Biomarker Analysis Services for Iga Nephropathy
Protheragen offers specialized biomarker analysis services tailored for IgA Nephropathy research and therapeutic development. Our comprehensive biomarker panel is designed to enhance the understanding of disease pathophysiology, supporting the advancement of drug discovery projects from early target identification through preclinical development. Please note that all of our services are exclusively focused on drug discovery and preclinical research applications; we do not provide clinical diagnostic services.
The foundation of effective therapeutic intervention lies in the precise discovery and identification of relevant biomarkers. Protheragen's biomarker discovery services are integral to drug development pipelines, enabling the identification of molecular indicators associated with IgA Nephropathy. Our process encompasses high-throughput screening of candidate molecules, followed by rigorous validation to ensure relevance to disease mechanisms. Through iterative screening, we refine and validate biomarker candidates using robust experimental models and state-of-the-art analytical platforms.
Multi Omics: We employ a cutting-edge multi-omics approach, integrating genomics, transcriptomics, proteomics, and metabolomics to provide a comprehensive study of biological systems relevant to IgA Nephropathy. This approach enables the identification of DNA, RNA, protein, and metabolite biomarkers, giving insight into complex disease pathways such as immune dysregulation, complement activation, and inflammatory cascades. By leveraging multi-omics technologies, we facilitate the exploration of molecular networks underlying IgA Nephropathy pathogenesis.
Candidate Validation: Our candidate validation strategies involve systematic assessment of biomarker association with IgA Nephropathy pathophysiology. We conduct preliminary screening using in vitro and in vivo models, followed by orthogonal validation methods to confirm biological relevance. Criteria for prioritizing promising candidates include specificity to disease pathways, reproducibility across experimental systems, and potential for translational application in drug development.
Diverse Technological Platforms: Protheragen provides custom assay development capabilities, adapting technological platforms to meet the specific requirements of each biomarker and research objective. Our platforms are compatible with a wide range of sample types and allow for the integration of multiple analytical modalities to ensure comprehensive and accurate biomarker measurement.
Immunoassays: We offer a suite of immunoassays including ELISA, chemiluminescent, and multiplex platforms for sensitive and specific quantification of protein biomarkers.
Mass Spectrometry: Our LC-MS/MS capabilities enable precise measurement of proteins, peptides, and metabolites, supporting both targeted and discovery-based analyses.
Flow Cytometry: Multiparametric flow cytometry is employed for cellular biomarker analysis, allowing for high-content characterization of immune cell populations and surface markers.
Molecular Diagnostics: We utilize advanced molecular diagnostics for the detection and quantification of nucleic acid biomarkers, including gene expression and epigenetic modifications.
Histopathology And Imaging: Our histopathology and imaging services provide spatial and morphological context for biomarker localization in tissue samples, supporting integrative pathophysiological studies.
Rigorous Method Validation: All assay methods undergo rigorous validation in accordance with established research guidelines. Performance characteristics such as sensitivity, specificity, accuracy, precision, linearity, and reproducibility are thoroughly assessed. Quality control measures are implemented throughout the validation process to ensure reliability and consistency of biomarker quantification.
Our quantitative analysis capabilities encompass the absolute and relative measurement of biomarker levels, utilizing validated standard curves, internal controls, and advanced data analysis software. This ensures robust and reproducible quantification across a range of sample types and analytical platforms.
Sample Analysis: We handle a diverse array of sample types, including serum, plasma, urine, tissue lysates, and cell culture supernatants. Our analysis protocols are standardized for consistency and optimized for each biomarker class. Comprehensive quality assurance procedures are in place to monitor sample integrity, prevent contamination, and ensure data reliability.
