Augurin
Augurin, encoded by the CRISPLD2 gene, is a secreted protein involved in various biological processes, including cell adhesion, inflammation, and tissue development. Its precise physiological functions are still areas of ongoing research, but it is understood to play a role in regulating cellular interactions and extracellular matrix remodeling.
Biological Basis
The CRISPLD2 gene provides instructions for making the augurin protein. This protein is characterized by its cysteine-rich domains, which are common in proteins involved in cell-surface interactions and signaling pathways. As a secreted protein, augurin is believed to exert its effects by interacting with other molecules in the extracellular environment, influencing cell behavior and tissue organization. Its involvement in developmental processes suggests a fundamental role in shaping tissues and organs.
Clinical Relevance
Research has linked variations in the CRISPLD2 gene and augurin protein levels to a range of clinical conditions. These include inflammatory diseases, such as asthma and chronic obstructive pulmonary disease (COPD), where augurin may influence airway remodeling and inflammatory responses. Its role in cell adhesion and tissue development also suggests potential implications in wound healing and certain types of cancer, though further research is needed to fully elucidate these connections.
Social Importance
Understanding augurin's functions and its associations with various health conditions holds significant social importance. By clarifying its roles in inflammation and tissue development, research on augurin could contribute to the development of new diagnostic markers or therapeutic targets for diseases like asthma, COPD, and potentially certain cancers. This knowledge could ultimately lead to improved treatments and better health outcomes for affected individuals, impacting public health initiatives and personalized medicine approaches.
Methodological and Statistical Considerations
Many investigations into augurin operate with moderate sample sizes, which can limit the power to detect genetic associations with modest effect sizes, potentially leading to false negative findings . Among these, variants within genes like CFH, BCHE, LINC01322, SKIC2, and MED16 contribute to a spectrum of cellular processes, from immune regulation to gene expression, potentially influencing the molecular mechanisms underlying traits associated with "augurin" or similar complex biological phenomena.
The rs34813609 variant is associated with the CFH gene, which encodes Complement Factor H, a critical regulator of the alternative complement pathway, a part of the innate immune system. CFH functions to protect host cells from complement-mediated damage by preventing uncontrolled activation of the complement cascade. Variations in CFH can impair this regulatory function, leading to chronic inflammation and tissue injury, which has been implicated in conditions like age-related macular degeneration and atypical hemolytic uremic syndrome. Dysregulation of the complement system can also contribute to inflammation observed in cardiovascular and renal diseases, suggesting a potential link to overlapping traits within the scope of augurin. [1]
Another variant, rs11447348, is located near both the LINC01322 and BCHE genes. BCHE encodes butyrylcholinesterase, an enzyme primarily found in the plasma and liver, which metabolizes choline esters and various drugs. Genetic differences in BCHE can alter its enzymatic activity, affecting drug metabolism and potentially influencing lipid metabolism, as the enzyme has been linked to triglyceride levels in some populations. [2] LINC01322 is a long intergenic non-coding RNA, whose precise function is still being investigated, but lncRNAs are known to regulate gene expression through diverse mechanisms, potentially impacting metabolic pathways or cellular responses relevant to augurin.
Finally, the rs453821 variant is linked to SKIC2 (also known as EXOSC3), and rs35267984 is associated with MED16. SKIC2 is a core component of the exosome complex, a crucial cellular machinery responsible for RNA degradation and processing, maintaining RNA quality control and regulating gene expression. Dysfunctional RNA processing can have widespread effects on cellular physiology and development. MED16 is a subunit of the Mediator complex, a key transcriptional coactivator that bridges gene-specific regulatory proteins to RNA polymerase II, thereby controlling the transcription of nearly all protein-coding genes. [3] Variations in MED16 can thus broadly impact gene expression patterns, influencing cellular responses to stress, metabolism, and development, providing a broad mechanistic link to complex traits and their potential implications with augurin.
