| Claim/Topic | Evidence summary (1-2 sentences) | Species (human/mouse) | Study type (review/primary; RNA-seq; qPCR; in vivo model) | Quantitative/statistical details | Citation (context id) |
|---|---|---|---|---|---|
| Identity and alias verification | SCGB1C1 is explicitly listed as **Secretoglobin family 1C member 1 / Secretoglobin RYD5**, confirming that the target gene symbol matches the RYD5 alias used in the literature. A separate review also names it **SCGB1C1 (ligand binding protein RYD5, RYD5)**. | Human | Review; primary/review background | Alias/identity confirmation; no effect size reported | (pqac-00000006, pqac-00000009) |
| Family membership and core definition | SCGB1C1 belongs to the **secretoglobin** family; secretoglobins are described as **small, secreted, dimeric proteins**, with dimerization occurring prior to secretion. This supports the UniProt precursor/secreted-protein annotation and secretoglobin-family assignment. | Human/general mammalian family | Review | Qualitative family definition; no SCGB1C1-specific statistics | (pqac-00000009, pqac-00000014) |
| Structural/evolutionary support for SCGB1C1 as SCGB1C/RYD5 | Evolutionary analysis places SCGB1C1/RYD5 in the **SCGB1C** subfamily, notes the expected secretoglobin/uteroglobin fold, and reports conserved residues consistent with ligand binding. | Human with comparative vertebrate context | Evolutionary/comparative analysis | Qualitative structural inference; no human quantitative expression values | (pqac-00000001) |
| Upper airway / sinonasal expression | In human sinonasal mucosa, SCGB1C1/RYD5 mRNA was detected, and the authors state that all SCGBs except SCGB1D2 were expressed in sinonasal mucosa. This establishes human upper-airway expression. | Human | Primary study; qPCR in sinonasal tissue | Control n=16, CRSsNP n=20, CRSwNP n=20; expression reported as ΔCT relative to GAPDH | (pqac-00000007, pqac-00000019) |
| Respiratory tract expression | A review table of secretoglobin-expressing tissues marks SCGB1C1 as present in the **respiratory tract**, consistent with airway epithelial/barrier-tissue expression. Another review describes SCGB1C1 as relevant to lung epithelial protection and airway mucosal defense. | Human | Review | Qualitative tissue presence; no numerical expression value in excerpt | (pqac-00000010, pqac-00000011) |
| Olfactory/olfactory mucosa association | A human secretoglobin-family review reports SCGB1C1 localized to **Bowman’s glands in the olfactory mucosa** and proposes that it acts as an **odorant-binding protein** with likely small hydrophobic ligands. Human olfactory transcriptomics also notes especially high overexpression of SCGB1C1 among secreted proteins in olfactory epithelium. | Human | Review; RNA-seq transcriptomics | Olfactory RNA-seq identified 196 non-OR genes overexpressed >6× vs control tissues (gene-specific fold not given in excerpt) | (pqac-00000004, pqac-00000017, pqac-00000018) |
| Cytokine regulation in normal nasal mucosa | In ex vivo cultured normal human nasal mucosa, **IFN-γ down-regulated SCGB1C1**, whereas **IL-4 and IL-13 up-regulated** it; **IL-1β and TNF-α showed no significant effect**. This indicates SCGB1C1 is cytokine-responsive in upper-airway mucosa. | Human | Primary study; ex vivo tissue culture + qPCR | n=6; significance thresholds shown as #P < 0.05 and *P < 0.01 vs untreated mucosa, but SCGB1C1-specific exact p-values not given in excerpt | (pqac-00000007, pqac-00000019) |
| Disease association in CRS / nasal polyps | SCGB1C1/RYD5 expression was reported as **increased specifically in CRSwNP** and significantly different between CRSwNP and CRSsNP, whereas it was not highlighted as increased in CRSsNP. This supports a phenotype-associated transcriptional shift in polyp disease. | Human | Primary study; qPCR in disease tissue | Cohorts: control n=16, CRSsNP n=20, CRSwNP n=20; expression shown as ΔCT, but no SCGB1C1-specific fold-change/p-value in excerpt | (pqac-00000007, pqac-00000008, pqac-00000019) |
| Airway host defense / common cold interpretation | Review evidence states SCGB1C1 is important for **protection of lung epithelial cells**, can **recognize and remove pathogens from airway mucosa**, and appears involved in the development/susceptibility of the **common cold**, supporting an extracellular mucosal-defense role. | Human | Review | Qualitative interpretation; no direct mechanistic receptor identified | (pqac-00000011) |
| URTI susceptibility biomarker signal in athletes | A pilot blood-transcriptomics study found **low SCGB1C1 expression** in athletes with **high IL-5**, and proposed SCGB1C1 as a marker of susceptibility to upper respiratory tract infections. | Human | Primary study; blood microarray/pilot biomarker study | n=10 elite kayakers; fold-change **3.17**; corrected p-value **0.00065** | (pqac-00000003) |
| Allergic airway inflammation suppression | In an OVA-induced asthma mouse model, intranasal recombinant SCGB1C1 reduced airway hyperresponsiveness, eosinophilic inflammation, goblet cell hyperplasia, and serum IgE, while increasing regulatory T cells. This is the strongest direct functional evidence currently available for SCGB1C1 immunomodulation. | Mouse | Primary study; in vivo model | BALF eosinophils **p=0.049**; peribronchiolar inflammation **p<0.001**; perivascular inflammation **p=0.012**; total IgE **p=0.037**; OVA-specific IgE **p=0.009**; BALF IL-5 **p=0.039**; LLN IL-4 **p=0.040**; BALF IL-10 **p=0.011**; BALF TGF-β **p=0.026**; Tregs **p=0.042**; four independent experiments in triplicate | (pqac-00000002, pqac-00000005, pqac-00000013) |
| EV-linked pulmonary gene in asthma context | SCGB1C1 expression was decreased in asthmatic mouse lungs and increased after adipose stem cell-derived extracellular vesicle treatment, nominating it as one of the pulmonary genes associated with anti-allergic effects of EV therapy. | Mouse | Primary study summarized in later paper/review | Directional expression change reported; exact SCGB1C1 fold-change not given in excerpt | (pqac-00000005, pqac-00000013) |
| Ovarian carcinoma expression | SCGB1C1/RYD5 was included among eight secretoglobin genes assayed in ovarian tissues and reported as **overexpressed in ovarian carcinoma compared with normal ovary**. This supports expression outside the airway and possible biomarker relevance in epithelial cancers. | Human | Primary study; qRT-PCR tumor profiling | 53 ovarian carcinomas vs 30 normal ovaries; no SCGB1C1-specific fold-change stated in excerpt | (pqac-00000012) |
| Open Targets disease links | Open Targets lists low-evidence associations of SCGB1C1 with **benign prostatic hyperplasia, uterine fibroid, lipoma, neurodegenerative disease, and cataract**. All listed associations in the retrieved record trace to a single literature source (**PMID: 34031600**) from the study identifier “Glutamatergic Neuron-Survival-CRISPRa,” so these links should be treated as weak and indirect. | Human | Database aggregation | Scores: neurodegenerative disease **0.3011**; benign prostatic hyperplasia **0.0895**; cataract **0.0882**; uterine fibroid **0.0875**; lipoma **0.0858**; each with evidence size=1 | (pqac-00000000) |


*Table: This table summarizes key functional-annotation evidence for human SCGB1C1 (UniProt Q8TD33), including identity verification, secretoglobin-family context, tissue expression, regulation, disease associations, and quantitative results from recent and foundational studies. It is useful as a compact evidence map linking major claims to specific cited contexts.*