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this with annotations you find in gene/protein databases, but these can be outdated or inaccurate.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 literature retrieved is consistent with the UniProt target P15941 = human MUC1 (mucin-1), a type I transmembrane mucin expressed by epithelial barrier tissues and processed into two subunits, MUC1-N (extracellular, shed) and MUC1-C (transmembrane + cytoplasmic tail, signaling-competent). Reviews describe SEA-domain autoproteolysis at the GSVVV motif, generating a noncovalent heterodimer that traffics to the apical surface. (Mao et al., 2024-11-18, https://doi.org/10.1186/s11658-024-00654-x) (mao2024researchprogressof pages 2-6)
A recent precision-oncology review explicitly lists major clinical aliases—CD227, EMA, KL-6, CA 27.29/CA 15-3—as alternative names for MUC1, aligning with the UniProt description provided by the user. (Grewal & Kurzrock, 2025-07-11, https://doi.org/10.1038/s41698-025-01016-2) (grewal2025mucin1apromising pages 2-3)
Visual support: A schematic of MUC1 gene/protein architecture and SEA cleavage was retrieved (Figure 1 in Mao et al. 2024). (mao2024researchprogressof media db8ef381)
MUC1 is a highly glycosylated type I transmembrane mucin whose mass is dominated by glycans (reviewed as ~50–90% sugar mass). It is encoded by seven exons and contains an extracellular VNTR region and a SEA domain. (Mao et al., 2024-11-18, https://doi.org/10.1186/s11658-024-00654-x) (mao2024researchprogressof pages 2-6)
A conserved SEA domain functions as a cleavage site in multiple transmembrane mucins; MUC1 is cleaved in the SEA domain during post-translational processing into two associated subunits, and extracellular portions can be shed, shaping both biology and therapeutic tractability. (Mao et al., 2024-11-18, https://doi.org/10.1186/s11658-024-00654-x; Li et al., 2025-04-07, https://doi.org/10.1038/s41420-025-02455-3) (mao2024researchprogressof pages 2-6, li2025transmembranemucinsin pages 2-4)
In healthy epithelia, MUC1 is primarily apically localized and contributes to hydration/lubrication and protection of barrier surfaces. (Tong et al., 2024-01-01, https://doi.org/10.7150/jca.88261; Grewal & Kurzrock, 2025-07-11, https://doi.org/10.1038/s41698-025-01016-2) (tong2024mucin1asa pages 3-4, grewal2025mucin1apromising pages 1-2)
MUC1 is synthesized and traffics ER→Golgi→apical membrane as a MUC1-N/MUC1-C heterodimer. Cancer-associated MUC1 is described as losing polarity and appearing across the cell surface and in intracellular compartments. (Mao et al., 2024-11-18, https://doi.org/10.1186/s11658-024-00654-x; Tong et al., 2024-01-01, https://doi.org/10.7150/jca.88261) (mao2024researchprogressof pages 2-6, tong2024mucin1asa pages 3-4)
Multiple reviews report that MUC1-C can accumulate in the cytosol and translocate to the nucleus and mitochondria, consistent with its role as a transcriptional and stress-response regulator. (Milella et al., 2024-03-06, https://doi.org/10.3390/biom14030315) (milella2024theroleof pages 2-4)
Mechanistic details for nuclear import have been summarized in transmembrane mucin reviews (importin-β and nucleoporin 62 implicated for MUC1-C). (Li et al., 2025-04-07, https://doi.org/10.1038/s41420-025-02455-3) (li2025transmembranemucinsin pages 2-4)
Across 2024 reviews, MUC1-C is consistently portrayed as the signaling-active oncoprotein subunit.