Defining Augurin: Conceptual Frameworks and Operational Parameters
Augurin represents a quantifiable physiological or biochemical parameter, similar to other metabolic or cardiovascular traits, whose precise definition is critical for both research and clinical application. Operational definitions specify how the trait is measured and characterized. For instance, Body Mass Index (BMI) is precisely defined as weight in kilograms divided by the square of height in meters (kg m−2). [2] Similarly, a calcified lesion, relevant in cardiovascular imaging, is defined by specific imaging characteristics, such as an area of at least three connected pixels with a CT attenuation greater than 130 Hounsfield Units. [4] The consistent application of such operational definitions, including standardized measurement protocols, is vital. For blood pressure, this involves trained personnel, specific equipment like a mercury sphygmomanometer, measurement on the right arm after a 15-minute rest in a sitting position, and the use of an average of duplicate measures to enhance reliability. [5]
Measurement approaches for augurin, as for other traits, vary widely depending on the nature of the parameter. These range from direct anthropometric measures, such as height and body weight [5] to sophisticated laboratory assays. Examples include immuno-turbidmetry for urinary albumin concentration, particle enhanced immunephelometry for Cystatin-C, and enzymatic-colorimetric methods for serum urate. [6] Rigorous quality control is paramount, evidenced by requirements for excellent intra- and inter-reader reproducibility for coronary artery calcification measurements and reported inter-assay and intra-assay coefficients of variation for biomarkers like Cystatin-C. [4] Furthermore, data often undergo transformations, such as natural log transformation for non-normally distributed traits like triglycerides, BMI, insulin, glucose, and C-reactive protein, to meet statistical assumptions for analysis. [5]
Classification Systems and Severity Grading of Augurin
Like other health-related traits, augurin can be categorized using established classification systems to delineate distinct health or disease states. This often involves setting specific thresholds that convert continuous measurements into categorical diagnoses. For example, chronic kidney disease (CKD) is defined based on criteria established by the National Kidney Foundation Kidney Disease Outcome Quality Initiative working group. [6] Similarly, hyperuricemia is defined by specific serum urate concentration thresholds, which are differentiated by sex (e.g., >7.5 mg/dl in men and >6.2 mg/dL in women). [7] Such categorical classifications are essential for clinical diagnosis, public health surveillance, and determining eligibility for interventions.
Severity gradations provide a more nuanced assessment of augurin-related conditions, enabling stratification of risk and guiding therapeutic strategies. For instance, the extent of subclinical atherosclerosis is quantified by scores such as the modified Agatston Score, applied to both coronary artery calcification (CAC) and abdominal aortic calcification (AAC). [4] This scoring system integrates the area of calcified lesions with a weighted CT attenuation score, providing a dimensional measure of disease burden. Complex conditions like the metabolic syndrome also exemplify a composite classification approach, defined by a "new world-wide definition" that integrates multiple metabolic parameters. [8] These systems allow for a spectrum of severity to be recognized, moving beyond simple presence or absence of a condition.
Measurement and Diagnostic Criteria for Augurin
Establishing robust diagnostic and measurement criteria for augurin is fundamental for both clinical identification of affected individuals and rigorous research. Clinical criteria frequently rely on specific thresholds or cut-off values. For example, the diagnosis of hyperuricemia is based on serum urate concentrations exceeding 7.5 mg/dl for men and 6.2 mg/dL for women. [7] For research purposes, criteria can also include specific exclusion conditions, such as excluding individuals who had not fasted before blood collection or those with diabetes from analyses of lipid traits. [5] These clear criteria ensure consistency in patient care and comparability across studies.
The measurement of augurin often involves a combination of direct biomarkers and derived measures. Common biomarkers include C-reactive protein, various lipid components (High-Density Lipoprotein (HDL), Low-Density Lipoprotein (LDL), triglycerides), glucose, and insulin. [5] Derived measures are also crucial for accounting for physiological variations or providing more clinically relevant indices. For instance, the ankle-brachial index (ABI) is calculated as a ratio of the average systolic blood pressure in the ankle to that in the arm [4] and the urine albumin/creatinine ratio (UACR) is used to normalize urinary albumin excretion for urine concentration. [6] Furthermore, specific adjustments to measurements, such as adding 15 mmHg to systolic blood pressure (SBP) and 10 mmHg to diastolic blood pressure (DBP) for individuals on blood pressure medication, are sometimes applied to standardize data for analysis. [5]
Nomenclature and Related Phenotypes
Standardized terminology is essential for clear communication and consistency in the study of augurin and its related phenotypes across research and clinical settings. Many physiological traits and their measurements are commonly referred to by specific abbreviations. These include Body Mass Index (BMI), Systolic Blood Pressure (SBP), Diastolic Blood Pressure (DBP), Triglycerides (TG), High-Density Lipoprotein (HDL), Low-Density Lipoprotein (LDL), Glomerular Filtration Rate (GFR), Chronic Kidney Disease (CKD), Intimal Medial Thickness (IMT), Coronary Artery Calcification (CAC), Abdominal Aortic Calcification (AAC), and Ankle Brachial Index (ABI). [5] The consistent use of these terms facilitates data exchange and understanding.
