The research report should be a detailed narrative explaining the function, biological processes, and localization of the gene product. Citations should be given for all claims.
You should prioritize authoritative reviews and primary scientific literature when conducting research. You can supplement
this with annotations you find in gene/protein databases, but these can be outdated or inaccurate.
We are specifically interested in the primary function of the gene - for enzymes, what reaction is catalyzed, and what is the substrate specificity? For transporters, what is the substrate? For structural proteins or adapters, what is the broader structural role? For signaling molecules, what is the role in the pathway.
We are interested in where in or outside the cell the gene product carries out its function.
We are also interested in the signaling or biochemical pathways in which the gene functions. We are less interested in broad pleiotropic effects, except where these elucidate the precise role.
Include evidence where possible. We are interested in both experimental evidence as well as inference from structure, evolution, or bioinformatic analysis. Precise studies should be prioritized over high-throughput, where available.
The target gene/protein in this report is human SCGB1C1, which is explicitly referred to in authoritative sources as “Secretoglobin family 1C member 1” and also as “Secretoglobin RYD5”, confirming that the gene symbol SCGB1C1 matches the UniProt-described protein identity and the literature alias RYD5. (mootz2022secretoglobinsinthe pages 26-30, lu2011thecytokinedrivenregulation pages 1-2)
Secretoglobins (SCGBs) are described as small, secreted, dimeric proteins expressed by secretory tissues of barrier organs. Family-level biochemical behavior includes dimerization prior to secretion, which is linked to stability against heat/pH/proteases. (lu2011thecytokinedrivenregulation pages 1-2, mootz2022secretoglobinsinthe pages 6-9)
Implication for SCGB1C1: SCGB1C1/RYD5 should be treated primarily as a secreted extracellular protein acting at mucosal surfaces, rather than as an intracellular enzyme or transporter, consistent with the “precursor/secreted” framing in the gene family literature. (lu2011thecytokinedrivenregulation pages 1-2, mootz2022secretoglobinsinthe pages 6-9)
SCGB1C1 is repeatedly labeled in the airway literature as “ligand binding protein RYD5”, but direct, human biochemical ligand-binding assays were not present in the retrieved excerpts. (lu2011thecytokinedrivenregulation pages 1-2, lu2011thecytokinedrivenregulation pages 4-6)
An expert review of the human SCGB gene superfamily states that SCGB1C1 is localized to Bowman’s glands in the olfactory mucosa and is thought to act as an odorant-binding protein, with ligands suggested to be small hydrophobic molecules (functional inference based on localization and family properties rather than direct human binding measurements in the excerpt). (jackson2011updateofthe pages 3-4)
Concurrently, an airway-focused immunology review places SCGB1C1 within mucosal host defense, stating it is important for protection of lung epithelial cells and can “recognize and remove pathogens from the airway mucosa,” with a suggested connection to common cold susceptibility. (mootz2022secretoglobinsinthe pages 6-9)
Current synthesis: The best-supported current model from tool-retrieved sources is that SCGB1C1 is a secreted mucosal protein with two plausible, non-exclusive roles: (i) binding/transport of hydrophobic ligands/odorants in the olfactory/nasal environment; and (ii) immunomodulatory or innate-defense functions in airway mucosa. However, receptors and downstream signaling mechanisms for SCGB proteins remain poorly characterized overall. (jackson2011updateofthe pages 3-4, mootz2022secretoglobinsinthe pages 6-9)
A primary human sinonasal study assayed multiple secretoglobins and detected SCGB1C1/RYD5 mRNA in sinonasal mucosa (SCGB family members except SCGB1D2 were detected). (lu2011thecytokinedrivenregulation pages 4-6)
In ex vivo cultured normal human nasal mucosa, SCGB1C1 showed cytokine responsiveness:
- IFN-γ down-regulated SCGB1C1
- IL-4 and IL-13 up-regulated SCGB1C1
- IL-1β and TNF-α had no significant effect
These experiments were reported with n = 6 tissues, and significance was evaluated versus untreated mucosa. (lu2011thecytokinedrivenregulation pages 4-6)
Interpretation: This pattern links SCGB1C1 to the local Th2 vs Th1 cytokine milieu, consistent with SCGB family roles in airway disease immunoregulation. (lu2011thecytokinedrivenregulation pages 4-6, mootz2022secretoglobinsinthe pages 6-9)
