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Sports and Lifestyle
The right choice of sports activities for children and adults will let you not only achieve high results, but also protect yourself from injury. The specification in injury prediction goes as far as indicating the risk of rupture or fracture of specific ligaments or bones.
Main | Sports and Lifestyle
In professional sports, genotyping makes it possible to identify potential champions — the genetic profile of the so-called "elite athletes" is known — that is of the athletes who have the highest rank awards at world championships and the Olympics. It is also important for sports coaches to know the personal characteristics of each of the players in order to correctly distribute them on the field, this way they always know who is the fastest or hardiest, who is not afraid of stress, and who can become a hero by taking "risk" decisions.
Genotyping can also assess the likelihood of such a dramatic complication of sports activities as the sudden death of players on the field. Timely measures taken can prevent a tragic event.
Genotyping in sports
Research areas
Sistema-BioTech will let you know about the most important indicators of the state of health, the impact of training on your health.
Stress resistance
4
Injury prevention
1
2
Choice of sports
Endurance
3
Why do you need a sports genetic test?
A genetic test makes it possible to determine the direction in physical development and the sport in which a person is able to achieve the best performance. Genetic profiling in sports is indicated for adults and children. In the first case, it can be a guiding light to achieve the final goal, as well as help in planning the training process, distributing sports loads and improving current performance. In the case of children, profiling helps to determine which sport is suitable for doing professionally and which activities the child will perform well. This is also important for the internal motivation of both the child and the adult.
How does it work?
In order to pass the test, it is enough to choose the desired option and submit the biomaterial (buccal epithelium). In a few days you will receive a detailed report with recommendations.
The panel contents:
Genetic predisposition to sports injury
This test is recommended for people involved in team sports, participating in running, competitions, tournaments, races. Before starting preparations for a future sporting event, it is important to assess your strength and body reserves. The design of the genetic panel combined those genetic points, which, according to numerous scientific studies, deal with the body’s predisposition to the formation of collagen, the absorption of trace elements and a number of other specific properties, the combination of which can lead to injury.
The choice of sport — power or speed
The panel contents:
This test is recommended for those who purposefully strive for victories. Genetically, there are two types of people — some of which are predisposed to high-speed sports — running, swimming, biathlon, triathlon, tennis, football, etc. Others prone to rapid muscle gain, capable of long static loads and easy weight gaining. Both types are diametrically opposed to each other, and this tendency is taken into account by the genetic panel of sports choice. It contains the points responsible for the formation of muscle mass, the synthesis of proteins responsible for the metabolic rate, and also analyzes the gene responsible for the "impoverishment" of bone and muscle mass.
The panel contents:
Genetic Predisposition for Endurance
The gene panel takes into account the characteristics of the body in relation to the choice of sports load and an adequate response to them. This panel makes it possible to understand which category a particular genotype belongs to — "sprinters" or "wrestlers".
The panel contents:
Risk of Achilles tendinopathy
With increased sports loads associated with high activity in athletes, the risk of collagen depletion in the fibers that form muscles and tendons increases. A deficiency in the produced protein, with a corresponding mutation in the gene, indicates the necessity for taking drugs and vitamins in order to reduce this risk.
The panel contents:
Risk of anterior cruciate ligament tear
This panel analyzes 2 key genes responsible for the performance of muscle mass and ligamentous apparatus. Identification of changes in these genes with an unfavorable combination of these changes gives a high probability of injury risk at high loads. This test is indicated for athletes planning to increase their load, before a competition, or to improve their current performance. Awareness of the possible individual risks will allow you to more accurately plan your vitamin intake schedule, adjust your diet and exercise regime.
The panel contents:
Risk of femoral compression fractures
The panel analyzes three genes, one of which encodes a protein responsible for bone density. Changes in this gene can affect the quality of the protein produced by the body, and as a result, directly affect the strength or fragility of bones. The other two genes are sources of information for the production of the collagen molecule. Type I collagen is the most abundant form of collagen in the human body. A lack of this critical protein is at the root of bone fragility.
The panel contents:
Genetic predisposition to stress resistance
The genes analyzed in the panel encode proteins that are responsible for the quantity and quality of the produced hormone cortisol, one of the important components in the fight against stress and increasing endurance.
