Hwp1
 | This article needs additional citations for verification. (January 2017) |
| Hyphal wall protein 1 | |||||||
|---|---|---|---|---|---|---|---|
| Identifiers | |||||||
| Organism | |||||||
| Symbol | Hwp1 | ||||||
| UniProt | C4YHA6 | ||||||
| |||||||
| Hyphal wall protein 1 | |||||||
|---|---|---|---|---|---|---|---|
| Identifiers | |||||||
| Organism | |||||||
| Symbol | Hwp1 | ||||||
| UniProt | P46593 | ||||||
| |||||||
Hwp1 (Hyphal wall protein 1) is a protein (glycoprotein) located on the surface of an opportunistic diploid fungus called Candida albicans.
This "hyphal" denomination is due to Hwp1 appears exclusively on the surface of a projection called hyphae that emerges from the surface of this fungus.
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Candida Albicans Yeast forms (round-to-oval) -
Candida Albicans Hyphal forms (filamentous projections called hyphaes emerging from round-to-oval forms)
Hwp1 is particularly important because it is a substrate of mammalian transglutaminase.[1]
This transglutaminase ability has two implications, one (in fungus pathogenicity) proved, and the other (in food proteins potential pathogenicity) hypothetical.
Fungus pathogenicity
Hwp1 has been proven to be involved in oral candidiasis. Candida albicans Hwp1 allows through the use of transglutaminase from the host (human beings, for example) to adhere to human epithelial cells with the strength of a covalent, isopeptide bond (the same strength in which human body proteins are built). This ability is highly related with Candida albicans being the prevalent Candida species in all types of candidiasis. Other candida species don't have the Hwp1 protein.
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Hwp1 - Gluten molecular mimicry
Hwp1 of Candida albicans shares similar sequence homology of amino acids with gliadin (α- and γ-gliadins) of gluten protein. This homology appears between fragments of hwp1 sequence and α-gliadin and γ-gliadin T-cell epitopes in celiac disease.[2][3][4]
See also
References
- ^ Williams DW, Jordan RP, Wei XQ, Alves CT, Wise MP, Wilson MJ, Lewis MA (2013). "Interactions of Candida albicans with host epithelial surfaces". Journal of Oral Microbiology. 5: 22434. doi:10.3402/jom.v5i0.22434. PMC 3805843. PMID 24155995.
- ^ Stepniak D, Koning F (2006). "Celiac disease--sandwiched between innate and adaptive immunity". Human Immunology. 67 (6): 460–8. doi:10.1016/j.humimm.2006.03.011. PMID 16728270.
- ^ Goldman DL, Huffnagle GB (2009). "Potential contribution of fungal infection and colonization to the development of allergy". Medical Mycology. 47 (5): 445–56. doi:10.1080/13693780802641904. PMID 19384753.
- ^ Meresse B, Ripoche J, Heyman M, Cerf-Bensussan N (2009). "Celiac disease: from oral tolerance to intestinal inflammation, autoimmunity and lymphomagenesis". Mucosal Immunology. 2 (1): 8–23. doi:10.1038/mi.2008.75. PMID 19079330.