Growth Regulated Alpha Protein

Introduction

Growth regulated alpha protein (GROα), also known as CXCL1, is a small signaling protein belonging to the CXC chemokine family. Chemokines are critical mediators of immune responses, primarily functioning to attract immune cells, such as neutrophils, to specific locations in the body. GROα plays a multifaceted role in biological processes, including inflammation, cell proliferation, angiogenesis (the formation of new blood vessels), and tissue repair. Understanding the factors that influence GROα levels is important as they can serve as indicators for various physiological and pathological conditions.

Biological Basis

At a molecular level, GROα functions as a potent chemoattractant, guiding neutrophils to sites of inflammation or injury by binding to specific receptors on their surface. The levels of GROα in circulation can be influenced by genetic variations. For example, the single nucleotide polymorphism (SNP)rs12075 , located on chromosome 1q23.2, has been identified in genome-wide association studies as significantly associated with the concentration of GROα. This variant resides within the ACKR1 gene, which encodes the Atypical Chemokine Receptor 1. ACKR1 is known to bind multiple cytokines and also functions as the Duffy antigen, a human erythrocyte blood group antigen. The association between rs12075 and GROα levels suggests that this genetic variant may affect how GROα interacts with the ACKR1 receptor, thereby impacting its availability and function in the bloodstream.^[1]

Clinical Relevance

Fluctuations in GROα levels carry significant clinical implications. As a pro-inflammatory chemokine, elevated GROα concentrations are frequently observed in various inflammatory conditions, infectious diseases, and certain types of cancer. Investigating the genetic determinants of GROα levels, such as thers12075 variant, can offer valuable insights into individual susceptibility to these diseases. This understanding may also pave the way for more personalized treatment approaches. For instance, genetic variations that alter the binding of GROα to receptors like ACKR1could modulate the body’s inflammatory response, potentially influencing disease progression or severity.

Social Importance

The study of proteins like GROα and their genetic underpinnings is of considerable social importance. By identifying specific genetic variants that influence protein concentrations, researchers can gain a deeper understanding of the fundamental biological mechanisms driving various diseases, especially those involving inflammation and immune system dysfunction. This knowledge is crucial for advancing the development of novel diagnostic tools, prognostic markers, and targeted therapeutic interventions. Furthermore, comprehending how genetic background influences protein expression can help explain observed differences in disease prevalence and treatment responses across diverse populations, contributing to more effective and equitable healthcare strategies.

Methodological and Statistical Constraints

The interpretation of findings regarding growth regulated alpha protein is subject to several methodological and statistical limitations. Many studies, particularly those focused on polygenic scores (PGS) or heritability estimates, face challenges due to still limited sample sizes, which can diminish statistical power and lead to the exclusion of proteins with low heritability estimates . This suggests thatrs12075 can directly modulate GROa levels by influencing receptor-ligand interactions, impacting immune cell recruitment and inflammatory responses. While the variant rs2814778 in the nearby CADM3-AS1 region is also implicated in genetic regulation, its precise mechanism concerning GROa levels requires further elucidation.^[2] The CXCL1 gene itself, which encodes GROa, is a central player in inflammation and tissue repair, and its expression is tightly regulated by a complex interplay of genetic factors. Variants such as rs3117604 , rs115711101 , and rs3117600 in the PF4V1-CXCL1 region, or rs116152597 , rs2115691 , and rs3097412 within the CXCL1-HNRNPA1P55 locus, can influence CXCL1 transcription or mRNA stability, thereby modulating GROa production.^[3] Similarly, variants like rs614822 , rs138657097 , and rs569108954 in the CXCL1P1-PF4 region may affect CXCL1 levels through mechanisms involving the CXCL1 pseudogene (CXCL1P1) or the platelet factor 4 (PF4) gene, both of which are located in close proximity and can interact in a regulatory network.^[4] Another related chemokine, CXCL2, also known as GROb, is influenced by variants like rs6811077 in the PPBPP2-CXCL2 region, which can contribute to the overall chemokine milieu and indirectly affect GROa-mediated processes.