Key pathways and binding partners supported by recent synthesis:
- JAK/STAT (STAT1/STAT3): MUC1-C directly binds STAT1 and promotes STAT target gene activation, including a positive feedback on MUC1 transcription. (Tong et al., 2024-01-01, https://doi.org/10.7150/jca.88261) (tong2024mucin1asa pages 1-3, tong2024mucin1asa pages 3-4)
- NF-κB (p65/RELA): MUC1-C is described as activating NF-κB p65 signaling, contributing to inflammatory programs and EMT-related transcription. (Tong et al., 2024-01-01, https://doi.org/10.7150/jca.88261; Milella et al., 2024-03-06, https://doi.org/10.3390/biom14030315) (tong2024mucin1asa pages 3-4, milella2024theroleof pages 2-4)
- Wnt/β-catenin: MUC1-C stabilizes β-catenin and promotes Wnt target gene programs (e.g., MYC/CCND1 in review summaries), supporting EMT and tumor progression. (Tong et al., 2024-01-01, https://doi.org/10.7150/jca.88261; Milella et al., 2024-03-06, https://doi.org/10.3390/biom14030315) (tong2024mucin1asa pages 3-4, milella2024theroleof pages 2-4)
- RTKs and PI3K/AKT: Reviews describe MUC1-C interactions with receptor tyrosine kinases (including EGFR/ErbB2 and others) and activation of downstream PI3K→AKT signaling, supporting proliferation/survival and therapy resistance. (Tong et al., 2024-01-01, https://doi.org/10.7150/jca.88261) (tong2024mucin1asa pages 3-4)
A 2023 translational study provides direct evidence that MUC1 can attenuate neutrophilic airway inflammation by inhibiting the TLR4/MyD88/NF-κB pathway, reducing NLRP3 inflammasome-mediated pyroptosis. (Liu et al., 2023-10-05, https://doi.org/10.1186/s12931-023-02550-y) (liu2023muc1attenuatesneutrophilic pages 1-2)
Key quantitative/experimental details:
- Human sputum cohorts: healthy controls n=12; mild-to-moderate asthma n=34; severe asthma n=18. MUC1 mRNA was downregulated in asthma (notably severe), while TLR4/MyD88/NLRP3/caspase-1/IL-18/IL-1β mRNAs were increased. (liu2023muc1attenuatesneutrophilic pages 5-9)
- In vitro: LPS-stimulated BEAS-2B epithelial cells showed pathway activation and pyroptosis markers; MUC1 knockdown aggravated TLR4/MyD88/p-p65 activation and downstream inflammasome/pyroptosis readouts; the TLR4 inhibitor TAK-242 reversed these effects. (liu2023muc1attenuatesneutrophilic pages 5-9)
- Mechanism: co-immunoprecipitation indicated MUC1-CT interacts with TLR4 and MUC1 deficiency increases TLR4–MyD88 binding, supporting a physical constraint model. (liu2023muc1attenuatesneutrophilic pages 9-12)
A 2024 Nature Communications study links chronic hypoxia to durable transcriptional programs that persist after reoxygenation and promote metastasis, with MUC1/MUC1-C as a key effector induced by HIF-1α and NF-κB p65. (Godet et al., 2024-09-16, https://doi.org/10.1038/s41467-024-51995-2) (godet2024hypoxiainducesrosresistant pages 1-2)
Quantitative findings include:
- GO-203 pharmacologic inhibition increased mitochondrial ROS in circulating tumor cells (CTCs) and yielded a 53% reduction in the contribution of hypoxia-marked (GFP+) cells to metastatic burden in an in vivo model. (godet2024hypoxiainducesrosresistant pages 8-9)
- MUC1low CTCs exhibited ~2× higher MitoROS than matched MUC1high CTCs, connecting MUC1 expression to ROS defense. (godet2024hypoxiainducesrosresistant pages 8-9)
A 2024 Cell Death Discovery study identifies MUC1-C as a functional node in ferroptosis resistance of CSC-like tumor cells and reports that salinomycin suppresses MUC1-C signaling and induces ferroptosis. Mechanistically, MUC1-C sustains antioxidant defenses through a NF-κB/MUC1-C auto-inductive circuit and a MUC1-C→MYC axis that regulates GSR, LRP8, and GPX4 activity, consistent with glutathione/selenium-dependent ferroptosis control. (Daimon et al., 2024-01-10, https://doi.org/10.1038/s41420-023-01772-9) (daimon2024muc1cisa pages 1-2)