Why do you need a sports genetic test?
The duration of the research is 10 working days.
A genetic test makes it possible to determine the direction in physical development and the sport in which a person is able to achieve the best performance. Genetic profiling in sports is indicated for adults and children. In the first case, it can be a guiding light to achieve the final goal, as well as help in planning the training process, distributing sports loads and improving current performance. In the case of children, profiling helps to determine which sport is suitable for doing professionally and which activities the child will perform well. This is also important for the internal motivation of both the child and the adult.
How does it work?
In order to pass the test, it is enough to choose the desired option and submit the biomaterial (buccal epithelium). In a few days you will receive a detailed report with recommendations.
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Sistema-BioTech LLC, 109 235, Moscow, st. 1st Kuryanovskaya, 34, building 11, fl. 5
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The COL1A1 gene provides instructions for making part of a large molecule called Collagen Type I. Collagens are a family of proteins that strengthen and support many tissues in the body, including cartilage, bones, tendons, skin, and the white part of the eye (sclera). Type I collagen is the most abundant form of collagen in the human body. A lack of this critical protein is at the root of bone fragility. The gene variants probably affect the production of type I collagen, but not the structure of the molecule. Variants of changes in the gene can cause an imbalance between the expression of COL1A1 and COL1A2 proteins, which leads to instability of collagen fibers. The resulting abnormal type I collagen fibrils weaken the connective tissue, which increases the risk of tendon and ligament injuries.
Variations in the COL1A1 gene may be associated with low bone mineral density, an increased risk of osteoporosis, fractures, and degeneration of the intervertebral discs.
Variations in the COL1A1 gene may be associated with low bone mineral density, an increased risk of osteoporosis, fractures, and degeneration of the intervertebral discs.
The COL5A1 gene provides instructions for making the type V collagen component. Type V collagen regulates the width of these fibrils and controls the assembly of other types of collagen into fibrils in several tissues, and is an important structural component of tendons and other connective tissues. Gene variants can lead to inter-individual variability in fibrillogenesis, differences in mechanical properties and susceptibility of the musculoskeletal system to soft tissue injury, and differences in flexibility and endurance while running.
The presence of changes in the COL5A1 gene in humans is associated with a predisposition to chronic Achilles tendon disease, ruptures of the anterior cruciate ligament, muscle spasms connected with physical activity. This fact is important for identifying a genetic predisposition to tendopathies during active training.
The presence of changes in the COL5A1 gene in humans is associated with a predisposition to chronic Achilles tendon disease, ruptures of the anterior cruciate ligament, muscle spasms connected with physical activity. This fact is important for identifying a genetic predisposition to tendopathies during active training.
The VDR gene codes for the nuclear hormone receptor for vitamin D3. The vitamin D receptor has been found in many tissues and organs, including the gastrointestinal tract, genitourinary system, endocrine organs, and the culture of musculoskeletal cell lines. VDR regulates the expression of genes involved in a variety of biological functions, including organ development, cell cycle control, calcium and phosphate homeostasis in bone metabolism, and xenobiotic detoxification. An important role in the progression of osteoporosis is played by metabolic disorders and reduced sensitivity to vitamin D. Variations in the gene can affect the stability of the gene transcript. It is associated with an increased risk of low bone mineral density and, consequently, vertebral and non-vertebral fractures.
The TNC gene encodes the extracellular matrix protein tenascin C. Tenascin is an oligomeric glycoprotein consisting, like fibronectin, of 2 subunits connected by a disulfide bond. This molecule is also called "hexabrachion", since it has 6 "arms" extending radially from one site. Due to this structure, tenascin can interact with a large number of ligands, which include various extracellular matrix molecules. In mature tissues, small amounts of tenascin are found in tendons and cartilage, and its synthesis is increased in healing wounds. In normal ligaments of adults, tenascin is most actively expressed at the sites of application of physical activity — muscle-tendon and tendon-bone junctions. This protein is also expressed around the cells and collagen fibers of the Achilles tendon.