Augurin is frequently studied within a broader context of interconnected metabolic and cardiovascular phenotypes. These related concepts encompass conditions such as insulin resistance, the metabolic syndrome [9] and subclinical atherosclerosis. [4] Understanding augurin's relationship with these broader syndromes and intermediate phenotypes, which can indicate inflammation or risk for cardiovascular events, is critical for a comprehensive assessment of an individual's health. [10] The adoption of standardized vocabularies and consistent nomenclature is key to integrating findings from diverse studies and advancing the understanding of complex biological pathways.
Metabolic and Biochemical Presentation
Individuals influenced by augurin may present with a spectrum of altered metabolic and biochemical profiles, including variations in serum uric acid, lipid concentrations, and liver enzyme levels. Hyperuricemia, a common manifestation, is clinically defined by serum urate concentrations exceeding 7.5 mg/dl (450 µmol/l) in men and 6.2 mg/dL (372 µmol/l) in women, and is directly associated with an increased risk of gout. [7] Lipid profiles, including those implicated in polygenic dyslipidemia, also show significant influence, correlating with the risk of coronary artery disease. [11] Furthermore, augurin may affect plasma levels of various liver enzymes and other intermediate metabolites, which can be assessed on a continuous scale to provide detailed insights into potentially affected pathways. [12]
Assessment of these metabolic indicators typically involves collecting serum samples after a 12-hour fasting period, with participants resting for 15 minutes prior to collection. [7] Serum uric acid is measured using enzymatic-colorimetric methods, such as those from Bayer or Roche Diagnostics, or with autoanalyzers employing the uricase or phosphotungstic acid reagent methods. [7] These methods demonstrate high reliability, with intra-assay coefficients of variation as low as 0.5% and inter-assay coefficients around 1.7%. [7] Variability in these presentations can be influenced by age and sex, with distinct hyperuricemia thresholds for men and women, and population-based studies have revealed heterogeneity across different ethnic groups, such as Caucasian and African American populations. [7]
Cardiovascular and Renal Health Markers
Augurin's influence may extend to cardiovascular and renal systems, manifesting as markers of subclinical atherosclerosis and altered kidney function. A key indicator is carotid intima-media thickness (IMT), which reflects subclinical atherosclerosis and serves as a prognostic indicator for cardiovascular risk. [4] Renal function, another critical aspect, can be assessed through parameters such as creatinine clearance, which typically ranges from 80.00–140.00, with observed means around 80.63 (28.17) in various cohorts. [13] Additionally, levels of calcium and phosphorous, which are endocrine-related traits, provide further insights into renal and metabolic bone health. [6]
Objective assessment methods are crucial for these markers. Carotid IMT is precisely measured using carotid ultrasonography, employing a standardized protocol with high-resolution transducers (7.5 MHz for the common carotid artery and 5.0 MHz for the internal carotid artery) on imaging units like the Toshiba SSH-140A. [4] Calcium and phosphorous concentrations are determined using standard colorimetric methods, often with instruments from Roche Diagnostics. [6] These measurements are typically obtained at study entry and at subsequent follow-up examinations, with covariates like blood pressure, height, weight, and diabetes status adjusted for in analyses. [4] Inter-individual variability and age-sex adjusted residuals are often considered to account for phenotypic diversity and atypical presentations in diagnostic evaluations. [6]
Endocrine and Hematological Indicators
The clinical presentation of augurin may also involve a range of endocrine and hematological indicators. Endocrine traits such as thyroid-stimulating hormone (TSH), luteinizing hormone (LH), follicle-stimulating hormone (FSH), and dehydroepiandrosterone sulfate (DHEAS) can be affected, signaling potential imbalances in hormonal regulation. [6] Furthermore, augurin is correlated with variations in serum-transferrin levels, a protein involved in iron transport, and may influence hemostatic factors and other hematological phenotypes. [14] These specific protein quantitative trait loci (pQTLs) can explain a substantial portion of the genetic variation observed in these circulating protein levels. [14]
Measurement approaches for these indicators are diverse and specific. TSH levels are typically determined using chemoluminescence assays, with a lower detection limit of 0.01 mU/L. [6] DHEAS concentrations are assessed on serum samples via radioimmunoassay. [6] Hemostatic factors and other hematological phenotypes are frequently analyzed using multivariable adjusted residuals derived from comprehensive measurements. [3] These methods allow for the objective quantification of these traits, highlighting inter-individual differences and age-related changes. The diagnostic significance lies in identifying specific "red flags" or prognostic indicators within these endocrine and hematological profiles that can correlate with broader clinical phenotypes associated with augurin. [6]
Management, Treatment, and Prevention of Augurin
Effective management of augurin, a condition characterized by dysregulation of uric acid levels leading to hyperuricemia and potentially gout, involves a multifaceted approach encompassing pharmacological interventions, diligent clinical monitoring, strategies for risk reduction, and the exploration of novel therapeutic avenues. The goal is to maintain serum uric acid levels within a healthy range, prevent acute gout attacks, and mitigate long-term complications.
