversidad genética individual de su perro.

La información sobre las pruebas individuales en este pack está disponible en la sección “Pruebas incluidas” en esta página. Aceptamos muestras de animales de cualquier edad. Normalmente, el tiempo de respuesta de las pruebas realizadas en nuestras propias instalaciones es de 10 días hábiles después de la recepción de la muestra. Para las pruebas subcontratadas, el llamado “laboratorio externo” o “laboratorio externo de patentes”, el tiempo de respuesta es de al menos 20 días hábiles después de la recepción de su muestra. Tenga en cuenta que los 20 días hábiles mencionados son una estimación, ya que el tiempo de envío a estos laboratorios externos o instalaciones de patentes puede variar debido a retrasos inesperados.

Algunas pruebas incluidas son realizadas por un laboratorio externo. CombiBreed se encarga de la mediación entre usted como cliente y el laboratorio externo. En estos casos, CombiBreed no se hace responsable del comportamiento del cliente y / o contratista.

CombiBreed Norwegian Elkhound (Black)

Este pack está diseñado para proporcionarle información vital sobre la salud genética, los rasgos y la diversidad de su perro, e incluye pruebas de ADN para numerosas enfermedades y / o rasgos importantes. Además, también calculamos el Coeficiente de Endogamia (COI) y el porcentaje de Heterocigosidad del ADN de tu perro. El COI muestra el grado de endogamia de su perro, mientras que el porcentaje de heterocigosidad es una medida de la diversidad genética individual de su perro.

La información sobre las pruebas individuales en este pack está disponible en la sección “Pruebas incluidas” en esta página. Aceptamos muestras de animales de cualquier edad. Normalmente, el tiempo de respuesta de las pruebas realizadas en nuestras propias instalaciones es de 10 días hábiles después de la recepción de la muestra. Para las pruebas subcontratadas, el llamado “laboratorio externo” o “laboratorio externo de patentes”, el tiempo de respuesta es de al menos 20 días hábiles después de la recepción de su muestra. Tenga en cuenta que los 20 días hábiles mencionados son una estimación, ya que el tiempo de envío a estos laboratorios externos o instalaciones de patentes puede variar debido a retrasos inesperados.

Algunas pruebas incluidas son realizadas por un laboratorio externo. CombiBreed se encarga de la mediación entre usted como cliente y el laboratorio externo. En estos casos, CombiBreed no se hace responsable del comportamiento del cliente y / o contratista.

CombiBreed Biewer Terrier

Este pack CombiBreed está diseñado para brindarle información vital sobre la salud genética, los rasgos y la diversidad de su Fox Terrier e incluye pruebas de ADN para numerosas enfermedades y / o rasgos importantes. Además, también calculamos el Coeficiente de Consanguinidad (COI) y el porcentaje de Heterocigosidad del ADN de tu perro. El COI muestra el grado de endogamia de tu perro, mientras que el porcentaje de heterocigosidad es una medida de la diversidad genética individual de tu perro.

La información sobre las pruebas individuales de este paquete está disponible en la sección “Pruebas incluidas” de esta página. Aceptamos muestras de animales de cualquier edad. Normalmente, el tiempo de respuesta de las pruebas realizadas en nuestras propias instalaciones es de 10 días hábiles después de la recepción de la muestra. En el caso de las pruebas subcontratadas, denominadas “laboratorio externo” o “laboratorio externo de patentes”, el tiempo de respuesta es de al menos 20 días hábiles después de la recepción de su muestra. Tenga en cuenta que los 20 días hábiles mencionados son una estimación, ya que el tiempo de envío a estos laboratorios externos o instalaciones de patentes puede variar debido a retrasos inesperados.

Algunas de las pruebas incluidas son realizadas por un laboratorio externo. CombiBreed se encarga de la mediación entre usted como cliente y el laboratorio externo. En estos casos, CombiBreed no se hace responsable del comportamiento del cliente y/o del contratista.

A-Locus (Agouti)

The Agouti gene (ASIP gene) is responsible for the production of a protein that regulates the distribution of black pigment (eumelanin) within the hair shaft. This gene is also known as the A-locus and is responsible for ticking and causes the individual hairs to have bands of light and heavy pigmentation. The agouti band can be seen in both black-based and red-based colours. The Coat Colour Agouti test (K757) tests for the genetic status of the A-locus. The A-locus has two variants (alleles). The allele A is dominant and produces ticked coat, hair shafts with alternating bands of yellow and black colour, ending with black tips (similar to the coat of a wild mouse or rabbit).The recessive allele produces a cat that is “self”coloured (solid). Only when the cat has two copies of the recessive allele a the coat colour is solid.

Another system of pigmentation in cats produces the tabby patterns of dark stripes interspersed with the lighter agouti tipped hairs. Hairs in the darker stripes do not have the shift between black and yellow pigment production and remain uniformly dark. The effect of the agouti protein on orange pigment is limited, thus tabby striping may still be seen on cats that are a/a for agouti.