Beyond direct chemokine regulation, other genetic loci also contribute to the intricate network that influences protein levels. The rs1246397 variant, associated with the AREG-BTC region, involves growth factors amphiregulin (AREG) and betacellulin (BTC), which are crucial for cell proliferation and tissue repair, and their altered levels can indirectly impact the broader growth factor environment, including GROa.^[5] Variants like rs13131508 in the AFP-AFM region, involving alpha-fetoprotein (AFP) and afamin (AFM), which are plasma proteins involved in transport and antioxidant functions, may also reflect systemic physiological states that influence cytokine levels. Furthermore, variants in genes involved in metabolism, such asrs491641 , rs189986015 , and rs75078633 in MTHFD2L (encoding methylenetetrahydrofolate dehydrogenase 2 like), or epigenetic regulation, such as rs7088799 in JMJD1C (encoding Jumonji C domain-containing protein 1C), can broadly affect cellular health and inflammatory responses, indirectly modulating GROa production.^[6] The immune-related HLA-DRB6 gene, with variant rs35467127 , is part of the major histocompatibility complex (MHC) and plays a role in immune recognition; variations here can influence the immune system’s baseline activity and inflammatory potential, thus indirectly affecting growth factor levels like GROa.

Defining Growth Regulated Alpha Protein

The of growth regulated alpha protein refers to the quantitative assessment of this specific protein’s concentration within biological fluids, primarily plasma. This process involves precise laboratory techniques to determine the abundance of the protein, which is considered a component of the broader “plasma proteome” or “circulating proteins”.^[4] Operational definitions for such measurements commonly include several key steps to ensure data quality and comparability. These steps encompass the initial sample collection and handling, the application of standardized quantification platforms such as those certified by SomaLogic Inc. or using the OLINK method, and subsequent data processing.^{[2], [4]} Further operational refinements involve data transformations, such as natural logarithm, log10, or inverse-normalization, to achieve a more normal distribution of protein levels, which is crucial for statistical analyses.^{[2], [4], [6], [7]}Additionally, measured protein levels are typically adjusted for various covariates, including age, sex, body mass index, genetic principal components reflecting ancestry, and technical factors like protein analysis batch or duration between blood draw and processing.^{[2], [4], [6], [7], [8]}These adjustments aim to minimize confounding factors and isolate the specific variability attributable to genetic or environmental influences on the protein’s concentration.

Classification of Genetic Influences on Protein Levels

Growth regulated alpha protein, like other circulating proteins, can be categorized based on the genetic factors that influence its levels. A primary classification system in this context is the concept of “protein quantitative trait loci” (pQTLs), which are genomic regions associated with variations in protein abundance.^[4] These pQTLs are further subtyped into “cis-pQTLs” and “trans-pQTLs” based on their genomic proximity to the gene encoding the measured protein.^{[4], [7], [8]} Cis-pQTLs are genetic variants located within a defined distance, often 1 megabase (Mb) upstream or downstream, of the gene that codes for the protein, implying a direct, local regulatory effect.^{[7], [8]} In contrast, trans-pQTLs are genetic variants situated on different chromosomes or at a greater distance from the protein-coding gene, suggesting more complex, indirect regulatory mechanisms, such as influencing transcription factors or other intermediary proteins.^[4]The identification and classification of cis- and trans-pQTLs for proteins like growth regulated alpha protein are crucial for understanding the genetic architecture of the proteome and for elucidating regulatory pathways, offering insights into potential causal relationships between genetic variations, protein levels, and disease endpoints through approaches like Mendelian randomization.^[4]

Criteria and Standardized Terminology

The accurate and reproducible of growth regulated alpha protein relies on stringent diagnostic and criteria, alongside standardized terminology. Key terms include “protein ,” which is recognized within standardized vocabularies such as the Experimental Factor Ontology (EFO) as “EFO_0004747”.^[6] Quality control (QC) is integral to these measurements, with criteria often including the exclusion of individual assays where a significant percentage of samples fall below the lower detection limit or where inter-plate coefficients of variation exceed established thresholds.^{[1], [4]} These rigorous QC steps ensure the reliability of the quantitative data.

