| Category | Key findings | Quantitative/statistical data | Key sources (author year, journal) | URL |
|---|---|---|---|---|
| Identity/features | Human CRISP3 is verified as cysteine-rich secretory protein 3, also called SGP28, matching UniProt P54108; it is a secreted CRISP/CAP-family glycoprotein detected as ~29 kDa unglycosylated and ~31 kDa glycosylated forms in seminal plasma (pqac-00000001, pqac-00000016, pqac-00000023) | Two seminal-plasma isoforms: 29 kDa and 31 kDa; human CRISP3 is described as a 245-aa extracellular/secreted protein in prostate-cancer literature (pqac-00000001, pqac-00000012, pqac-00000023) | Belardin 2019, *Andrology*; Udby 2005, *Journal of Andrology*; Ribeiro 2011, *PLoS ONE* | https://doi.org/10.1111/andr.12555; https://doi.org/10.2164/jandrol.04132; https://doi.org/10.1371/journal.pone.0022317 |
| Localization & expression | CRISP3 is present in neutrophil specific/gelatinase granules, plasma, saliva, sweat, and seminal plasma; in the male tract it localizes to secretory epithelium throughout, with strongest expression in cauda epididymis and ampulla/vas deferens, and seminal-plasma CRISP3 is free in solution rather than prostasome-associated (pqac-00000014, pqac-00000016, pqac-00000019, pqac-00000020, pqac-00000025) | Reported concentrations: saliva ~22 µg/mL, plasma ~6 µg/mL, sweat ~0.15 µg/mL, seminal plasma ~11 µg/mL; tissue levels low in testis/caput-corpus epididymis (~0.025 mg CRISP3 per mg protein) and high in cauda epididymis/vas deferens (~4.5 mg/mg protein) (pqac-00000019, pqac-00000025) | Udby 2005, *Journal of Andrology*; Bjartell 2007, *Clinical Cancer Research*; Edström 2010 (thesis/monograph context) | https://doi.org/10.2164/jandrol.04132; https://doi.org/10.1158/1078-0432.ccr-06-3031 |
| Binding partners/mechanisms | Recent mechanistic work shows human CRISP3 binds PMCA4b via its N-terminal CAP domain; unlike hCRISP1/rCRISP4 it did not inhibit PMCA4b-mediated Ca2+ extrusion. CRISP3 also interacts with PSP94/MSMB in seminal plasma, and A1BG binds CRISP-family proteins with nanomolar affinity and inhibits sterol binding/export, supporting roles in extracellular ligand binding rather than a defined enzymatic reaction (pqac-00000008, pqac-00000009, pqac-00000010, pqac-00000017) | A1BG coexpression blocked sterol secretion by >50%; CRISP3-A1BG interaction described as nanomolar affinity; PMCA4b interaction mapped to the CAP domain, while hCRISP3 did not reduce PMCA4b Ca2+ clearance in the 2024 assay system (pqac-00000008, pqac-00000009, pqac-00000010) | Miya 2024, *Andrology*; Atab 2024, *Journal of Biological Chemistry* | https://doi.org/10.1111/andr.13549; https://doi.org/10.1016/j.jbc.2024.107910 |
| Disease/biomarker applications | In sepsis, plasma CRISP3 is elevated and shows biomarker potential in trauma cohorts. In prostate cancer, CRISP3 is a direct ERG target and is strongly overexpressed in TMPRSS2-ERG fusion-positive tumors. In varicocele-associated infertility, seminal CRISP3 rises markedly and falls after surgery, supporting use as an inflammation-linked seminal biomarker (pqac-00000007, pqac-00000018, pqac-00000012, pqac-00000013, pqac-00000015, pqac-00000023) | Sepsis: meta-analysis of 23 datasets SMD 0.90 (95% CI 0.50-1.30), p<0.001; cohort 1 OR 1.004 (1.002-1.006), AUC 0.811 (0.681-0.905); cohort 2 OR 1.002 (1.001-1.003), AUC 0.772 (0.701-0.834). Prostate cancer: >50-fold upregulation in fusion-positive tumors, ~53-fold vs TMPRSS2-ERG-negative, 63% IHC overexpression, ERG-CRISP3 correlation rs=0.65, p<0.001. Varicocele: seminal CRISP3 increased 67.5-fold (29 kDa) and 5.2-fold (31 kDa); after varicocelectomy decreased 5.6-fold and 4.3-fold (pqac-00000007, pqac-00000018, pqac-00000012, pqac-00000013, pqac-00000015, pqac-00000023) | Zhang 2024, *Frontiers in Immunology*; Ribeiro 2011, *PLoS ONE*; Bjartell 2007, *Clinical Cancer Research*; Belardin 2019, *Andrology* | https://doi.org/10.3389/fimmu.2024.1492538; https://doi.org/10.1371/journal.pone.0022317; https://doi.org/10.1158/1078-0432.ccr-06-3031; https://doi.org/10.1111/andr.12555 |


*Table: This table compiles core evidence for human CRISP3 (UniProt P54108), spanning identity, localization, binding partners, and disease/biomarker relevance. It emphasizes recent 2024 studies while anchoring them to foundational localization and prostate-cancer literature.*