The COL1A1 gene provides instructions for making part of a large molecule called Collagen Type I. Collagens are a family of proteins that strengthen and support many tissues in the body, including cartilage, bones, tendons, skin, and the white part of the eye (sclera). Type I collagen is the most abundant form of collagen in the human body. A lack of this critical protein is at the root of bone fragility. The gene variants probably affect the production of type I collagen, but not the structure of the molecule. Variants of changes in the gene can cause an imbalance between the expression of COL1A1 and COL1A2 proteins, which leads to instability of collagen fibers. The resulting abnormal type I collagen fibrils weaken the connective tissue, which increases the risk of tendon and ligament injuries.
Variations in the COL1A1 gene may be associated with low bone mineral density, an increased risk of osteoporosis, fractures, and degeneration of the intervertebral discs.
Variations in the COL1A1 gene may be associated with low bone mineral density, an increased risk of osteoporosis, fractures, and degeneration of the intervertebral discs.
The COL5A1 gene provides instructions for making the type V collagen component. Type V collagen regulates the width of these fibrils and controls the assembly of other types of collagen into fibrils in several tissues, and is an important structural component of tendons and other connective tissues. Gene variants can lead to inter-individual variability in fibrillogenesis, differences in mechanical properties and susceptibility of the musculoskeletal system to soft tissue injury, and differences in flexibility and endurance while running.
The presence of changes in the COL5A1 gene in humans is associated with a predisposition to chronic Achilles tendon disease, ruptures of the anterior cruciate ligament, muscle spasms connected with physical activity. This fact is important for identifying a genetic predisposition to tendopathies during active training.
The presence of changes in the COL5A1 gene in humans is associated with a predisposition to chronic Achilles tendon disease, ruptures of the anterior cruciate ligament, muscle spasms connected with physical activity. This fact is important for identifying a genetic predisposition to tendopathies during active training.
The VDR gene codes for the nuclear hormone receptor for vitamin D3. The vitamin D receptor has been found in many tissues and organs, including the gastrointestinal tract, genitourinary system, endocrine organs, and the culture of musculoskeletal cell lines. VDR regulates the expression of genes involved in a variety of biological functions, including organ development, cell cycle control, calcium and phosphate homeostasis in bone metabolism, and xenobiotic detoxification. An important role in the progression of osteoporosis is played by metabolic disorders and reduced sensitivity to vitamin D. Variations in the gene can affect the stability of the gene transcript. It is associated with an increased risk of low bone mineral density and, consequently, vertebral and non-vertebral fractures.
The TNC gene encodes the extracellular matrix protein tenascin C. Tenascin is an oligomeric glycoprotein consisting, like fibronectin, of 2 subunits connected by a disulfide bond. This molecule is also called "hexabrachion", since it has 6 "arms" extending radially from one site. Due to this structure, tenascin can interact with a large number of ligands, which include various extracellular matrix molecules. In mature tissues, small amounts of tenascin are found in tendons and cartilage, and its synthesis is increased in healing wounds. In normal ligaments of adults, tenascin is most actively expressed at the sites of application of physical activity - muscle-tendon and tendon-bone junctions. This protein is also expressed around the cells and collagen fibers of the Achilles tendon.
The ACE gene encodes an angiotensin-converting enzyme (ACE) that catalyzes the breakdown of angiotensin I into the physiologically active peptide angiotensin II. Angiotensin II is a powerful vasopressor and aldosterone-stimulating peptide that controls blood pressure and fluid and electrolyte balance. ACE also inactivates the vasodilator protein bradykinin. Accordingly, the encoded enzyme increases blood pressure. It has been established that individuals with the I/I genotype of the ACE gene are characterized by a higher relative content of slow fibers and a low content of fast fibers compared to those with the D/D genotype. "Slow" muscle fibers contract slowly, tire slowly, anaerobic glycolysis predominates. Variations in the gene are associated with the development of speed, strength and muscle mass.
The AGT gene encodes angiotensinogen. This protein is expressed in the liver and is cleaved by the enzyme renin in response to a decrease in blood pressure. The resulting product, angiotensin I, is then cleaved by the angiotensinogen-converting enzyme (ACE) to the physiologically active enzyme angiotensin II. This protein is involved in maintaining blood pressure, in the pathogenesis of hypertension. Gene variations are associated with higher plasma angiotensinogen levels, which consequently can lead to higher blood pressure and a predisposition to increased levels of strength and speed.