Furthermore, the statistical analysis of protein levels employs specific criteria for identifying significant associations with genetic variants. This includes the application of statistical models, such as linear regression, after appropriate data transformations and covariate adjustments.^{[2], [4], [6]} Significance thresholds, such as Bonferroni-adjusted P-values (e.g., 3.8 × 10−11 for discovery or 1.08 × 10−4 for replication), are applied to account for multiple comparisons in genome-wide association studies (GWAS), ensuring that reported associations for protein levels are statistically robust.^{[2], [8], [9]}

Molecular Identity and Cellular Role of GROa

Growth regulated alpha protein (GROa), also known as Chemokine (C-X-C motif) Ligand 1 (CXCL1), functions as a cytokine, a type of signaling protein involved in cell-to-cell communication.^[1] As an oncogene-alpha, GROa plays a role in various cellular processes, including inflammation and immune responses. These proteins are typically secreted by cells to exert their effects on target cells, often by binding to specific receptors on the cell surface.^[6] The of such secreted proteins, along with membrane and intracellular proteins, provides insights into cellular functions and regulatory networks.^[7] A key interaction for GROa involves the ACKR1 receptor, which is encoded by a gene located at 1q23.2.^[1] ACKR1 serves as a receptor for multiple cytokines and is also recognized as a human erythrocyte blood group antigen.^[1] The binding of GROa to ACKR1 can modulate its circulating levels and signaling activity, influencing downstream molecular and cellular pathways. This receptor interaction highlights GROa’s involvement in complex biological networks that regulate immune surveillance and other physiological processes.

Genetic Determinants of GROa Levels

The concentration of growth regulated alpha protein in the body is significantly influenced by genetic factors, with specific genetic variants (SNPs) acting as protein quantitative trait loci (pQTLs).^[4] These pQTLs can be classified as cis-pQTLs, located near the gene coding for the protein, or trans-pQTLs, located further away and often affecting regulatory pathways that indirectly influence protein levels.^[9] For GROa, the genetic variant rs12075 has been identified as significantly associated with its circulating levels, alongside other cytokines like eotaxin and MCP1.^[1] The variant rs12075 is situated within the ACKR1 gene, suggesting that its influence on GROa levels is mediated through altered binding of cytokines, including GROa, to the ACKR1 receptor.^[1] This genetic mechanism can impact the availability and activity of GROaby modifying receptor affinity or expression, thereby affecting the protein’s overall concentration. Genetic variants can also influence protein levels directly by altering gene expression or indirectly by changing the protein’s structure, which might affect its stability, function, or even its detection by assays (an “epitope effect”).^[3] Understanding these genetic mechanisms is crucial for deciphering regulatory check-points that determine biomarker concentrations.^[4]

Systemic Context and Clinical Relevance of GROa

As a circulating cytokine, growth regulated alpha protein serves as a biomarker, providing insights into systemic biological states and pathophysiological processes.^[4] The of proteins like GROain plasma, cerebrospinal fluid, or tissue offers a window into the body’s homeostatic balance and potential disruptions. The platform used for protein quantification covers a wide range of proteins, including those relevant to human diseases such as neurodegenerative and cardiovascular conditions, reflecting the broad utility of proteomic analysis in biomarker discovery.^[7]The study of pQTLs, particularly trans-pQTLs, can reveal previously unknown regulatory pathways and establish causal relationships between protein biomarkers and disease risk through methods like Mendelian randomization.^[4] For a protein like GROa, which is implicated in cellular signaling and inflammation, its systemic levels can reflect ongoing physiological or pathological processes across various tissues and organs. Understanding the genetic and environmental factors that govern GROalevels can therefore provide valuable insights into disease mechanisms and potential therapeutic targets.^[4]