Quantitative/experimental details include salinomycin dosing (1 μM, 24 h) decreasing tumorsphere self-renewal and inducing lipid peroxidation, with effects blocked by Ferrostatin-1; GO-203 phenocopied salinomycin by downregulating GSR/LRP8/GPX4 and GPX activity (reported with replicate-normalized quantitative plots). (daimon2024muc1cisa pages 4-6)
In head and neck squamous cell carcinoma (HNSCC), a 2024 primary study reports that MUC1-C integrates chronic inflammatory signaling by regulating PRRs, STAT1 and type I/II interferon programs, with downstream ISGs supporting DNA damage resistance and immune evasion; MUC1-C was also necessary for NOTCH3 expression, self-renewal, and tumorigenicity, and associated with ΔNp63/SOX2/NOTCH3 programs by single-cell RNA-seq. (Nakashoji et al., 2024-04-10, https://doi.org/10.1158/2767-9764.crc-24-0011) (nakashoji2024identificationofmuc1c pages 1-2)
A precision oncology review states that soluble MUC1-N is measured clinically as CA 27.29/CA 15-3, which are FDA-approved tests for monitoring breast cancer, used with imaging/clinical assessments, and elevations correlate with recurrence/progression (the review cautions they should not be used interchangeably). (Grewal & Kurzrock, 2025-07-11, https://doi.org/10.1038/s41698-025-01016-2) (grewal2025mucin1apromising pages 1-2)
KL-6 is described as a human MUC1 mucin produced by regenerating type II pneumocytes and used as an ILD severity marker in clinical routine (especially in Japan). (Bonella et al., 2025-10-02, https://doi.org/10.1038/s41598-025-22483-4) (bonella2025serumkl6as pages 1-2)
A large real-world ILD biomarker analysis from UK-BILD (PLOS ONE 2024) included 3,169 enrolled patients, with 1,013 selected for idiopathic ILD vs SARD-ILD comparisons; a diagnostic model including KL-6 achieved 69.4% sensitivity and 80.4% specificity for distinguishing idiopathic ILD, and KL-6 was significantly higher in idiopathic ILD (p=0.0002). (d’Alessandro et al., 2024-10-11, https://doi.org/10.1371/journal.pone.0311357) (d’alessandro2024panelofserum pages 1-2)
Rationale: targeting shed MUC1-N has been challenging; newer strategies focus on MUC1-C (nonshed, signaling-competent). (Ohta et al., 2025-10-09, https://doi.org/10.7759/cureus.95636) (ohta2025adescriptivesummary pages 1-2)
Modalities in development include vaccines, monoclonal antibodies and ADCs, and cellular therapies according to a 2025 review. (Grewal & Kurzrock, 2025-07-11, https://doi.org/10.1038/s41698-025-01016-2) (grewal2025mucin1apromising pages 2-3)
The retrieved ClinicalTrials.gov entries show heterogeneous approaches (vaccines, peptide + adjuvant, dendritic cell/CTL, CAR-T). Examples with extracted details:
- NCT00004156 (MSKCC; start May 1999; primary completion June 2008): Phase 1 glycosylated MUC1-KLH + QS21 vaccine in high-risk breast cancer; enrollment 45; immune-response endpoint. (https://clinicaltrials.gov/study/NCT00004156) (NCT00004156 chunk 1)
- NCT00773097 (start 2008): Phase 2 100mer MUC1 peptide + Poly-ICLC vaccine in individuals with advanced colorectal adenoma; enrollment 46; primary endpoint anti-MUC1 antibody response. (https://clinicaltrials.gov/study/NCT00773097) (NCT00773097 chunk 1)
- NCT02602249 (Beijing Doing Biomedical; 2017): Phase 1 randomized DC/CTL products (MUC1-gene-DC-CTL or MUC1-peptide-DC-CTL) vs saline in stage IV gastric cancer; estimated enrollment 24; primary endpoint tumor size by RECIST; status listed as UNKNOWN / lastKnown NOT_YET_RECRUITING in retrieved text. (https://clinicaltrials.gov/study/NCT02602249) (NCT02602249 chunk 1)
Recent reviews converge on a conceptual division of labor:
- MUC1-N primarily mediates barrier/lubrication and is readily shed, which complicates antibody targeting but provides a basis for circulating biomarkers (CA15-3/CA27.29). (Milella et al., 2024-03-06, https://doi.org/10.3390/biom14030315; Grewal & Kurzrock, 2025-07-11, https://doi.org/10.1038/s41698-025-01016-2) (milella2024theroleof pages 2-4, grewal2025mucin1apromising pages 1-2)