The Coat Colour Agouti test (A-Locus) enclose the following results:

A-locus	Coat Colour
A/A	Agouti coat colour
A/a	Agouti coat colour
a/a	Solid, “Self” coloured

Goniodysgenesis and Glaucoma (GG)

Goniodysgenesis and Glaucoma (GG) affects the development of the eye’s drainage system. It is caused by an autosomal recessive mutation in the Olfactomedin-Like 3 (OLFML3 gene). This gene is involved in the creation of a protein that supports cell structure and is involved in blood vessel formation. Specifically in Border Collies, affected dogs are at severe high risk for having a malformed or partially closed drainage angle, which prevents fluid from exiting the eye properly. This is called goniodysgenesis and can lead to glaucoma, though the effect of the mutation is variable.

¡Neuva preuba! Trombastenia de Glanzmann (GT) 2

Quarter Horses y los pura sangre pueden verse afectados por una variante de la trombastenia de Glanzmann (GT), causada por una mutación recesiva en el gen ITGA2B. Este trastorno hemorrágico causa plaquetas defectuosas, lo que resulta en una incapacidad para que la sangre se coagule adecuadamente. Los signos clínicos generalmente se caracterizan por sangrado de la piel, las membranas mucosas y las encías, y también pueden incluir hematomas, epistaxis (sangrado nasal) y hemorragia gastrointestinal.

La trombastenia de Glanzmann en el Quarter Horse y el pura sangre se puede analizar con la prueba CombiBreed Trombastenia de Glanzmann (GT) 2 – Caballo, con el número de prueba P392.

P392 Trombastenia de Glanzmann (GT) 2 – Caballo

Tail Length (Brachyury, T-Locus, Natural Bobtail) – Dog

The bobtail or brachyury trait is caused by an autosomal dominant mutation in the T-box transcription factor T (TBXT) gene. The TBXT or T-gene encodes transcription factors that play critical roles in embryonic development, especially the tail and spine. A single copy of the mutation (heterozygous) causes the bobtail look, but two copies (homozygous mutant) disrupt development so severely that the embryo cannot survive. This makes the mutation homozygous lethal.

The tested mutation was originally discovered in the Pembroke Welsh Corgi, but also causes distinctive short tails in multiple other breeds, mainly sheepdogs and hunting breeds.

MDR1 Multi Resistencia a Medicamentos – Gato

Multi Drug Resistance 1 (MDR1), sometimes known as Ivermectin Sensitivity, is a disorder that affects the blood-brain barrier. As a result, affected animals can be in effect poisoned when given certain drugs as part of standard veterinary procedures. In cats, a variant of the disease is caused by a recessive mutation to the gene ABCB1.

It is estimated that this mutation occurs in approximately 4% of domestic cats.

Curly Coat with or without Hypotrichosis (SP6- and KRT25-related) – Horse

A curly coat in horses, known particularly as the distinctive trait of the American Bashkir Curly Horse, is caused by a complex interaction between two separate genes, KRT25 (P317) and SP6 (DNA test P330). These same genes can also cause hypotrichosis: a loss of tail and mane hair.

A horse with a genotype with GG and CC (GC/GC) is entirely unaffected, and will develop a straight coat with normal thickness. A genotype of GC/GT or GT/GT causes a curly coat. A genotype of GC/AT or GC/AC causes curly coat and incomplete hypotrichosis (scanty tail). Finally, a genotype of AC/AC causes a curly coat with complete hypotrichosis (string tail).

Hereditary Footpad Hyperkeratosis (FAM83G-related)

Hereditary Footpad Hyperkeratosis (HFH) is a skin disorder of the footpads, which causes the development of thick, painful, callus-like growths. This variant of the disease, known as Palmoplantar Hyperkeratosis or Digital Hyperkeratosis (DH), is found in the Irish Terrier and Kromfohrländer. It is caused by a recessive mutation to the gene FAM83G.

Coat Colour C-Locus Colourpoint (Siam, Mink, Burma)

Coat colour in cats is controlled by a wide range of different genes working together. One of these genes involved is the Tyrosinase (TYR) gene. This gene produces an enzyme that is required for melanin production, which gives skin, hair, and eyes their colour. Mutations in this gene cause various degrees of Type 1 Oculocutaneous Albinism (OCA1), a failure to produce pigment. This can range between the distinctive point colouration of the Burmese and Siamese cat, to complete albinism.

Two known autosomal recessive mutations in TYR have been associated with colourpoints: a pattern of colouration that causes a cat’s body to be pale and their extremities to be dark. It is directly caused by temperature differences in which the darker parts of the cat are colder, while the lighter parts are warmer. The first mutation is designated as “cb” and is responsible for Burmese-type point colouration or Burmese colourpoint. The second mutation is designated as “cs” and is responsible for Siamese-type point colouration or Siamese colourpoint. Cats that carry one “cb” allele and one “cs” allele will display Tonkinese or Mink colourpoints instead, an intermediate color between Siamese and Burmese. The “cb” and “cs” variants are both tested here.