Pharmacological Management of Uric Acid Levels
Pharmacological treatment for conditions associated with elevated uric acid primarily relies on medications aimed at lowering serum urate concentrations. Allopurinol is considered a mainstay of treatment for gout, alongside other agents such as probenecid, benzbromarone, and colchicine, which are also prescribed for gout cases. [15] Despite its widespread use, the efficacy of allopurinol can be limited by various factors including drug dosing, patient intolerance, potential drug-drug interactions, and treatment failure, with studies indicating that only a minority of patients achieve optimal uric acid levels. [15]
The limitations of existing therapies highlight the ongoing need for improved and more effective treatment options. Newer agents like febuxostat show promise in managing uric acid levels. [15] Furthermore, the identification of genes influencing uric acid levels may pave the way for discovering novel proteins and molecular mechanisms, which could serve as targets for the development of new drugs to enhance gout treatment. [15]
Clinical Monitoring and Early Intervention
Regular monitoring of serum uric acid levels is crucial for the diagnosis and ongoing management of hyperuricemia. Hyperuricemia is clinically defined by serum urate concentrations exceeding 7.5 mg/dl (450 µmol/l) in men and 6.2 mg/dL (372 µmol/l) in women, measured using enzymatic-colorimetric methods. [7] These measurements are typically performed after a fasting period, utilizing diagnostic tools such as reagent kits and autoanalyzers. [15]
Beyond initial diagnosis, continuous monitoring is essential to assess the effectiveness of pharmacological interventions and to adjust treatment as necessary, especially given that many patients may not achieve target uric acid levels with standard treatments. [15] The emerging understanding of genetic risk factors, such as those associated with GLUT9, offers the potential for personalized medicine, where genetic risk scores could help predict an individual's response to medications or their predisposition to gout complications, including joint destruction. [15]
Preventive Strategies and Risk Reduction
Preventive strategies for conditions related to elevated uric acid focus on identifying individuals at risk and implementing early interventions to prevent the onset or progression of hyperuricemia and gout. The discovery of specific genetic loci associated with uric acid concentration and gout risk provides a powerful tool for risk stratification. [15] Such genetic insights could establish a "strong genetic risk gradient" that informs personalized medicine approaches, allowing for targeted preventive measures in individuals identified as high-risk. [15]
Early detection of hyperuricemia, based on established clinical definitions, is a primary step in risk reduction, as it allows for timely initiation of uric acid-lowering therapies before the development of symptomatic gout or its complications. [7] While the provided studies emphasize genetic associations and pharmacological treatments, these findings underscore the importance of understanding individual predispositions to guide proactive management and prevent adverse health outcomes.
Future Directions and Novel Therapies
The landscape of managing conditions related to uric acid is continuously evolving, with significant potential emerging from genetic research. The identification of genes influencing uric acid levels offers a unique opportunity to uncover novel proteins and molecular mechanisms that regulate urate homeostasis. [15] These discoveries are critical for the development of new drug targets, which could lead to more effective and personalized treatments for gout and hyperuricemia, addressing the current limitations of existing medications. [15]
Future research aims to integrate genetic risk information into clinical practice, potentially through genetic risk scores, to predict patient response to medications or susceptibility to specific gout complications. [15] This move towards personalized medicine, coupled with the development of promising novel agents like febuxostat, signifies a shift towards more tailored and effective therapeutic strategies for individuals affected by augurin. [15]
The SLC2A9 Gene and Urate Transport Biology
The SLC2A9 gene encodes the GLUT9 protein, a member of the facilitative glucose transporter family (SLC2A proteins). While initially recognized for its structural similarity to glucose transporters, GLUT9 has been definitively characterized as a crucial urate transporter, playing a central role in maintaining uric acid balance within the body. [16] This protein exhibits a highly conserved hydrophobic motif within its exofacial vestibule, a structural feature critical for determining its substrate selectivity and enabling its function as a urate anion exchanger. [16] The ability of GLUT9 to transport urate is fundamental to its physiological role, distinguishing it from other SLC2A family members primarily involved in glucose transport.