In the same sinonasal qPCR cohort (controls n=16; CRSsNP n=20; CRSwNP n=20), SCGB1C1/RYD5 was reported as increased specifically in CRSwNP (nasal polyposis) with a significant difference between CRSwNP and CRSsNP. Expression was presented as ΔCT vs GAPDH (where a CT shift of 1 corresponds to ~2× change). (lu2011thecytokinedrivenregulation pages 4-6)
A separate 2023 RNA-seq study of CRS phenotypes (CRSwNP n=22; CRSsNP n=11; controls n=15) provides updated transcriptomic context for CRS, reinforcing that CRS is heterogeneous and strongly endotype-linked (e.g., CRSwNP being T2 endotype in that cohort). While the excerpted pages primarily describe cohort structure and DEG counts rather than SCGB1C1-specific fold changes, this represents a modern framework in which SCGB1C1 changes (as reported in earlier targeted qPCR) plausibly reflect endotype-associated epithelial programs. (urbancic2023transcriptomicdifferentiationof pages 1-2, urbancic2023transcriptomicdifferentiationof pages 2-4)
Human olfactory epithelium RNA-seq identified a set of non-olfactory receptor genes overexpressed in olfactory epithelium versus controls (>6× criterion), and within this broader analysis SCGB1C1 appears among notably enriched secreted-protein signals (the excerpt highlights “especially high overexpression” for SCGB1C1 among secreted proteins). (olender2016thehumanolfactory pages 1-2, olender2016thehumanolfactory pages 2-4)
Separately, the human SCGB superfamily review explicitly states SCGB1C1 is localized to Bowman’s glands in olfactory mucosa and is thought to be an odorant-binding protein (inference toward odorant carrier function). (jackson2011updateofthe pages 3-4)
Across the retrieved sources, SCGB1C1 is not described as catalyzing a chemical reaction or transporting solutes across membranes. It is consistently treated as a secreted protein and/or ligand-binding protein. (lu2011thecytokinedrivenregulation pages 1-2, mootz2022secretoglobinsinthe pages 6-9)
The strongest direct statement in the retrieved corpus about SCGB1C1’s “primary function” is the olfactory-mucosa localization plus the explicit interpretation that it may act as an odorant-binding protein, with ligands suggested to be small hydrophobic molecules. (jackson2011updateofthe pages 3-4)
Evolutionary/structural analysis of the broader SCGB1C subfamily also supports a ligand-binding-capable fold and conserved residues consistent with ligand binding in SCGB1C sequences, lending plausibility to a hydrophobic ligand-binding function (though this is not human biochemical validation). (karn2025abroadgenome pages 7-9)
An authoritative airway immunoregulation review states that SCGB1C1 is important for protection of lung epithelial cells, and that it recognizes and removes pathogens from airway mucosa, implying an extracellular innate defense function. (mootz2022secretoglobinsinthe pages 6-9)
Key uncertainty: The same review emphasizes that receptors and molecular mechanisms for secretoglobins remain largely unknown, so SCGB1C1’s downstream signaling partners and whether its effects are direct (e.g., binding/pathogen aggregation) or indirect (immune modulation) remains unresolved in the tool-retrieved text. (mootz2022secretoglobinsinthe pages 6-9)
A 2024 study tested recombinant SCGB1C1 in an ovalbumin (OVA) mouse asthma model using intranasal administration (5 μg/50 μL) before OVA challenge and reported multi-level improvements consistent with anti-allergic activity and immune regulation. Key quantitative outcomes included:
- BALF eosinophils decreased (p = 0.049) (kim2024scgb1c1playsa pages 2-5)
- Peribronchiolar inflammation score decreased (p < 0.001) and perivascular inflammation score decreased (p = 0.012) (kim2024scgb1c1playsa pages 2-5)
- Serum total IgE decreased (p = 0.037) and OVA-specific IgE decreased (p = 0.009) (kim2024scgb1c1playsa pages 2-5)
- BALF IL-5 decreased (p = 0.039) and LLN IL-4 decreased (p = 0.040) (kim2024scgb1c1playsa pages 2-5)
- BALF IL-10 increased (p = 0.011) and TGF-β increased (p = 0.026) (kim2024scgb1c1playsa pages 2-5)
- CD4+CD25+Foxp3+ Tregs in LLNs increased (p = 0.042) (kim2024scgb1c1playsa pages 2-5)
Although this is a murine model (not direct human physiology), it is currently the most explicit mechanistic/functional intervention evidence in the retrieved set, supporting a role for SCGB1C1 in shifting inflammatory balance toward regulatory/anti-inflammatory responses, consistent with secretoglobin immunoregulatory themes. (kim2024scgb1c1playsa pages 2-5, mootz2022secretoglobinsinthe pages 6-9)