Genetic Control of Protein Abundance

The circulating levels of growth-regulated alpha protein are substantially influenced by genetic factors, with protein quantitative trait loci (pQTLs) playing a pivotal role in determining its plasma concentration.^[2]These genetic variations, including single nucleotide polymorphisms (SNPs), can exert their effects through bothcis- and trans-mechanisms. Cis-pQTLs are typically located within 1 Mb upstream or downstream of the gene encoding the protein, directly affecting its expression, transcription, or stability.^[7] In contrast, trans-pQTLs influence protein levels indirectly, often by regulating an intermediary gene or pathway that then impacts the target protein.^[4] This genetic control over protein levels, observed across a significant portion of the human proteome, underscores the importance of an individual’s genetic makeup in shaping their protein landscape.^[2] Understanding these genetic determinants is crucial for elucidating the mechanisms of post-transcriptional gene regulation and how genetic variation translates into observable differences in protein abundance.^[7] For instance, specific SNPs linked to protein levels have been identified within transcription factor binding sites and DNase hypersensitivity peaks, indicating a direct impact on gene expression.^[1] The ability of trans-pQTLs to uncover previously unknown regulatory pathways, based on in-vivo human observations, provides valuable insights into the causal flow from genetic variants to protein concentrations.^[4]

Receptor-Mediated Signaling and Intracellular Cascades

Growth-regulated alpha protein, as a chemokine, engages in specific signaling pathways primarily through its interactions with cellular receptors. A notable example involves the atypical chemokine receptorACKR1, also known as DARC, which is known to bind to various cytokines including growth-regulated oncogene-a (GROa).^[1] Genetic variants, such as rs12075 located within the ACKR1 gene, have been associated with altered levels of GROa, suggesting that variations in receptor function can influence the availability or clearance of the protein.^[1] This interaction implies a mechanism where receptor binding can modulate the circulating concentration of GROa, potentially through sequestration, internalization, or altered turnover rates.

Beyond direct receptor binding, the effects of proteins like GROa often propagate through intracellular signaling cascades, such as the mitogen-activated protein kinase (MAPK) cascade, a pathway extensively involved in cellular growth, differentiation, and stress responses.^[7] The identification of pQTLs for components like MAP2K4 (Dual specificity mitogen-activated protein kinase kinase 4) suggests that genetic variations can affect these downstream signaling elements.^[2]Such impacts could alter the cellular response to growth-regulated alpha protein, or influence its synthesis and release, ultimately contributing to the observed plasma levels.

Transcriptional and Post-Transcriptional Regulatory Mechanisms

The regulation of growth-regulated alpha protein levels encompasses sophisticated transcriptional and post-transcriptional control mechanisms that fine-tune its expression. Gene regulation, often modulated by genetic variants residing in regulatory regions, dictates the efficiency with which theGROa gene is transcribed into messenger RNA (mRNA).^[1] Following transcription, a complex array of post-transcriptional processes, including mRNA stability, translation efficiency, and regulated protein degradation, further determines the final protein concentration within cells and in circulation.^[7] Understanding these tissue-specific genetic controls is essential for uncovering the intricate details of post-transcriptional gene regulation.

While specific details for growth-regulated alpha protein are not extensively provided, protein modification represents a common post-translational regulatory mechanism that significantly impacts protein function, stability, localization, and interactions. These modifications can activate or inactivate proteins and contribute to intricate feedback loops that maintain cellular homeostasis or enable rapid responses to environmental cues. Furthermore, protein-altering variants (PAVs) or genetic variants in high linkage disequilibrium with them can directly modify the protein’s structure, potentially affecting its stability, biological activity, or even its detectability by specific assay methods.^[3]

Integrated Network Interactions and Pathway Crosstalk

The regulation and biological role of growth-regulated alpha protein are not isolated events but are embedded within complex biological networks, characterized by extensive pathway crosstalk. Research employing graphical modeling has revealed intricate connections among numerous proteins, where pQTL variants serve as nodes influencing protein-protein correlation networks.^[2]This systems-level perspective demonstrates how a single genetic variant can impact multiple proteins, or conversely, how the levels of a key protein like growth-regulated alpha protein can be affected by the convergence of various genetic association signals.^[2] Pathway crosstalk occurs when components or signals from one biological pathway influence another, leading to a coordinated and often amplified cellular response. For example, a trans-pQTL identified for growth-regulated alpha protein might exert its effect through an intermediarycis-gene, which then modulates the target protein’s levels.^[4] These network interactions highlight hierarchical regulation, where upstream genetic factors or protein changes can cascade through a complex network, leading to emergent properties and diverse biological outcomes that extend beyond the function of individual components.