PPARG is an important nuclear transcription factor involved in the regulation of glucose and lipid metabolism, as well as ovarian steroidogenesis. It regulates energy balance and enhances insulin sensitivity. The carriage of the G allele is associated with a decrease in the activity of the PPARγ2 receptor isoform. The consequence of this is the suppression of lipolysis in adipocytes and a decrease in the level of circulating fatty acids. Variations in the PPARG gene are associated with high values of BMI in athletes, maximum voluntary strength (MPS), and its increase in response to exercise.
The ACTN3 gene encodes a member of the gene family that binds alpha-actin proteins. The encoded protein is mainly expressed in skeletal muscle and functions as a structural component of the sarcomeric Z-line. This protein is involved in the cross-linking of actin containing thin filaments. Deficiency of alpha-actinin-3 protein is observed in various forms of muscular dystrophy. Variations in the gene are associated with greater muscle damage and the need for longer recovery from hard exercise and reduced skeletal muscle speed.
The ACE gene encodes an angiotensin-converting enzyme (ACE) that catalyzes the breakdown of angiotensin I into the physiologically active peptide angiotensin II. Angiotensin II is a powerful vasopressor and aldosterone-stimulating peptide that controls blood pressure and fluid and electrolyte balance. ACE also inactivates the vasodilator protein bradykinin. Accordingly, the encoded enzyme increases blood pressure. It has been established that individuals with the I/I genotype of the ACE gene are characterized by a higher relative content of slow fibers and a low content of fast fibers compared to those with the D/D genotype. "Slow" muscle fibers contract slowly, tire slowly, anaerobic glycolysis predominates. Variations in the gene are associated with the development of speed, strength and muscle mass.
The AGT gene encodes angiotensinogen. This protein is expressed in the liver and is cleaved by the enzyme renin in response to a decrease in blood pressure. The resulting product, angiotensin I, is then cleaved by the angiotensinogen-converting enzyme (ACE) to the physiologically active enzyme angiotensin II. This protein is involved in maintaining blood pressure, in the pathogenesis of hypertension. Gene variations are associated with higher plasma angiotensinogen levels, which consequently can lead to higher blood pressure and a predisposition to increased levels of strength and speed.
PPARG is an important nuclear transcription factor involved in the regulation of glucose and lipid metabolism, as well as ovarian steroidogenesis. It regulates energy balance and enhances insulin sensitivity. The carriage of the G allele is associated with a decrease in the activity of the PPARγ2 receptor isoform. The consequence of this is the suppression of lipolysis in adipocytes and a decrease in the level of circulating fatty acids. Variations in the PPARG gene are associated with high values of BMI in athletes, maximum voluntary strength (MPS), and its increase in response to exercise.
The ACTN3 gene encodes a member of the gene family that binds alpha-actin proteins. The encoded protein is mainly expressed in skeletal muscle and functions as a structural component of the sarcomeric Z-line. This protein is involved in the cross-linking of actin containing thin filaments. Deficiency of alpha-actinin-3 protein is observed in various forms of muscular dystrophy. Variations in the gene are associated with greater muscle damage and the need for longer recovery from hard exercise and reduced skeletal muscle speed.
The ACE gene encodes an angiotensin-converting enzyme (ACE) that catalyzes the breakdown of angiotensin I into the physiologically active peptide angiotensin II. Angiotensin II is a powerful vasopressor and aldosterone-stimulating peptide that controls blood pressure and fluid and electrolyte balance. ACE also inactivates the vasodilator protein bradykinin. Accordingly, the encoded enzyme increases blood pressure. It has been established that individuals with the I/I genotype of the ACE gene are characterized by a higher relative content of slow fibers and a low content of fast fibers compared to those with the D/D genotype. "Slow" muscle fibers contract slowly, tire slowly, anaerobic glycolysis predominates. Variations in the gene are associated with the development of speed, strength and muscle mass.
The NOS3 gene is a candidate for explaining individual differences in health and exercise-related phenotypes. The frequency of the TT genotype is significantly higher in strength athletes. The NOS3 gene variation is associated with elite performance in power sports competitions (throwing, jumping, sprinting), and the T allele has a positive effect. The mechanism by which this allele variant may improve power performance is still to be elucidated.