A 2023 CRS RNA-seq study provides an updated, phenotype/endotype-resolved context: it reports substantial DEG changes and emphasizes that CRSwNP in their cohort aligned with T2 inflammation while CRSsNP was predominantly non-T2. This modern stratification is important for interpreting older findings of SCGB1C1 elevation in CRSwNP, as SCGB1C1 is Th2-cytokine responsive in nasal mucosa (IL-4/IL-13 upregulation). (urbancic2023transcriptomicdifferentiationof pages 2-4, urbancic2023transcriptomicdifferentiationof pages 1-2, lu2011thecytokinedrivenregulation pages 4-6)
A pilot study in elite athletes evaluated whole-genome expression in blood and reported that SCGB1C1 expression was low in athletes with high IL-5, with fold change 3.17 and adjusted p = 0.00065; the authors proposed SCGB1C1 expression as a potential marker of susceptibility to upper respiratory tract infections. (orysiak2016expressionofscgb1c1 pages 1-2)
An expert review similarly notes SCGB1C1’s potential as a parameter for susceptibility to respiratory infections in contexts such as elite athletes, though this remains in an exploratory biomarker stage rather than clinical implementation. (mootz2022secretoglobinsinthe pages 6-9)
The 2024 murine asthma work operationalizes a translational concept: intranasal delivery of recombinant SCGB1C1 as a mucosal anti-inflammatory biologic to reduce airway hyperresponsiveness and eosinophilic inflammation, with statistical significance across multiple endpoints. This is preclinical and does not yet constitute a human therapy, but it is a concrete “real-world” intervention implementation in animal models. (kim2024scgb1c1playsa pages 2-5)
In ovarian carcinoma profiling, SCGB1C1/RYD5 was one of eight secretoglobin genes measured by qRT-PCR and was reported to be overexpressed in ovarian carcinomas vs normal ovaries (53 tumors vs 30 normals), indicating that SCGB1C1 may appear in secretoglobin-based expression panels in epithelial cancers. (bignotti2013secretoglobinexpressionin pages 1-2)
A high-authority review in Allergy frames secretoglobins as key elements of epithelial barrier immune control, cytokine-responsive, and potentially useful for diagnostic assessment of epithelial activity. It also notes that many family members remain superficially examined, consistent with SCGB1C1’s relatively sparse mechanistic literature. (mootz2022secretoglobinsinthe pages 6-9)
The same review emphasizes that little is known about receptors or molecular mechanisms for SCGB proteins, which is a central limitation in assigning SCGB1C1 to a specific signaling pathway with defined receptor-ligand interactions. (mootz2022secretoglobinsinthe pages 6-9)
Open Targets lists low-evidence associations between SCGB1C1 and several diseases (benign prostatic hyperplasia, uterine fibroid, lipoma, neurodegenerative disease, cataract), each supported by a single evidence item and tracing to PMID:34031600 in the retrieved record; these should be treated as hypothesis-generating rather than definitive SCGB1C1 disease mechanisms. (OpenTargets Search: -SCGB1C1)
| 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 | (mootz2022secretoglobinsinthe pages 26-30, lu2011thecytokinedrivenregulation pages 1-2) |
| 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 | (lu2011thecytokinedrivenregulation pages 1-2, mootz2022secretoglobinsinthe pages 6-9) |
| 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 | (karn2025abroadgenome pages 7-9) |
| 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 | (lu2011thecytokinedrivenregulation pages 4-6) |
| 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 | (mootz2022secretoglobinsinthe pages 26-30, mootz2022secretoglobinsinthe pages 6-9) |
| 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) | (jackson2011updateofthe pages 3-4, olender2016thehumanolfactory pages 1-2, olender2016thehumanolfactory pages 2-4) |
| 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 | (lu2011thecytokinedrivenregulation pages 4-6) |
| 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 | (lu2011thecytokinedrivenregulation pages 4-6, lu2011thecytokinedrivenregulation pages 6-9) |
| 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 | (mootz2022secretoglobinsinthe pages 6-9) |
| 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 | (orysiak2016expressionofscgb1c1 pages 1-2) |
| 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 | (kim2024scgb1c1playsa pages 2-5, kim2024scgb1c1playsa pages 1-2) |
| 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 | (kim2024scgb1c1playsa pages 1-2, kim2024scgb1c1playsa pages 2-5) |
| 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 | (bignotti2013secretoglobinexpressionin pages 1-2) |
| 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 | (OpenTargets Search: -SCGB1C1) |
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.