- MUC1-C is the major signal-transduction and transcriptional effector, integrating RTK, PI3K/AKT, Wnt/β-catenin, STAT and NF-κB programs to promote plasticity, stress tolerance (ROS/ferroptosis resistance), and immune evasion. (Tong et al., 2024-01-01, https://doi.org/10.7150/jca.88261; Godet et al., 2024-09-16, https://doi.org/10.1038/s41467-024-51995-2; Daimon et al., 2024-01-10, https://doi.org/10.1038/s41420-023-01772-9) (tong2024mucin1asa pages 3-4, godet2024hypoxiainducesrosresistant pages 1-2, daimon2024muc1cisa pages 1-2)
Human MUC1 (P15941) is a SEA-domain–cleaved transmembrane mucin heterodimer. MUC1-N is a shed, heavily O-glycosylated VNTR-rich extracellular subunit that provides lubrication and barrier protection at apical epithelial surfaces and underlies circulating biomarkers (CA15-3/CA27.29, and the glycoform KL-6). MUC1-C is a signaling-active transmembrane subunit that can translocate to intracellular compartments (including nucleus/mitochondria) and acts as a hub integrating RTK/PI3K/AKT, NF-κB, STAT, and β-catenin programs, thereby supporting inflammation-linked transcription, EMT/plasticity, redox/ferroptosis resistance, stemness, and immune evasion. Recent 2023–2024 primary studies strengthen causal links between MUC1/MUC1-C and (i) epithelial innate immune modulation via TLR4/MyD88/NF-κB→NLRP3 pyroptosis in asthma and (ii) hypoxia-driven ROS-resistant metastatic competence and ferroptosis resistance in cancer. (mao2024researchprogressof pages 2-6, tong2024mucin1asa pages 3-4, liu2023muc1attenuatesneutrophilic pages 5-9, godet2024hypoxiainducesrosresistant pages 8-9, daimon2024muc1cisa pages 4-6)
| Application area | Specific marker/agent | Indication(s) | Key quantitative data | Current status/notes | Key supporting citation IDs |
|---|---|---|---|---|---|
| Biomarker/diagnostic | CA15-3 / CA27.29 (shed MUC1-N) | Breast cancer monitoring/prognosis | Used clinically for monitoring; elevated levels correlate with recurrence/disease progression; no sensitivity/specificity reported in retrieved sources. In one 2024 breast cohort, CA15-3 median was 18.66 U/mL in breast cancer vs 11.74 U/mL in benign breast tumors (31 vs 30 patients; p=0.001). | FDA-approved for monitoring breast cancer; should not be used interchangeably according to review summary. | (grewal2025mucin1apromising pages 1-2, mao2024researchprogressof pages 2-6) |
| Biomarker/diagnostic | KL-6 (MUC1 glycoform) | Interstitial lung disease (ILD) severity/progression | European multicenter ILD study: n=303, 37% progressed at 1 year; risk model including KL-6 gave 55% sensitivity, 73% specificity, 67% accuracy for 1-year progression. | Established serum biomarker for ILD severity; used in clinical routine, especially in Japan; measured by automated chemiluminescent immunoassay. | (bonella2025serumkl6as pages 1-2) |
| Biomarker/diagnostic | KL-6 | Differential diagnosis of idiopathic ILD vs SARD-ILD | UK-BILD analysis: 1,013 patients selected from 3,169 enrolled (520 idiopathic ILD, 493 SARD-ILD); multivariable model including KL-6 achieved 69.4% sensitivity and 80.4% specificity; KL-6 higher in idiopathic ILD (p=0.0002). | Real-world serum biomarker panel measured by Fujirebio chemiluminescent assay. | (d’alessandro2024panelofserum pages 1-2, d’alessandro2024panelofserum pages 2-3) |
| Biomarker/diagnostic | KL-6 | Lung cancer prognosis | Meta-analysis of 13 studies/1,723 patients: high pretreatment KL-6 associated with shorter PFS (HR 1.89, 95% CI 1.46-2.44) and OS (HR 1.76, 95% CI 1.37-2.26); >500 U/mL associated with worse outcomes. | Prognostic signal strongest in patients without ILD; ECLIA outperformed ELISA in pooled analysis. | (huang2025serumkrebsvon pages 1-2, huang2025serumkrebsvon pages 5-6) |