Pathophysiological Implications and Therapeutic Avenues

Dysregulation of growth-regulated alpha protein levels or its associated pathways can have significant pathophysiological implications, contributing to the development and progression of various diseases. As a protein whose levels are under substantial genetic control, it holds potential as a biomarker, and understanding its underlying genetic determinants provides crucial knowledge for elucidating disease mechanisms.^[4]The advanced proteomic platforms used for its are designed to cover proteins known to be relevant to human diseases, including neurodegenerative and cardiovascular conditions, suggesting its potential involvement in these pathologies.^[7]Identifying pQTLs for growth-regulated alpha protein allows for the rigorous evaluation of whether observed associations between the protein and disease are causal, often utilizing methodologies like Mendelian randomization.^[4]If a causal link is established, targeting upstream factors that influence growth-regulated alpha protein levels could represent a promising therapeutic strategy. For instance, modulating the activity or expression of its receptorACKR1or other components within its regulatory network might offer avenues for intervention in diseases where growth-regulated alpha protein plays a pathological role.^[1]

Diagnostic and Prognostic Utility

The of proteins, such as growth regulated alpha protein, holds significant diagnostic utility by serving as biomarkers for various human diseases. These measurements contribute to the discovery of novel indicators for disease states, including neurodegenerative and cardiovascular conditions.^[7]By quantifying protein levels in biological samples, clinicians can gain insights into ongoing pathological processes, aiding in early detection or characterization of disease activity. The reliability and consistency of protein platforms, validated across different cohorts and methods, support their use in clinical settings for biomarker discovery.^[6]Beyond diagnosis, protein measurements offer substantial prognostic value, informing predictions of disease progression and long-term outcomes. Genetic studies have identified protein quantitative trait loci (pQTLs) that influence circulating protein levels, and these genetic associations can be leveraged in Mendelian randomization (MR) analyses to assess the causal relationship between a protein biomarker and disease risk.^[4]Such approaches can help determine if altered protein levels, potentially including growth regulated alpha protein, are causally involved in disease development, thereby informing more precise prognostic assessments and identifying individuals at higher risk for adverse events. Understanding these causal links can also guide the prediction of treatment response, as interventions targeting specific protein pathways could be more effective.

Risk Stratification and Personalized Medicine

Protein measurements are integral to advanced risk stratification strategies, enabling the identification of individuals at elevated risk for specific diseases. By examining the genetic architecture influencing protein levels, such as through whole-genome sequence analysis of the plasma proteome, researchers can uncover novel insights into complex conditions like cardiovascular disease.^[8] This allows for the development of polygenic scores (PGS) that predict individual protein levels, correlating with measured protein concentrations and providing a genetic predisposition marker.^[9] Such genetic and proteomic profiling can help delineate high-risk subgroups within seemingly healthy populations, facilitating targeted screening and early intervention efforts.

The integration of protein measurements into personalized medicine approaches allows for more precise prevention strategies and treatment selection. Understanding the regulatory pathways influenced by pQTLs can reveal upstream factors that affect protein concentrations, offering potential targets for therapeutic intervention.^[4]For instance, if a protein like growth regulated alpha protein is found to be causally involved in a disease, identifying its genetic determinants and associated regulatory mechanisms could lead to tailored treatments or preventive measures based on an individual’s unique genetic and proteomic profile. This personalized approach moves beyond broad treatment guidelines to consider individual biological nuances, optimizing patient care.