References
(mootz2022secretoglobinsinthe pages 26-30): Martine Mootz, Constanze A. Jakwerth, Carsten B. Schmidt‐Weber, and Ulrich M. Zissler. Secretoglobins in the big picture of immunoregulation in airway diseases. Allergy, 77:767-777, Aug 2022. URL: https://doi.org/10.1111/all.15033, doi:10.1111/all.15033. This article has 54 citations and is from a highest quality peer-reviewed journal.
(lu2011thecytokinedrivenregulation pages 1-2): Xiang Lu, Nan Wang, Xiao-Bo Long, Xue-Jun You, Yong-Hua Cui, and Zheng Liu. The cytokine-driven regulation of secretoglobins in normal human upper airway and their expression, particularly that of uteroglobin-related protein 1, in chronic rhinosinusitis. Respiratory Research, Dec 2011. URL: https://doi.org/10.1186/1465-9921-12-28, doi:10.1186/1465-9921-12-28. This article has 49 citations and is from a domain leading peer-reviewed journal.
(mootz2022secretoglobinsinthe pages 6-9): Martine Mootz, Constanze A. Jakwerth, Carsten B. Schmidt‐Weber, and Ulrich M. Zissler. Secretoglobins in the big picture of immunoregulation in airway diseases. Allergy, 77:767-777, Aug 2022. URL: https://doi.org/10.1111/all.15033, doi:10.1111/all.15033. This article has 54 citations and is from a highest quality peer-reviewed journal.
(lu2011thecytokinedrivenregulation pages 4-6): Xiang Lu, Nan Wang, Xiao-Bo Long, Xue-Jun You, Yong-Hua Cui, and Zheng Liu. The cytokine-driven regulation of secretoglobins in normal human upper airway and their expression, particularly that of uteroglobin-related protein 1, in chronic rhinosinusitis. Respiratory Research, Dec 2011. URL: https://doi.org/10.1186/1465-9921-12-28, doi:10.1186/1465-9921-12-28. This article has 49 citations and is from a domain leading peer-reviewed journal.
(jackson2011updateofthe pages 3-4): Brian C Jackson, David C Thompson, Mathew W Wright, Monica McAndrews, Alfred Bernard, Daniel W Nebert, and Vasilis Vasiliou. Update of the human secretoglobin (scgb) gene superfamily and an example of 'evolutionary bloom' of androgen-binding protein genes within the mouse scgb gene superfamily. Human Genomics, 5:691-702, Oct 2011. URL: https://doi.org/10.1186/1479-7364-5-6-691, doi:10.1186/1479-7364-5-6-691. This article has 110 citations and is from a peer-reviewed journal.
(urbancic2023transcriptomicdifferentiationof pages 1-2): Jure Urbančič, Tanja Košak Soklič, Ajda Demšar Luzar, Irena Hočevar Boltežar, Peter Korošec, and Matija Rijavec. Transcriptomic differentiation of phenotypes in chronic rhinosinusitis and its implications for understanding the underlying mechanisms. International Journal of Molecular Sciences, 24:5541, Mar 2023. URL: https://doi.org/10.3390/ijms24065541, doi:10.3390/ijms24065541. This article has 6 citations.
(urbancic2023transcriptomicdifferentiationof pages 2-4): Jure Urbančič, Tanja Košak Soklič, Ajda Demšar Luzar, Irena Hočevar Boltežar, Peter Korošec, and Matija Rijavec. Transcriptomic differentiation of phenotypes in chronic rhinosinusitis and its implications for understanding the underlying mechanisms. International Journal of Molecular Sciences, 24:5541, Mar 2023. URL: https://doi.org/10.3390/ijms24065541, doi:10.3390/ijms24065541. This article has 6 citations.
(olender2016thehumanolfactory pages 1-2): Tsviya Olender, Ifat Keydar, Jayant M. Pinto, Pavlo Tatarskyy, Anna Alkelai, Ming-Shan Chien, Simon Fishilevich, Diego Restrepo, Hiroaki Matsunami, Yoav Gilad, and Doron Lancet. The human olfactory transcriptome. BMC Genomics, Aug 2016. URL: https://doi.org/10.1186/s12864-016-2960-3, doi:10.1186/s12864-016-2960-3. This article has 143 citations and is from a peer-reviewed journal.