The alleles of the mentioned mutations are equal in dominance. They are recessive to the normal genotype (C) and dominant over the alleles for complete albinism (c and c2).

Ehlers-Danlos Syndrome Type 7 – Doberman

Ehlers-Danlos Syndromes (EDS) are a group of connective tissue disorders, causing loose skin and joint hypermobility. The variant analysed in this test, Ehlers-Danlos Syndrome type VII (Type 7, also known as Dermatosparaxis) is found in the Doberman Pinscher, and is caused by a recessive mutation to the gene ADAMTS2. Similar variants of Dermatosparaxis also affect the Alapaha Blue Blood Bulldog, Pit Bull Terrier and the Catahoula Leopard Dog.

Osteopatía Craneomandibular (CMO) – Basset Hound

Craniomandibular Osteopathy (CMO), also known as Lion Jaw, is a skeletal disorder that generally occurs in young, growing dogs under 1 year old, and causes painful growth of the jawbone. It is caused by a dominant mutation with incomplete penetrance to the Solute Carrier Family 37 Member 2 (SLC37A2) gene.

The variant analysed in this test occurs in the Basset Hound. A related variant has been observed in the Cairn Terrier, Scottish Terrier and West Highland White Terrier.

Coat Colour E-Locus (6 variants) – Dog

Coat colour in dogs is influenced by multiple interacting genes, one of which is the Extension or E-Locus, corresponding to the MC1R (melanocortin 1 receptor) gene. MC1R controls pigment production by switching between phaeomelanin (red/yellow) and eumelanin (black/brown). The normal E allele allows for dark pigment formation, while other loci like B and D can further modify the final coat colour.

Recessive e mutations (e1, e2, e3) disable MC1R, resulting in light coats—ranging from cream to red—when two copies are present. These e variants are breed-specific but functionally equivalent.

Dominant mutations at the E-Locus alter pigment distribution instead of production. The Eg (Grizzle) mutation, found in Salukis and Afghan Hounds, creates a dark-topped “Grizzle” or “Domino” pattern with a distinct widow’s peak. The Em (Melanistic Mask) mutation darkens the muzzle and face, though it can be hidden by an already dark coat.

Among all E-locus alleles, Em is most dominant, followed by Eg, while all e variants are equally recessive.

Canine Multiple System Degeneration (CMSD) – Kerry Blue Terrier

Canine Multiple System Degeneration (CMSD) is a progressive, heritable neurological disorder. It is caused by a mutation in the Serine Active Site Containing 1 (SERAC1) gene and is inherited in an autosomal recessive manner. The mutation in the SERAC1 gene causes disruption of phospholipid remodeling and cholesterol trafficking, which are essential for healthy mitochondrial function and neuronal survival. This leads to degeneration of specific brain regions, resulting in the progressive movement disorder seen in Kerry Blue Terriers.

Myosin Heavy Chain Myopathy (MYHM)

Myosin-Heavy Chain Myopathy (MHYM), also known as Immune-Mediated Myositis (IMM), is an autoimmune disorder found in the Quarter Horse, American Paint and Appaloosa. The disease causes bouts of acute, rapid-onset muscle atrophy as the horse’s immune system attacks its own muscles. The disease is caused by a co-dominant mutation to the gene MYH1.

Coat Colour Tabby (3 variants)

A tabby cat is a cat with a dark striped or spotted pattern on a paler background. Domestic cats exhibit heritable variation of tabby markings – mackerel vs. blotched. The gene responsible for tabby pattern variation is identified as Laeverin (LVRN), also known as Transmembrane aminopeptidase Q (Taqpep). This gene is involved in control of melanocortin signalling. Three recessive mutations of this gene are identified to date that have a clear effect on the rise of the “blotched” pattern. Without mutations, the cat will display the mackerel tabby markings.

Progressive Retinal Atrophy (MERTK-PRA)

Progressive Retinal Atrophy (PRA) is a large group of genetic diseases in which the retina gradually degenerates over time, causing a progressive loss of vision. The specific variant of the disease analysed in this test is known as MERTK-PRA and is found in the Swedish Vallhund. It is caused by an autosomal recessive mutation to the MER proto-oncogene, tyrosine kinase (MERTK) gene.

Von Willebrand Disease Type 3 – Shetland Sheepdog

Von Willebrand Disease Type 3 (vWD3) in Shetland Sheepdogs is considered the most severe form of Von Willebrand Disease. This variant is caused by a specific autosomal recessive mutation in the von Willebrand factor (vWF) gene. This mutation leads to a significant reduction or complete absence of the functional von Willebrand Factor (vWF). vWF is vital for normal blood clotting, as it plays a key role in platelet adhesion and stabilising a clotting protein known as Factor VIII. As a result, this mutation can cause serious and spontaneous bleeding episodes, even in the absence of trauma.

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