The PPARA gene encodes the PPAR-alpha subtype, which is a nuclear transcription factor. The main function of the PPARα protein is the regulation of lipid metabolism, glucose and energy homeostasis, as well as body weight through the regulation of the expression of genes involved in peroxisomal and mitochondrial oxidation. During aerobic exercise, an increase in the utilization of fatty acids (FA) occurs due to an increase in the expression of the PPARA gene and the cascade of genes regulated by it, which ultimately improves the oxidative capacity of skeletal muscles. With low expression of the PPARA gene, the ability of tissues to efficiently β-oxidize FAs decreases, and tissue metabolism switches to the glycolytic method of obtaining energy. Overexpression of the PPARA gene leads to a decrease in glucose utilization and an increase in FA oxidation. In a group of Russian athletes there has been found a relationship between the PPARA gene variant and the risk of developing LVMH. It is more common in athletes involved in sports with the manifestation of mixed qualities of variable power.
The ACE gene encodes an angiotensin-converting enzyme (ACE) that catalyzes the breakdown of angiotensin I into the physiologically active peptide angiotensin II. Angiotensin II is a powerful vasopressor and aldosterone-stimulating peptide that controls blood pressure and fluid and electrolyte balance. ACE also inactivates the vasodilator protein bradykinin. Accordingly, the encoded enzyme increases blood pressure. It has been established that individuals with the I/I genotype of the ACE gene are characterized by a higher relative content of slow fibers and a low content of fast fibers compared to those with the D/D genotype. "Slow" muscle fibers contract slowly, tire slowly, anaerobic glycolysis predominates. Variations in the gene are associated with the development of speed, strength and muscle mass.
The NOS3 gene is a candidate for explaining individual differences in health and exercise-related phenotypes. The frequency of the TT genotype is significantly higher in strength athletes. The NOS3 gene variation is associated with elite performance in power sports competitions (throwing, jumping, sprinting), and the T allele has a positive effect. The mechanism by which this allele variant may improve power performance is still to be elucidated.
The PPARA gene encodes the PPAR-alpha subtype, which is a nuclear transcription factor. The main function of the PPARα protein is the regulation of lipid metabolism, glucose and energy homeostasis, as well as body weight through the regulation of the expression of genes involved in peroxisomal and mitochondrial oxidation. During aerobic exercise, an increase in the utilization of fatty acids (FA) occurs due to an increase in the expression of the PPARA gene and the cascade of genes regulated by it, which ultimately improves the oxidative capacity of skeletal muscles. With low expression of the PPARA gene, the ability of tissues to efficiently β-oxidize FAs decreases, and tissue metabolism switches to the glycolytic method of obtaining energy. Overexpression of the PPARA gene leads to a decrease in glucose utilization and an increase in FA oxidation. In a group of Russian athletes there has been found a relationship between the PPARA gene variant and the risk of developing LVMH. It is more common in athletes involved in sports with the manifestation of mixed qualities of variable power.
The TNC gene encodes the extracellular matrix protein tenascin C. Tenascin is an oligomeric glycoprotein, which, similarly to fibronectin, consists of 2 subunits connected by a disulfide bond. This molecule is also called "hexabrachion", since it has 6 "arms" extending radially from one site. Due to this structure, tenascin can interact with a large number of ligands, which include various molecules of the extracellular matrix. In mature tissues, small amounts of tenascin are found in tendons and cartilage, and its synthesis is increased in healing wounds. In normal ligaments of adults, tenascin is most actively expressed at the sites of application of physical activity — muscle-tendon and tendon-bone junctions. This protein is also expressed around the cells and collagen fibers of the Achilles tendon. Variations in the gene are associated with an increased risk of developing Achilles tendinopathy.
The MMP3 gene encodes a protein from the matrix metalloproteinase (MMP) family that is involved in the destruction of the extracellular matrix in normal physiological processes such as embryonic development, tissue reproduction and remodeling, as well as disease processes such as arthritis and metastasis. Most MMPs are secreted as inactive proproteins, which are activated upon cleavage by extracellular proteinases. This gene encodes an enzyme that degrades fibronectin, laminin, collagens III, IV, IX, and X, and cartilage proteoglycans. Variations in the MMP3 gene are associated with the risk of developing Achilles tendinopathy.