Genetic Associations and Disease Mechanisms

The study of protein levels, including growth regulated alpha protein, reveals important associations with various comorbidities and overlapping disease phenotypes. Genetic variants can displaycis-associations with increased or decreased levels of specific proteins, and concordant trans-associations with other proteins or disease endpoints.^[2] For example, certain genetic variants are linked to altered levels of proteins like APOEand are associated with Alzheimer’s disease, or influence glycans linked to rheumatoid arthritis risk or cancer antigen 19-9.^[2] These findings highlight how protein measurements can illuminate shared biological pathways or predispositions underlying seemingly distinct conditions, offering a more comprehensive view of patient health.

Investigating the genetic basis of protein levels, through approaches like protein quantitative trait loci (pQTL) mapping, provides crucial insights into fundamental disease mechanisms. pQTLs can identify previously unknown regulatory pathways in vivo, establishing a clear direction of causality from genetic variation to protein concentration.^[4]This deeper understanding of regulatory checkpoints is essential for biomarkers causally involved in disease, as it allows for the targeting of upstream factors. By elucidating how genetic variants influence the abundance of proteins like growth regulated alpha protein, researchers can pinpoint molecular drivers of disease, paving the way for novel therapeutic targets and a better understanding of disease pathophysiology.

Key Variants

RS ID	Gene	Related Traits
rs3117604 rs115711101 rs3117600	PF4V1 - CXCL1	chemokine (C-X-C motif) ligand 1 growth-regulated alpha protein
rs116152597 rs2115691 rs3097412	CXCL1 - HNRNPA1P55	growth-regulated alpha protein
rs614822 rs138657097 rs569108954	CXCL1P1 - PF4	growth-regulated alpha protein
rs1246397	AREG - BTC	growth-regulated alpha protein
rs12075 rs2814778	ACKR1, CADM3-AS1	basophil count C-C motif chemokine 2 level leukocyte quantity self reported educational attainment monocyte count
rs13131508	AFP - AFM	growth-regulated alpha protein
rs491641 rs189986015 rs75078633	MTHFD2L	growth-regulated alpha protein
rs7088799	JMJD1C	interleukin 10 amount of early activation antigen CD69 (human) in blood C-X-C motif chemokine 5 growth-regulated alpha protein level of ataxin-10 in blood
rs35467127	HLA-DRB6, HLA-DRB6	basal cell carcinoma BMI-adjusted waist circumference BMI-adjusted waist-hip ratio growth-regulated alpha protein
rs6811077	PPBPP2 - CXCL2	growth-regulated alpha protein

Frequently Asked Questions About Growth Regulated Alpha Protein

These questions address the most important and specific aspects of growth regulated alpha protein based on current genetic research.

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1. Why do I seem to get inflamed more easily than my friends?

Your body’s inflammatory response, partly driven by proteins like GROα, can differ due to genetics. A specific variant, rs12075 , influences GROα levels, which might make you more prone to inflammation than others. This variant affects how GROα interacts with a receptor called ACKR1, impacting its availability.

2. My sibling and I live similarly, but our health issues differ. Why?

Even with similar lifestyles, genetic differences can influence how your body produces key proteins like GROα. These variations, such as the rs12075 variant near the ACKR1 gene, can lead to different GROα levels, affecting your individual susceptibility to inflammatory conditions or how your immune system responds.

3. Does my genetic background make me more prone to certain illnesses?

Yes, your genetics can influence your body’s GROα levels, a protein involved in inflammation and immune responses. Variations like rs12075 can alter these levels, potentially affecting your susceptibility to inflammatory conditions, infections, or even certain types of cancer. This understanding can offer insights into your personal disease risk.

4. Can my body’s inflammation response be “too strong” or “too weak”?

Yes, your inflammatory response, partly regulated by GROα, can vary. Genetic factors, like the rs12075 variant, can influence your GROα levels, potentially leading to an overactive or underactive inflammatory response. This can impact how effectively your body fights infections or manages chronic inflammation.