High Throughput Capabilities: Our high-throughput analytical platforms support multiplexed biomarker analysis, enabling simultaneous measurement of multiple targets within a single sample. This approach maximizes efficiency, conserves precious biological material, and accelerates data generation for large-scale preclinical studies.
| Gene Target | Biological Function | Application as a Biomarker |
|---|---|---|
| TNF superfamily member 13 (TNFSF13) | TNF superfamily member 13 (TNFSF13), also known as APRIL (A Proliferation-Inducing Ligand), is a cytokine belonging to the tumor necrosis factor (TNF) ligand family. TNFSF13 is primarily involved in the regulation of B cell development, survival, and differentiation. It binds to specific receptors, including TACI (transmembrane activator and CAML interactor), BCMA (B-cell maturation antigen), and heparan sulfate proteoglycans. Through these interactions, TNFSF13 promotes B cell proliferation, supports antibody production, and contributes to the maintenance of plasma cells. Additionally, it plays a role in immune homeostasis and has been implicated in modulating immune responses and inflammation. | TNFSF13 has been studied as a biomarker in various clinical contexts, particularly in immune-mediated disorders and hematological malignancies. Elevated levels of TNFSF13 have been observed in the serum of patients with autoimmune diseases such as systemic lupus erythematosus and rheumatoid arthritis. It has also been investigated in the context of multiple myeloma and other B cell-related malignancies, where its expression may reflect disease activity or burden. Furthermore, TNFSF13 levels have been explored as a potential indicator of transplant outcomes and immune dysregulation. |
| TNF superfamily member 13b (TNFSF13B) | TNF superfamily member 13b (TNFSF13B), also known as B cell-activating factor (BAFF), is a cytokine that plays a critical role in the regulation of B cell development, survival, and differentiation. TNFSF13B binds to receptors such as BAFF-R (TNFRSF13C), TACI (TNFRSF13B), and BCMA (TNFRSF17) on B cells, promoting their maturation and maintenance. The protein is primarily produced by myeloid cells and stromal cells, and its signaling is essential for the maintenance of peripheral B cell populations and the formation of germinal centers. Dysregulation of TNFSF13B expression can impact immune homeostasis and is associated with autoimmunity. | TNFSF13B has been used as a biomarker in various clinical and research settings, particularly in the context of autoimmune diseases and B cell-related disorders. Elevated levels of TNFSF13B in serum or plasma have been observed in systemic lupus erythematosus, rheumatoid arthritis, and multiple sclerosis, among others. Measurement of TNFSF13B concentrations can aid in disease characterization, assessment of disease activity, and monitoring of therapeutic responses, especially in conditions involving abnormal B cell activation or survival. |
| apolipoprotein A1 (APOA1) | Apolipoprotein A1 (APOA1) is the major protein component of high-density lipoprotein (HDL) particles in plasma. It plays a central role in the reverse transport of cholesterol from peripheral tissues to the liver for excretion. APOA1 acts as a cofactor for lecithin-cholesterol acyltransferase (LCAT), which is essential for the formation of mature HDL particles and the esterification of cholesterol. Additionally, APOA1 contributes to lipid binding, promotes cholesterol efflux from cells via interaction with ATP-binding cassette transporters (such as ABCA1), and exhibits anti-inflammatory and antioxidant properties. | APOA1 is commonly measured in clinical and research settings as an indicator of HDL quantity and function. Its plasma concentration is used to assess lipid metabolism, cardiovascular risk, and the efficacy of lipid-modifying therapies. Lower levels of APOA1 have been associated with increased risk of atherosclerotic cardiovascular disease, while higher levels are generally linked to a favorable lipid profile. APOA1 has also been investigated as a biomarker in other conditions, such as liver disease and certain inflammatory disorders, due to its involvement in lipid transport and systemic inflammation. |