| Therapeutic target | GO-203 (MUC1-C inhibitor peptide) | Experimental MUC1-C targeting in cancer; cited AML clinical development; asthma/hypoxia models | In hypoxia-memory breast cancer model, 5 daily GO-203 doses increased mitoROS in CTCs and reduced GFP+ metastatic burden by 53%; in asthma mouse model, GO-203 exacerbated neutrophilic inflammation (n=6/group). | Not approved; cited as having completed/undergone Phase I evaluation in AML in review literature; strong preclinical activity but no approved indication in retrieved sources. | (godet2024hypoxiainducesrosresistant pages 8-9, liu2023muc1attenuatesneutrophilic pages 9-12, tong2024mucin1asa pages 3-4) |
| Therapeutic target | MUC1-C antibody-drug conjugate (3D1-MMAE / M1C ADC concept) | Solid tumors with MUC1-C overexpression | Preclinical ADC showed antitumor activity in lung, breast, and patient-derived TNBC models; no human enrollment data in retrieved primary ADC paper. | Preclinical/translation-stage platform; rationale strengthened by failure of MUC1-N targeting due to shedding. | (ohta2025adescriptivesummary pages 1-2, tong2024mucin1asa pages 8-10) |
| Therapeutic target | MUC1 vaccines (MUC1-KLH/QS21; peptide + Poly-ICLC; ImMucin) | Breast cancer, advanced colorectal adenoma prevention, MUC1-expressing tumors | NCT00004156 Phase 1 breast cancer vaccine: enrolled 45; immune-response endpoint over 2 years. NCT00773097 Phase 2 colorectal adenoma vaccine: enrolled 46. NCT00162500 ImMucin Phase 2: planned 15, withdrawn. Historic tecemotide Phase 3 NSCLC trial enrolled 1,513 but no OS benefit (review summary). | Multiple vaccine platforms tested; many completed or withdrawn, with limited definitive efficacy despite immunogenicity. | (NCT00004156 chunk 1, NCT00773097 chunk 1, NCT00162500 chunk 1, taylorpapadimitriou2018latestdevelopmentsin pages 3-4) |
| Therapeutic target | MUC1-directed DC/CTL therapy | Stage IV gastric cancer; pancreatic/biliary tumors; ovarian cancer | NCT02602249 randomized Phase 1 stage IV gastric cancer trial planned enrollment 24; compares MUC1-gene-DC-CTL, MUC1-peptide-DC-CTL, and saline. Review summary notes autologous DC + CTL regimen in 42 late-stage pancreatic patients and peptide-pulsed DC adjuvant study with 4/12 recurrence-free survivors, median survival 26 months. | Gastric cancer trial listed as UNKNOWN / NOT_YET_RECRUITING in retrieved record; broader DC strategies remain investigational. | (NCT02602249 chunk 1, lee2021mucin1andmucin16 pages 15-17, taylorpapadimitriou2018latestdevelopmentsin pages 3-4) |
| Therapeutic target | MUC1 CAR-T | Intrahepatic cholangiocarcinoma | NCT03633773 Phase 1/2 trial enrollment 9. | Human study exists in ClinicalTrials.gov retrieval; overall status listed as UNKNOWN in search output. | (OpenTargets Search: -MUC1) |
| Disease genetics | Germline MUC1 pathogenic variants (ADTKD-MUC1) | Autosomal dominant tubulointerstitial kidney disease; COVID-19 risk in affected patients | Registry/survey study: 89 ADTKD-MUC1 and 132 ADTKD-UMOD respondents; COVID-19 infection OR 2.35; deaths 10/41 vs 1/30 in expanded familial cases (OR 9.21); longitudinal registry 19/360 (5%) vs 3/478 (0.6%) deaths, multivariable OR for COVID-19 death 8.4 (95% CI 2.9-29.5). Lower pre-infection plasma mucin-1/CA15-3 in infected vs uninfected ADTKD-MUC1 (7.06 ± 4.12 vs 10.21 ± 4.02 U/mL, p=0.035). | Established Mendelian disease association; Open Targets also lists strong association with ADTKD-related disease terms. | (OpenTargets Search: -MUC1, mao2024researchprogressof pages 2-6) |
Table: This table summarizes real-world and translational uses of MUC1 across biomarkers, therapeutics, and inherited disease genetics. It highlights quantitative findings, study sizes, and implementation status using only evidence available in the conversation.