The COL5A1 gene encodes a component of type V collagen. Type V collagen regulates the width of these fibrils and controls the assembly of other types of collagen into fibrils in several tissues, and is an important structural component of tendons and other connective tissues. Gene variants can lead to inter-individual variability in fibrillogenesis, differences in mechanical properties and susceptibility of the musculoskeletal system to soft tissue injury, and differences in flexibility and endurance while running. The presence of variations in the COL5A1 gene in humans is associated with a predisposition to chronic Achilles tendon disease, ruptures of the anterior cruciate ligament, muscle spasms connected with physical activity. This fact is important for identifying a genetic predisposition to tendopathies during active training.
The TNC gene encodes the extracellular matrix protein tenascin C. Tenascin is an oligomeric glycoprotein, which, similarly to fibronectin, consists of 2 subunits connected by a disulfide bond. This molecule is also called "hexabrachion", since it has 6 "arms" extending radially from one site. Due to this structure, tenascin can interact with a large number of ligands, which include various molecules of the extracellular matrix. In mature tissues, small amounts of tenascin are found in tendons and cartilage, and its synthesis is increased in healing wounds. In normal ligaments of adults, tenascin is most actively expressed at the sites of application of physical activity — muscle-tendon and tendon-bone junctions. This protein is also expressed around the cells and collagen fibers of the Achilles tendon. Variations in the gene are associated with an increased risk of developing Achilles tendinopathy.
The MMP3 gene encodes a protein from the matrix metalloproteinase (MMP) family that is involved in the destruction of the extracellular matrix in normal physiological processes such as embryonic development, tissue reproduction and remodeling, as well as disease processes such as arthritis and metastasis. Most MMPs are secreted as inactive proproteins, which are activated upon cleavage by extracellular proteinases. This gene encodes an enzyme that degrades fibronectin, laminin, collagens III, IV, IX, and X, and cartilage proteoglycans. Variations in the MMP3 gene are associated with the risk of developing Achilles tendinopathy.
The COL5A1 gene encodes a component of type V collagen. Type V collagen regulates the width of these fibrils and controls the assembly of other types of collagen into fibrils in several tissues, and is an important structural component of tendons and other connective tissues. Gene variants can lead to inter-individual variability in fibrillogenesis, differences in mechanical properties and susceptibility of the musculoskeletal system to soft tissue injury, and differences in flexibility and endurance while running. The presence of variations in the COL5A1 gene in humans is associated with a predisposition to chronic Achilles tendon disease, ruptures of the anterior cruciate ligament, muscle spasms connected with physical activity. This fact is important for identifying a genetic predisposition to tendopathies during active training.
The MMP3 gene encodes a protein from the matrix metalloproteinase (MMP) family that is involved in the destruction of the extracellular matrix in normal physiological processes such as embryonic development, tissue reproduction and remodeling, as well as disease processes such as arthritis and metastasis. Most MMPs are secreted as inactive proproteins, which are activated upon cleavage by extracellular proteinases. This gene encodes an enzyme that degrades fibronectin, laminin, collagens III, IV, IX, and X, and cartilage proteoglycans. Variations in the MMP3 gene are associated with the risk of anterior cruciate ligament tear.
The COL1A1 gene provides instructions for making part of a large molecule called Collagen Type I. Collagens are a family of proteins that strengthen and support many tissues in the body, including cartilage, bones, tendons, skin, and the white part of the eye (sclera). Type I collagen is the most abundant form of collagen in the human body. A lack of this critical protein is at the root of bone fragility. The gene variants probably affect the production of type I collagen, but not the structure of the molecule. Variants of changes in the gene can cause an imbalance between the expression of COL1A1 and COL1A2 proteins, which leads to instability of collagen fibers. The resulting abnormal type I collagen fibrils weaken the connective tissue, which increases the risk of tendon and ligament injuries. Variations in the COL1A1 gene are associated with an increased risk of anterior cruciate ligament tear.
The MMP3 gene encodes a protein from the matrix metalloproteinase (MMP) family that is involved in the destruction of the extracellular matrix in normal physiological processes such as embryonic development, tissue reproduction and remodeling, as well as disease processes such as arthritis and metastasis. Most MMPs are secreted as inactive proproteins, which are activated upon cleavage by extracellular proteinases. This gene encodes an enzyme that degrades fibronectin, laminin, collagens III, IV, IX, and X, and cartilage proteoglycans. Variations in the MMP3 gene are associated with the risk of anterior cruciate ligament tear.
