 Pulmonary Surfactant-Associated Protein C
"Pulmonary Surfactant-Associated Protein C" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus,
MeSH (Medical Subject Headings). Descriptors are arranged in a hierarchical structure,
which enables searching at various levels of specificity.
A pulmonary surfactant associated protein that plays a role in alveolar stability by lowering the surface tension at the air-liquid interface. It is a membrane-bound protein that constitutes 1-2% of the pulmonary surfactant mass. Pulmonary surfactant-associated protein C is one of the most hydrophobic peptides yet isolated and contains an alpha-helical domain with a central poly-valine segment that binds to phospholipid bilayers.
| Descriptor ID |
D037721
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| MeSH Number(s) |
D12.776.543.717 D12.776.816.750 D12.776.823.186
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| Concept/Terms |
Pulmonary Surfactant-Associated Protein C- Pulmonary Surfactant-Associated Protein C
- Pulmonary Surfactant Associated Protein C
- Surfactant Polypeptide SP-C
- SP-C, Surfactant Polypeptide
- Surfactant Polypeptide SP C
- SP-C protein
- SP C protein
- Pulmonary Surfactant Protein C
- Pulmonary Surfactant-Associated Protein SP-C
- Pulmonary Surfactant Associated Protein SP C
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Below are MeSH descriptors whose meaning is more general than "Pulmonary Surfactant-Associated Protein C".
Below are MeSH descriptors whose meaning is more specific than "Pulmonary Surfactant-Associated Protein C".
This graph shows the total number of publications written about "Pulmonary Surfactant-Associated Protein C" by people in this website by year, and whether "Pulmonary Surfactant-Associated Protein C" was a major or minor topic of these publications.
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| Year | Major Topic | Minor Topic | Total |
|---|
| 2016 | 0 | 1 | 1 | | 2019 | 0 | 1 | 1 | | 2020 | 1 | 0 | 1 |
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Below are the most recent publications written about "Pulmonary Surfactant-Associated Protein C" by people in Profiles.
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Chen Q, Rehman J, Chan M, Fu P, Dudek SM, Natarajan V, Malik AB, Liu Y. Angiocrine Sphingosine-1-Phosphate Activation of S1PR2-YAP Signaling Axis in Alveolar Type II Cells Is Essential for Lung Repair. Cell Rep. 2020 06 30; 31(13):107828.
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Dorry SJ, Ansbro BO, Ornitz DM, Mutlu GM, Guzy RD. FGFR2 Is Required for AEC2 Homeostasis and Survival after Bleomycin-induced Lung Injury. Am J Respir Cell Mol Biol. 2020 05; 62(5):608-621.
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Moore C, Blumhagen RZ, Yang IV, Walts A, Powers J, Walker T, Bishop M, Russell P, Vestal B, Cardwell J, Markin CR, Mathai SK, Schwarz MI, Steele MP, Lee J, Brown KK, Loyd JE, Crapo JD, Silverman EK, Cho MH, James JA, Guthridge JM, Cogan JD, Kropski JA, Swigris JJ, Bair C, Kim DS, Ji W, Kim H, Song JW, Maier LA, Pacheco KA, Hirani N, Poon AS, Li F, Jenkins RG, Braybrooke R, Saini G, Maher TM, Molyneaux PL, Saunders P, Zhang Y, Gibson KF, Kass DJ, Rojas M, Sembrat J, Wolters PJ, Collard HR, Sundy JS, O'Riordan T, Strek ME, Noth I, Ma SF, Porteous MK, Kreider ME, Patel NB, Inoue Y, Hirose M, Arai T, Akagawa S, Eickelberg O, Fernandez IE, Behr J, Mogulkoc N, Corte TJ, Glaspole I, Tomassetti S, Ravaglia C, Poletti V, Crestani B, Borie R, Kannengiesser C, Parfrey H, Fiddler C, Rassl D, Molina-Molina M, Machahua C, Worboys AM, Gudmundsson G, Isaksson HJ, Lederer DJ, Podolanczuk AJ, Montesi SB, Bendstrup E, Danchel V, Selman M, Pardo A, Henry MT, Keane MP, Doran P, Vašáková M, Sterclova M, Ryerson CJ, Wilcox PG, Okamoto T, Furusawa H, Miyazaki Y, Laurent G, Baltic S, Prele C, Moodley Y, Shea BS, Ohta K, Suzukawa M, Narumoto O, Nathan SD, Venuto DC, Woldehanna ML, Kokturk N, de Andrade JA, Luckhardt T, Kulkarni T, Bonella F, Donnelly SC, McElroy A, Armstong ME, Aranda A, Carbone RG, Puppo F, Beckman KB, Nickerson DA, Fingerlin TE, Schwartz DA. Resequencing Study Confirms That Host Defense and Cell Senescence Gene Variants Contribute to the Risk of Idiopathic Pulmonary Fibrosis. Am J Respir Crit Care Med. 2019 07 15; 200(2):199-208.
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Kim SJ, Cheresh P, Jablonski RP, Morales-Nebreda L, Cheng Y, Hogan E, Yeldandi A, Chi M, Piseaux R, Ridge K, Michael Hart C, Chandel N, Scott Budinger GR, Kamp DW. Mitochondrial catalase overexpressed transgenic mice are protected against lung fibrosis in part via preventing alveolar epithelial cell mitochondrial DNA damage. Free Radic Biol Med. 2016 12; 101:482-490.
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