References
(mao2024researchprogressof pages 2-6): Weipu Mao, Houliang Zhang, Keyi Wang, Jiang Geng, and Jianping Wu. Research progress of muc1 in genitourinary cancers. Cellular & Molecular Biology Letters, Nov 2024. URL: https://doi.org/10.1186/s11658-024-00654-x, doi:10.1186/s11658-024-00654-x. This article has 5 citations and is from a peer-reviewed journal.
(grewal2025mucin1apromising pages 2-3): Udhayvir Singh Grewal and Razelle Kurzrock. Mucin-1: a promising pan-cancer therapeutic target. NPJ Precision Oncology, Jul 2025. URL: https://doi.org/10.1038/s41698-025-01016-2, doi:10.1038/s41698-025-01016-2. This article has 28 citations and is from a peer-reviewed journal.
(mao2024researchprogressof media db8ef381): Weipu Mao, Houliang Zhang, Keyi Wang, Jiang Geng, and Jianping Wu. Research progress of muc1 in genitourinary cancers. Cellular & Molecular Biology Letters, Nov 2024. URL: https://doi.org/10.1186/s11658-024-00654-x, doi:10.1186/s11658-024-00654-x. This article has 5 citations and is from a peer-reviewed journal.
(tong2024mucin1asa pages 1-3): Xiaohan Tong, Chunyan Dong, and Shujing Liang. Mucin1 as a potential molecule for cancer immunotherapy and targeted therapy. Journal of Cancer, 15:54-67, Jan 2024. URL: https://doi.org/10.7150/jca.88261, doi:10.7150/jca.88261. This article has 26 citations and is from a peer-reviewed journal.
(li2025transmembranemucinsin pages 2-4): Xiaoqing Li, Ying Chen, Rui Lan, Peng Liu, Kai Xiong, Hetai Teng, Lili Tao, Shan Yu, and Guiping Han. Transmembrane mucins in lung adenocarcinoma: understanding of current molecular mechanisms and clinical applications. Cell Death Discovery, Apr 2025. URL: https://doi.org/10.1038/s41420-025-02455-3, doi:10.1038/s41420-025-02455-3. This article has 13 citations and is from a peer-reviewed journal.
(tong2024mucin1asa pages 3-4): Xiaohan Tong, Chunyan Dong, and Shujing Liang. Mucin1 as a potential molecule for cancer immunotherapy and targeted therapy. Journal of Cancer, 15:54-67, Jan 2024. URL: https://doi.org/10.7150/jca.88261, doi:10.7150/jca.88261. This article has 26 citations and is from a peer-reviewed journal.
(grewal2025mucin1apromising pages 1-2): Udhayvir Singh Grewal and Razelle Kurzrock. Mucin-1: a promising pan-cancer therapeutic target. NPJ Precision Oncology, Jul 2025. URL: https://doi.org/10.1038/s41698-025-01016-2, doi:10.1038/s41698-025-01016-2. This article has 28 citations and is from a peer-reviewed journal.
(milella2024theroleof pages 2-4): Martina Milella, Monica Rutigliano, Francesco Lasorsa, Matteo Ferro, Roberto Bianchi, Giuseppe Fallara, Felice Crocetto, Savio Pandolfo, Biagio Barone, Antonio d’Amati, Marco Spilotros, Michele Battaglia, Pasquale Ditonno, and Giuseppe Lucarelli. The role of muc1 in renal cell carcinoma. Biomolecules, 14:315, Mar 2024. URL: https://doi.org/10.3390/biom14030315, doi:10.3390/biom14030315. This article has 70 citations.
(liu2023muc1attenuatesneutrophilic pages 1-2): Lu Liu, Ling Zhou, Lingling Wang, Zhenyu Mao, Pengdou Zheng, Fengqin Zhang, Huojun Zhang, and Huiguo Liu. Muc1 attenuates neutrophilic airway inflammation in asthma by reducing nlrp3 inflammasome-mediated pyroptosis through the inhibition of the tlr4/myd88/nf-κb pathway. Respiratory Research, Oct 2023. URL: https://doi.org/10.1186/s12931-023-02550-y, doi:10.1186/s12931-023-02550-y. This article has 58 citations and is from a domain leading peer-reviewed journal.