The COL1A1 gene provides instructions for making part of a large molecule called Collagen Type I. Collagens are a family of proteins that strengthen and support many tissues in the body, including cartilage, bones, tendons, skin, and the white part of the eye (sclera). Type I collagen is the most abundant form of collagen in the human body. A lack of this critical protein is at the root of bone fragility. The gene variants probably affect the production of type I collagen, but not the structure of the molecule. Variants of changes in the gene can cause an imbalance between the expression of COL1A1 and COL1A2 proteins, which leads to instability of collagen fibers. The resulting abnormal type I collagen fibrils weaken the connective tissue, which increases the risk of tendon and ligament injuries. Variations in the COL1A1 gene are associated with an increased risk of anterior cruciate ligament tear.
The COL1A1 gene provides instructions for making part of a large molecule called Collagen Type I. Collagens are a family of proteins that strengthen and support many tissues in the body, including cartilage, bones, tendons, skin, and the white part of the eye (sclera). Type I collagen is the most abundant form of collagen in the human body. A lack of this critical protein is at the root of bone fragility. Variations in the gene are associated with an increased risk of femoral compression fractures.
The COL1A2 gene encodes the pro-alpha2 type I collagen, the triple helix of which consists of two alpha1 chains and one alpha2 chain. Variations in the gene are associated with an increased risk of femoral compression fractures.
The LRP5 gene encodes a protein (transmembrane low density lipoprotein receptor) involved in bone homeostasis. Variations are associated with lower bone mineral density, which is a risk for developing femoral compression fractures.
The COL1A1 gene provides instructions for making part of a large molecule called Collagen Type I. Collagens are a family of proteins that strengthen and support many tissues in the body, including cartilage, bones, tendons, skin, and the white part of the eye (sclera). Type I collagen is the most abundant form of collagen in the human body. A lack of this critical protein is at the root of bone fragility. Variations in the gene are associated with an increased risk of femoral compression fractures.
The COL1A2 gene encodes the pro-alpha2 type I collagen, the triple helix of which consists of two alpha1 chains and one alpha2 chain. Variations in the gene are associated with an increased risk of femoral compression fractures.
The LRP5 gene encodes a protein (transmembrane low density lipoprotein receptor) involved in bone homeostasis. Variations are associated with lower bone mineral density, which is a risk for developing femoral compression fractures.
The FKBP5 gene encodes a chaperone protein that regulates glucocorticoid receptor (GR) sensitivity. When FKBP5 binds to GR, it reduces the receptor’s affinity for cortisol and decreases its trafficking into the nucleus. This protein significantly reduces the production of cortisol. It mediates the inhibition of calcineurin. It also functionally interacts with the progensterone receptor. Variations in the FKBP5 gene are associated with insufficient cortisol recovery, increased anxiety, and decreased stress resistance.
The HTR1A gene encodes the 5-hydroxytryptamine (serotonin) receptor, which belongs to the family of transmembrane metabotropic G-protein-coupled receptors and is associated with a heterotrimeric inhibitory G-protein. Variations in the gene lead to an increase in the number of autoreceptors and, accordingly, to the 5-HT signal weakening, an increased level of anxiety, and a decrease in the level of stress tolerance.
The FKBP5 gene encodes a chaperone protein that regulates glucocorticoid receptor (GR) sensitivity. When FKBP5 binds to GR, it reduces the receptor’s affinity for cortisol and decreases its trafficking into the nucleus. This protein significantly reduces the production of cortisol. It mediates the inhibition of calcineurin. It also functionally interacts with the progensterone receptor. Variations in the FKBP5 gene are associated with insufficient cortisol recovery, increased anxiety, and decreased stress resistance.
The HTR1A gene encodes the 5-hydroxytryptamine (serotonin) receptor, which belongs to the family of transmembrane metabotropic G-protein-coupled receptors and is associated with a heterotrimeric inhibitory G-protein. Variations in the gene lead to an increase in the number of autoreceptors and, accordingly, to the 5-HT signal weakening, an increased level of anxiety, and a decrease in the level of stress tolerance.