| complement C3 (C3) | Complement C3 (C3) is a central component of the complement system, an essential part of the innate immune response. C3 is synthesized primarily in the liver and circulates in the blood in an inactive form. Upon activation by proteolytic cleavage, C3 is converted to C3a and C3b. C3b binds to the surface of pathogens, promoting opsonization and enhancing phagocytosis by immune cells. C3a acts as an anaphylatoxin, mediating inflammatory responses. C3 is also involved in the formation of the membrane attack complex and plays a role in the clearance of immune complexes and apoptotic cells. | Complement C3 levels are commonly measured in clinical laboratories as an indicator of complement system activity. Alterations in C3 concentrations have been associated with a variety of clinical conditions, including autoimmune diseases (such as systemic lupus erythematosus), infections, and certain kidney disorders (such as glomerulonephritis). Measurement of C3, often alongside other complement components, can aid in the assessment of disease activity, monitoring of disease progression, and evaluation of immune system function. |
| complement C5 (C5) | Complement C5 (C5) is a central component of the complement system, which is part of the innate immune response. Upon activation by complement convertases, C5 is cleaved into C5a and C5b fragments. C5a acts as a potent anaphylatoxin, mediating chemotaxis and activation of inflammatory cells, while C5b initiates the assembly of the membrane attack complex (MAC), leading to cell lysis. Thus, C5 plays a critical role in host defense against pathogens and in mediating inflammatory responses. | Levels of complement C5 and its activation products (such as C5a) have been measured in various clinical contexts to assess immune activation and inflammation. Altered C5 concentrations or activity have been reported in disorders involving complement dysregulation, such as autoimmune diseases (e.g., systemic lupus erythematosus), certain types of glomerulonephritis, and sepsis. Measurement of C5 or its fragments in biological fluids can provide information about complement activation status and has been investigated in disease monitoring and prognosis. |
| complement factor B (CFB) | Complement factor B (CFB) is a key component of the alternative pathway of the complement system, an essential part of the innate immune response. CFB encodes a serine protease that circulates in the blood as an inactive zymogen. Upon activation, CFB binds to complement component C3b, forming the C3bB complex. This complex is then cleaved by factor D, producing the active Bb fragment, which remains associated with C3b to form the C3 convertase (C3bBb). This enzyme complex amplifies the complement cascade by cleaving additional C3 molecules, leading to opsonization, inflammation, and cell lysis. Regulation of CFB activity is critical for preventing uncontrolled complement activation and tissue damage. | Complement factor B has been investigated as a biomarker in various clinical contexts, particularly those involving immune and inflammatory processes. Altered levels of CFB have been reported in association with autoimmune diseases, age-related macular degeneration, and certain kidney disorders such as atypical hemolytic uremic syndrome. Measurement of CFB levels or activity in biological fluids has been used in research and clinical studies to assess complement system activation and to explore disease mechanisms or monitor disease activity. |
| endothelin receptor type A (EDNRA) | Endothelin receptor type A (EDNRA) is a G protein-coupled receptor that binds endothelin-1 (ET-1), a potent vasoconstrictor peptide. Upon ligand binding, EDNRA activates intracellular signaling pathways, primarily through Gq proteins, leading to increased intracellular calcium and smooth muscle contraction. EDNRA is predominantly expressed in vascular smooth muscle cells and mediates vasoconstriction, regulation of blood pressure, and cell proliferation. It also plays roles in cardiovascular development and pathophysiological processes such as vascular remodeling and fibrosis. | EDNRA expression and activity have been studied as potential biomarkers in various cardiovascular and renal diseases. Elevated EDNRA levels have been observed in conditions such as pulmonary arterial hypertension, heart failure, and certain forms of hypertension. Assessment of EDNRA expression or signaling may provide information on disease presence, progression, or response to endothelin receptor antagonist therapies in these contexts. |