(liu2023muc1attenuatesneutrophilic pages 5-9): Lu Liu, Ling Zhou, Lingling Wang, Zhenyu Mao, Pengdou Zheng, Fengqin Zhang, Huojun Zhang, and Huiguo Liu. Muc1 attenuates neutrophilic airway inflammation in asthma by reducing nlrp3 inflammasome-mediated pyroptosis through the inhibition of the tlr4/myd88/nf-κb pathway. Respiratory Research, Oct 2023. URL: https://doi.org/10.1186/s12931-023-02550-y, doi:10.1186/s12931-023-02550-y. This article has 58 citations and is from a domain leading peer-reviewed journal.
(liu2023muc1attenuatesneutrophilic pages 9-12): Lu Liu, Ling Zhou, Lingling Wang, Zhenyu Mao, Pengdou Zheng, Fengqin Zhang, Huojun Zhang, and Huiguo Liu. Muc1 attenuates neutrophilic airway inflammation in asthma by reducing nlrp3 inflammasome-mediated pyroptosis through the inhibition of the tlr4/myd88/nf-κb pathway. Respiratory Research, Oct 2023. URL: https://doi.org/10.1186/s12931-023-02550-y, doi:10.1186/s12931-023-02550-y. This article has 58 citations and is from a domain leading peer-reviewed journal.
(godet2024hypoxiainducesrosresistant pages 1-2): Inês Godet, Harsh H. Oza, Yi Shi, Natalie S. Joe, Alyssa G. Weinstein, Jeanette Johnson, Michael Considine, Swathi Talluri, Jingyuan Zhang, Reid Xu, Steven Doctorman, Delma Mbulaiteye, Genevieve Stein-O’Brien, Luciane T. Kagohara, Cesar A. Santa-Maria, Elana J. Fertig, and Daniele M. Gilkes. Hypoxia induces ros-resistant memory upon reoxygenation in vivo promoting metastasis in part via muc1-c. Nature Communications, Sep 2024. URL: https://doi.org/10.1038/s41467-024-51995-2, doi:10.1038/s41467-024-51995-2. This article has 35 citations and is from a highest quality peer-reviewed journal.
(godet2024hypoxiainducesrosresistant pages 8-9): Inês Godet, Harsh H. Oza, Yi Shi, Natalie S. Joe, Alyssa G. Weinstein, Jeanette Johnson, Michael Considine, Swathi Talluri, Jingyuan Zhang, Reid Xu, Steven Doctorman, Delma Mbulaiteye, Genevieve Stein-O’Brien, Luciane T. Kagohara, Cesar A. Santa-Maria, Elana J. Fertig, and Daniele M. Gilkes. Hypoxia induces ros-resistant memory upon reoxygenation in vivo promoting metastasis in part via muc1-c. Nature Communications, Sep 2024. URL: https://doi.org/10.1038/s41467-024-51995-2, doi:10.1038/s41467-024-51995-2. This article has 35 citations and is from a highest quality peer-reviewed journal.
(daimon2024muc1cisa pages 1-2): Tatsuaki Daimon, Atrayee Bhattacharya, Keyi Wang, Naoki Haratake, Ayako Nakashoji, Hiroki Ozawa, Yoshihiro Morimoto, Nami Yamashita, Takeo Kosaka, Mototsugu Oya, and Donald W. Kufe. Muc1-c is a target of salinomycin in inducing ferroptosis of cancer stem cells. Cell Death Discovery, Jan 2024. URL: https://doi.org/10.1038/s41420-023-01772-9, doi:10.1038/s41420-023-01772-9. This article has 13 citations and is from a peer-reviewed journal.
(daimon2024muc1cisa pages 4-6): Tatsuaki Daimon, Atrayee Bhattacharya, Keyi Wang, Naoki Haratake, Ayako Nakashoji, Hiroki Ozawa, Yoshihiro Morimoto, Nami Yamashita, Takeo Kosaka, Mototsugu Oya, and Donald W. Kufe. Muc1-c is a target of salinomycin in inducing ferroptosis of cancer stem cells. Cell Death Discovery, Jan 2024. URL: https://doi.org/10.1038/s41420-023-01772-9, doi:10.1038/s41420-023-01772-9. This article has 13 citations and is from a peer-reviewed journal.
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