Cellular functions of GLUT9 are further influenced by molecular mechanisms such as alternative splicing, where different mRNA isoforms can lead to variations in protein structure and subsequent cellular trafficking. [16] These variations in protein isoforms can impact the efficiency and localization of GLUT9 within cells, thereby modulating its transport activity and overall contribution to uric acid homeostasis. [16] This complex regulatory network ensures that urate transport can be finely tuned, reflecting the body's dynamic metabolic needs and influencing systemic uric acid levels.
Genetic Contributions to Uric Acid Homeostasis
Genetic variations, particularly single nucleotide polymorphisms (SNPs), within the SLC2A9 gene are significant determinants of an individual's serum uric acid levels and susceptibility to conditions like gout. [15] Common nonsynonymous variants in GLUT9 have been directly associated with altered serum uric acid concentrations, highlighting the gene's critical role in genetic predisposition. [17] Beyond SLC2A9, the ABCG2 gene, which encodes an ATP-binding cassette (ABC) transporter, also harbors missense SNPs, such as rs2231142, that strongly associate with uric acid levels and gout risk. [15]
Gene expression patterns and regulatory networks play a crucial role in controlling the abundance and activity of these urate transporters. Alternative splicing, a process where a single gene can produce multiple protein isoforms, is a known mechanism that can be influenced by genetic variants and affect protein function. [18] While alternative splicing of GLUT9 is known to alter its trafficking, the impact of specific genetic variants on this process for SLC2A9 or ABCG2 in the context of uric acid regulation further illustrates the intricate genetic control over metabolic pathways. [16] These genetic mechanisms collectively contribute to the wide range of uric acid levels observed in the population, influencing individual health outcomes.
Renal Physiology and Systemic Uric Acid Homeostasis
The kidneys are the primary organs responsible for maintaining uric acid homeostasis, meticulously regulating its reabsorption and excretion to ensure stable systemic levels. [19] Both SLC2A9 (GLUT9) and ABCG2 are critically expressed in the apical membrane of human kidney proximal tubule cells, where they mediate the transport of urate. [15] The coordinated action of these and other renal transporters is essential for efficient urate handling, with SLC2A9 acting as a significant urate anion exchanger influencing blood urate levels. [20] Disruptions in this delicate balance, often due to genetic factors or environmental influences, can lead to either elevated or reduced uric acid concentrations throughout the body.
Systemic consequences of impaired renal urate regulation extend beyond the kidney itself. Uric acid circulates in the blood, and its concentration reflects the net balance between production and excretion. When renal function is compromised or transporter activity is altered, uric acid can accumulate systemically, leading to hyperuricemia. [21] This systemic dysregulation can affect various tissues and organs, contributing to broader metabolic and health issues, highlighting the interconnectedness of renal physiology with overall bodily homeostasis.
Pathophysiological Consequences of Uric Acid Dysregulation
Aberrant uric acid levels, particularly hyperuricemia, are directly implicated in several significant pathophysiological processes. Gout, a painful inflammatory arthritis, is a prime example, resulting from the crystallization of excess uric acid in joints and surrounding tissues. [15] The strong association of SLC2A9 and ABCG2 variants with both serum uric acid concentration and gout risk directly links the molecular mechanisms of urate transport to the development of this disease. [15] Understanding these genetic and molecular underpinnings is crucial for elucidating gout's etiology and identifying potential therapeutic targets.
Beyond gout, elevated uric acid levels are also recognized as a component and potential contributor to the metabolic syndrome and progressive renal disease. [21] These conditions often involve complex interactions between metabolic disruptions, inflammation, and organ damage. The presence of high uric acid can exacerbate existing conditions or contribute to their onset, emphasizing its role as a biomarker and potentially an active participant in broader systemic pathologies. [21] Therefore, maintaining optimal uric acid homeostasis is vital for preventing a spectrum of chronic health issues.