| immunoglobulin heavy constant alpha 1 (IGHA1) | Immunoglobulin heavy constant alpha 1 (IGHA1) encodes the constant region of the heavy chain of immunoglobulin A1 (IgA1), a subclass of IgA. IgA is the predominant antibody isotype found in mucosal secretions, such as saliva, tears, and intestinal fluids, and is also present in the circulation. The IGHA1 gene product contributes to the formation of the IgA1 molecule, which plays a critical role in immune defense by neutralizing pathogens and toxins at mucosal surfaces and facilitating their removal. IgA1 is produced by plasma cells and can exist as a monomer in serum or as a dimer in secretions, where it is associated with a joining (J) chain and a secretory component. The constant region encoded by IGHA1 determines the effector functions of the antibody, including interactions with Fc receptors and the complement system. | IGHA1 and its encoded protein, IgA1, have been utilized as biomarkers in various clinical contexts. Elevated serum or tissue levels of IgA1 have been associated with certain autoimmune and inflammatory diseases, such as IgA nephropathy, where aberrant glycosylation of IgA1 is a characteristic finding. Measurement of IgA1 can also assist in the assessment of immune status, mucosal immunity, and in the diagnosis of immunodeficiency disorders. Additionally, altered IgA1 levels have been investigated in the context of infections and some malignancies. Detection methods typically involve immunoassays targeting the IgA1 heavy chain or its glycosylation patterns. |
| nuclear receptor subfamily 3 group C member 1 (NR3C1) | Nuclear receptor subfamily 3 group C member 1 (NR3C1) encodes the glucocorticoid receptor (GR), a ligand-activated transcription factor belonging to the nuclear receptor superfamily. Upon binding glucocorticoids, NR3C1 translocates from the cytoplasm to the nucleus, where it regulates the expression of target genes involved in diverse physiological processes, including metabolism, immune response modulation, stress response, and cell proliferation. The receptor can act as a transcriptional activator or repressor, depending on the context and interacting cofactors. NR3C1 also mediates negative feedback regulation of the hypothalamic-pituitary-adrenal (HPA) axis. | NR3C1 expression, genetic variants, and epigenetic modifications have been studied as biomarkers in a range of contexts. Alterations in NR3C1 have been associated with glucocorticoid sensitivity or resistance in inflammatory and autoimmune disorders, as well as in certain cancers. NR3C1 methylation status and expression levels have been investigated in relation to psychiatric conditions, such as major depressive disorder and post-traumatic stress disorder, and as indicators of stress exposure. Additionally, NR3C1 is evaluated in pharmacogenomics to predict individual responses to glucocorticoid therapy. |
| tumor necrosis factor (TNF) | Tumor necrosis factor (TNF) is a pro-inflammatory cytokine primarily produced by activated macrophages, as well as by other immune and non-immune cells. TNF plays a central role in the regulation of immune responses, inflammation, cell proliferation, differentiation, and apoptosis. It acts by binding to two distinct receptors, TNFR1 and TNFR2, initiating signaling cascades that can lead to the activation of nuclear factor kappa B (NF-κB), mitogen-activated protein kinases (MAPKs), and caspases. Through these pathways, TNF contributes to the defense against infections, the orchestration of inflammatory responses, and the modulation of cellular survival and death. | TNF levels are measured in various biological fluids, such as serum or plasma, to assess the presence and extent of inflammation. Elevated TNF concentrations have been associated with a range of inflammatory and autoimmune diseases, including rheumatoid arthritis, inflammatory bowel disease, and sepsis. TNF measurement is used in research and clinical settings to monitor disease activity, evaluate therapeutic responses, and study the pathophysiology of inflammatory conditions. |
Explore Research Opportunities with Protheragen. Our biomarker research services and capabilities are designed to support exploratory and preclinical research in IgA Nephropathy. The biomarkers discussed herein are research targets only; we do not claim any biomarkers as validated or mandatory for any application. Our focus remains on facilitating discovery and mechanistic studies during preclinical development, with a commitment to scientific objectivity and rigor.
We invite you to connect with Protheragen to discuss collaborative opportunities in exploratory biomarker research for IgA Nephropathy. Let's advance scientific understanding together through open exchange and objective investigation.
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