| Year | Source type | System/tissue | Key PRG3-related findings (function/localization/disease/biomarker) | Quantitative data/statistics (if present) | URL/DOI |
|---|---|---|---|---|---|
| 2001 | Review / foundational primary synthesis | Human eosinophils, bone marrow; chromosome 11q12 locus | Confirmed that human **PRG3** encodes **hMBP2/MBPH (major basic protein homolog 2)**, a distinct paralog of **PRG2/MBP1**. PRG3 product localizes to **eosinophil secondary granules**, is less cationic than MBP1, and shows **cytotoxic/cytostimulatory activity** with generally reduced potency relative to MBP1; expression is more restricted than PRG2 and not established as a placental pregnancy-serum protein. (pqac-00000001, pqac-00000002, pqac-00000005, pqac-00000014, pqac-00000015) | hMBP2 mature mass ~**13,437 Da**; gene has **6 exons**; mRNA abundance in bone marrow library about **1.1%** vs **8.1%** for PRG2/hMBP1; pI about **8.7** vs **11.4** for MBP1; transcription reported ~**7-fold lower** than hMBP1 in IL-5–stimulated cells. (pqac-00000002, pqac-00000001) | https://doi.org/10.1034/j.1600-065x.2001.790119.x |
| 2011 | Review | Placenta, pregnancy serum, bone marrow/eosinophil lineage | Review of **proMBP/proMBP-2 biology** distinguished **PRG3/proMBP-2 (MBP-2)** from **PRG2/proMBP**. PRG3 shares homology and proximal promoter features with PRG2 but lacks the placental/pregnancy-serum role typical of proMBP1; MBP-2 shows similar biological activities to MBP with **lower potency**, supporting a role as a related eosinophil granule cationic effector rather than a major placental regulator. (pqac-00000003, pqac-00000011) | PRG3/MBP-2 pI **8.7** vs MBP/proMBP pI **11.4**; promoter differs by missing **C/EBP** site; PRG3 protein reportedly does **not** rise in pregnancy serum. (pqac-00000003, pqac-00000011) | https://doi.org/10.1095/biolreprod.110.090209 |
| 2016 | Omics / primary proteomics | Purified **human peripheral blood eosinophils** | Deep proteomics placed **PRG3 (bone marrow proteoglycan 3 / MBP2)** among the **major eosinophil granule proteins** and among the **top 15 most abundant eosinophil proteins**, supporting its status as a prominent eosinophil granule constituent and useful marker of eosinophil content/degranulation. (pqac-00000016, pqac-00000017) | **PRG3 ranked #12** among the **top 15 most abundant proteins** detected in eosinophils. (pqac-00000017) | https://doi.org/10.1021/acs.jproteome.6b00006 |
| 2016 | Primary mechanistic study | Human granulocytes/neutrophil phagosomes and granules; Candida killing assay | Study identified **MBPH/PRG3** in granulocyte granule/phagosome proteomes and grouped it with major basic protein family members having **membrane-disruptive antimicrobial activity**. MBPH and MBP were markedly depleted from phagosomes of G-CSF/dexamethasone–mobilized granulocytes, linking altered granule content to impaired **Candida albicans** killing. (pqac-00000007) | In mobilized granulocytes, MBPH and MBP were described as **virtually absent** from phagosomes; overall study reported a selective defect in **Candida yeast killing** despite preserved ROS production/phagocytosis. Exact PRG3-specific abundance not given in excerpt. (pqac-00000007) | https://doi.org/10.3324/haematol.2015.136630 |
| 2012 | Primary GWAS | Ashkenazi Jewish Crohn’s disease cohorts | GWAS implicated the **11q12.1 locus** containing **PRG3** as a biologically plausible Crohn’s disease susceptibility region, together with nearby eosinophil granule genes such as **PRG2**. This is association evidence rather than direct functional proof for PRG3. (pqac-00000010) | Discovery **907 cases / 2,345 controls**; replication **971 cases / 2,124 controls**. Signal at **11q12.1 rs11229030**, combined **OR 1.15**; replicated/new loci plus 3 NOD2 variants explained **11.2%** of AJ CD genetic variance. (pqac-00000010) | https://doi.org/10.1371/journal.pgen.1002559 |
| 2023 | Omics / clinical proteomics | Human **esophageal biopsies** in eosinophilic esophagitis (EoE), before/after PPI | PRG3 was one of four **eosinophil granule-derived proteins** (**PRG3, RNASE3, EPX, RNASE2**) differentially accumulated with response to proton-pump inhibitor therapy, highlighting PRG3 as a **tissue proteomic biomarker** of eosinophilic inflammation and treatment response. The study also noted PRG3 was detectable by proteomics but not prior transcriptomics. (pqac-00000009, pqac-00000018) | Cohort: **25 EoE** patients and **10 controls**. Responders had **166 DAP** post- vs pre-PPI (**100 up**, **66 down**); baseline responder vs non-responder comparison had **28 DAP** using **fold change >1.5** and **adjusted p ≤0.05**. Mean peak eosinophils fell **53.64 → 2.28**, **p<0.001** after 8 weeks PPI. PRG3-specific fold change not given in excerpt. (pqac-00000009, pqac-00000018) | https://doi.org/10.1101/2023.11.21.23298292 |
| 2023-2024 aggregation | Database / target-disease evidence integration | Open Targets PRG3 disease associations | Open Targets lists PRG3 disease associations including **hypertrophic cardiomyopathy, neoplasm, osteosarcoma, alcohol drinking, and glioma**. These are integrated evidence scores from literature, expression, and genetics rather than direct causal validation; for this target, PMIDs surfaced in the evidence include **27058420**, **22350417**, and **34594039**. (pqac-00000000) | Example integrated scores: **hypertrophic cardiomyopathy 0.1791**, **neoplasm 0.0968**, **osteosarcoma 0.0454**, **alcohol drinking 0.0878**, **glioma 0.0819**; evidence count shown as **4** for PRG3 across listed diseases. (pqac-00000000) | https://platform.opentargets.org/target/ENSG00000156575 |


*Table: This table compiles the most relevant curated and primary sources for human PRG3/MBP2/MBPH, spanning foundational identity/function papers, proteomics, disease genetics, and database-integrated disease associations. It is useful for quickly separating experimentally supported biology from association-level or biomarker-level evidence.*