Prognostic Assessment and Risk Stratification
augurin, characterized by specific genetic variations, offers substantial prognostic value for gout development and uric acid (UA) levels. A genetic risk score, derived from high-risk alleles across loci like SLC2A9, ABCG2, and SLC17A3, demonstrates a robust risk gradient for gout, identifying individuals at significantly elevated risk long before clinical disease onset. [15] For instance, individuals with six risk alleles exhibited a gout prevalence of 8–18% across studies, a notable increase from the 1–2% observed in those with no risk alleles. [15] This one-time genetic assessment provides a stable indicator of predisposition, contrasting with the inherent variability and measurement error associated with repeated UA level measurements. [15]
The utility of augurin extends to precise risk stratification, distinguishing individuals who may benefit most from early intervention. Research has shown that a genetic risk score can be associated with up to a 40-fold increased risk of developing gout, an effect size substantially greater than many environmental risk factors. [15] Furthermore, specific gene-by-sex interactions have been identified, where variants such as rs16890979 in SLC2A9 and rs2231142 in ABCG2 differentially influence UA levels and gout risk between men and women, highlighting the potential for sex-specific risk assessment and prevention strategies. [15] This detailed understanding allows for a more granular identification of high-risk individuals within diverse populations, including Caucasian and African American participants in studies like ARIC. [15]
Guiding Personalized Clinical Management
The insights provided by augurin can directly inform clinical decision-making, particularly in tailoring personalized medicine approaches for individuals at risk of gout. Knowledge of a patient's genetic profile, or their genetic risk score, could guide the selection or avoidance of medications known to elevate uric acid levels and potentially precipitate gout. [15] While current guidelines do not typically recommend prophylaxis for asymptomatic hyperuricemia, a robust genetic risk score might identify a subset of individuals for whom early intervention could be beneficial, warranting further investigation in controlled trials. [15]
Specific genetic variants, such as the Q141K variant in ABCG2 (rs2231142), are strong candidates for elevating gout risk by approximately 70% in both white and black populations, with a more pronounced effect in men. [15] This highlights the diagnostic utility of augurin in identifying individuals who may require closer monitoring or proactive management strategies to prevent disease progression and potential complications like joint destruction. [15] The ability to predict a patient's response to existing treatments, such as allopurinol, which often fails to achieve optimal UA levels in a significant proportion of patients, remains an area of active exploration for augurin's clinical application. [15]
Uncovering Disease Mechanisms and Therapeutic Avenues
augurin provides crucial insights into the underlying molecular mechanisms influencing uric acid homeostasis and gout pathogenesis. The identified genes, SLC2A9, ABCG2, and SLC17A3, are implicated in renal urate transport, suggesting their protein products are integral to regulating UA levels. [15] This functional understanding offers promising avenues for the discovery of novel proteins and pathways involved in UA metabolism, which could lead to a more comprehensive understanding of the disease. [15]
The elucidation of these genetic mechanisms is foundational for the development of desperately needed novel drug targets to improve the treatment of gout, a debilitating form of arthritis characterized by joint pain, inflammation, and potential disability. [15] Current treatments like allopurinol face limitations including dosing challenges, intolerance, and treatment failure, underscoring the need for new therapeutic strategies. [15] Exploring how augurin might differentially associate with specific gout complications, such as the severity of joint destruction or varied responses to existing medications, represents a critical area for future research to enhance patient care. [15]
Key Variants
| RS ID | Gene | Related Traits |
|---|---|---|
| rs34813609 | CFH | insulin growth factor-like family member 3 measurement vitronectin measurement rRNA methyltransferase 3, mitochondrial measurement secreted frizzled-related protein 2 measurement Secreted frizzled-related protein 3 measurement |
| rs11447348 | LINC01322, BCHE | transmembrane protein 59-like measurement ADP-ribosylation factor-like protein 11 measurement biglycan measurement protein TMEPAI measurement histone-lysine n-methyltransferase EHMT2 measurement |
| rs453821 | SKIC2 | DNA-directed RNA polymerases I and III subunit RPAC1 measurement protein measurement pro-FMRFamide-related neuropeptide FF measurement o-acetyl-ADP-ribose deacetylase MACROD1 measurement kallikrein-6 measurement |
| rs35267984 | MED16 | interleukin-34 measurement interleukin-37 measurement interleukin-10 receptor subunit alpha measurement protein measurement C-type lectin domain family 4 member D measurement |
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