(olender2016thehumanolfactory pages 2-4): Tsviya Olender, Ifat Keydar, Jayant M. Pinto, Pavlo Tatarskyy, Anna Alkelai, Ming-Shan Chien, Simon Fishilevich, Diego Restrepo, Hiroaki Matsunami, Yoav Gilad, and Doron Lancet. The human olfactory transcriptome. BMC Genomics, Aug 2016. URL: https://doi.org/10.1186/s12864-016-2960-3, doi:10.1186/s12864-016-2960-3. This article has 143 citations and is from a peer-reviewed journal.
(karn2025abroadgenome pages 7-9): Robert C Karn and Christina M Laukaitis. A broad genome survey reveals widespread presence of secretoglobin genes in squamate and archosaur reptiles that flowered into diversity in mammals. Genome Biology and Evolution, Feb 2025. URL: https://doi.org/10.1093/gbe/evaf024, doi:10.1093/gbe/evaf024. This article has 0 citations and is from a domain leading peer-reviewed journal.
(kim2024scgb1c1playsa pages 2-5): Sung-Dong Kim, Shin-Ae Kang, Sue-Jean Mun, Hak-Sun Yu, Hwan-Jung Roh, and Kyu-Sup Cho. Scgb1c1 plays a critical role in suppression of allergic airway inflammation through the induction of regulatory t cell expansion. International Journal of Molecular Sciences, 25:6282, Jun 2024. URL: https://doi.org/10.3390/ijms25116282, doi:10.3390/ijms25116282. This article has 3 citations.
(orysiak2016expressionofscgb1c1 pages 1-2): Joanna Orysiak, Jadwiga Malczewska-Lenczowska, and Miroslaw Bik-Multanowski. Expression of scgb1c1 gene as a potential marker of susceptibility to upper respiratory tract infections in elite athletes – a pilot study. Biology of Sport, 33(2):107-110, Mar 2016. URL: https://doi.org/10.5604/20831862.1196510, doi:10.5604/20831862.1196510. This article has 13 citations and is from a peer-reviewed journal.
(bignotti2013secretoglobinexpressionin pages 1-2): Eliana Bignotti, Renata A Tassi, Stefano Calza, Antonella Ravaggi, Elisa Rossi, Carla Donzelli, Paola Todeschini, Chiara Romani, Elisabetta Bandiera, Laura Zanotti, Mario Carnazza, Francesco Quadraro, Germana Tognon, Enrico Sartori, Sergio Pecorelli, Dana M Roque, and Alessandro D Santin. Secretoglobin expression in ovarian carcinoma: lipophilin b gene upregulation as an independent marker of better prognosis. Journal of Translational Medicine, Jul 2013. URL: https://doi.org/10.1186/1479-5876-11-162, doi:10.1186/1479-5876-11-162. This article has 18 citations and is from a peer-reviewed journal.
(OpenTargets Search: -SCGB1C1): Open Targets Query (-SCGB1C1, 5 results). Buniello, A. et al. (2025). Open Targets Platform: facilitating therapeutic hypotheses building in drug discovery. Nucleic Acids Research.
(lu2011thecytokinedrivenregulation pages 6-9): Xiang Lu, Nan Wang, Xiao-Bo Long, Xue-Jun You, Yong-Hua Cui, and Zheng Liu. The cytokine-driven regulation of secretoglobins in normal human upper airway and their expression, particularly that of uteroglobin-related protein 1, in chronic rhinosinusitis. Respiratory Research, Dec 2011. URL: https://doi.org/10.1186/1465-9921-12-28, doi:10.1186/1465-9921-12-28. This article has 49 citations and is from a domain leading peer-reviewed journal.
(kim2024scgb1c1playsa pages 1-2): Sung-Dong Kim, Shin-Ae Kang, Sue-Jean Mun, Hak-Sun Yu, Hwan-Jung Roh, and Kyu-Sup Cho. Scgb1c1 plays a critical role in suppression of allergic airway inflammation through the induction of regulatory t cell expansion. International Journal of Molecular Sciences, 25:6282, Jun 2024. URL: https://doi.org/10.3390/ijms25116282, doi:10.3390/ijms25116282. This article has 3 citations.