5. If I get a test for this protein, will it tell me everything?

A test measuring your GROα levels can provide valuable insights, but it won’t tell you everything. While genetics like the rs12075 variant play a role, many other factors, including unmeasured environmental influences or complex gene interactions, also affect these levels. Current tests also face limitations in generalizability across all populations.

6. Could my ancestry affect how useful a genetic test is for me?

Yes, your ancestry can definitely affect the accuracy of genetic insights. Studies on proteins like GROα are often based on populations of European descent, meaning their findings and predictive accuracy might be less reliable for individuals from other backgrounds, like Arab, South-East Asian, or African populations. More inclusive research is needed.

7. Does stress or my daily habits impact my inflammation levels?

While genetics play a significant role, unmeasured environmental factors and complex gene-environment interactions can also influence your GROα levels. This suggests that aspects like stress or lifestyle habits could potentially modulate your body’s inflammatory responses, though the full extent of these interactions is still being researched.

8. Is it true that doctors don’t fully understand all my body’s protein levels?

Yes, while much is known, a significant portion of the variability in proteins like GROα remains unexplained, a concept sometimes called “missing heritability.” This means current genetic models don’t fully capture all the complex genetic interactions or environmental factors influencing your protein levels, showing there are still knowledge gaps.

9. Why might my body react differently to an infection than someone else’s?

Your body’s response to infection, particularly the inflammatory component, can be influenced by your unique genetic makeup. Proteins like GROα are key in attracting immune cells, and genetic variations, such asrs12075 , can lead to different GROα levels, causing your immune system to react distinctly compared to others.

10. Could a genetic test for this protein help predict my future health?

Investigating genetic factors influencing proteins like GROα, such as the rs12075 variant, can offer valuable insights into your individual susceptibility to inflammatory conditions, infections, and certain cancers. This understanding could potentially pave the way for more personalized approaches to managing your health risks in the future.

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This FAQ was automatically generated based on current genetic research and may be updated as new information becomes available.

Disclaimer: This information is for educational purposes only and should not be used as a substitute for professional medical advice. Always consult with a healthcare provider for personalized medical guidance.

References

[1] Ahola-Olli AV, et al. “Genome-wide Association Study Identifies 27 Loci Influencing Concentrations of Circulating Cytokines and Growth Factors.” Am J Hum Genet, vol. 100, no. 1, 2017, pp. 40-50.

[2] Suhre K, et al. “Connecting genetic risk to disease end points through the human blood plasma proteome.”Nat Commun, vol. 8, 2017, p. 14357.

[3] Kalnapenkis A, et al. “Genetic determinants of plasma protein levels in the Estonian population.” Sci Rep, vol. 14, no. 1, 2024, p. 7694.

[4] Folkersen L, et al. “Mapping of 79 loci for 83 plasma protein biomarkers in cardiovascular disease.”PLoS Genet, vol. 13, no. 4, 2017, e1006706.

[5] Katz, D. H. et al. “Whole Genome Sequence Analysis of the Plasma Proteome in Black Adults Provides Novel Insights Into Cardiovascular Disease.” Circulation, vol. 144, no. 21, 2021, pp. 1676-1691.

[6] Sun BB, et al. “Genomic atlas of the human plasma proteome.” Nature, vol. 558, no. 7708, 2018, pp. 73-79.

[7] Yang C, et al. “Genomic atlas of the proteome from brain, CSF and plasma prioritizes proteins implicated in neurological disorders.” Nature Neuroscience, vol. 24, no. 8, 2021, pp. 1122-1133.

[8] Katz DH, et al. “Whole Genome Sequence Analysis of the Plasma Proteome in Black Adults Provides Novel Insights Into Cardiovascular Disease.”Circulation, vol. 145, no. 5, 2022, pp. 363-376.

[9] Thareja G, et al. “Differences and commonalities in the genetic architecture of protein quantitative trait loci in European and Arab populations.” Human Molecular Genetics, vol. 31, no. 23, 2022, pp. 3968-3982.