Lymphotoxin alpha
From Wikipedia, the free encyclopedia
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Lymphotoxin alpha (TNF superfamily, member 1)
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| PDB rendering based on 1tnr. | ||||||||||||||
| Available structures: 1tnr | ||||||||||||||
| Identifiers | ||||||||||||||
| Symbol(s) | LTA; LT; TNFB; TNFSF1 | |||||||||||||
| External IDs | OMIM: 153440 MGI: 104797 HomoloGene: 497 | |||||||||||||
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| RNA expression pattern | ||||||||||||||
| Orthologs | ||||||||||||||
| Human | Mouse | |||||||||||||
| Entrez | 4049 | 16992 | ||||||||||||
| Ensembl | ENSG00000204496 | ENSMUSG00000024402 | ||||||||||||
| Uniprot | P01374 | Q542S2 | ||||||||||||
| Refseq | NM_000595 (mRNA) NP_000586 (protein) |
NM_010735 (mRNA) NP_034865 (protein) |
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| Location | Chr 6: 31.65 - 31.65 Mb | Chr 17: 34.81 - 34.81 Mb | ||||||||||||
| Pubmed search | [1] | [2] | ||||||||||||
Lymphotoxin alpha (TNF superfamily, member 1), also known as LTA, is a human gene.
Lymphotoxin alpha, a member of the tumor necrosis factor family, is a cytokine produced by lymphocytes. LTA is highly inducible, secreted, and exists as homotrimeric molecule. LTA forms heterotrimers with lymphotoxin-beta which anchors lymphotoxin-alpha to the cell surface. LTA mediates a large variety of inflammatory, immunostimulatory, and antiviral responses. LTA is also involved in the formation of secondary lymphoid organs during development and plays a role in apoptosis.[1]
[edit] See also
[edit] References
[edit] Further reading
- Körner H, Sedgwick JD (1997). "Tumour necrosis factor and lymphotoxin: molecular aspects and role in tissue-specific autoimmunity.". Immunol. Cell Biol. 74 (5): 465–72. PMID 8912010.
- Wang Q (2005). "Molecular genetics of coronary artery disease.". Curr. Opin. Cardiol. 20 (3): 182–8. PMID 15861005.
- Copeland KF (2006). "Modulation of HIV-1 transcription by cytokines and chemokines.". Mini reviews in medicinal chemistry 5 (12): 1093–101. PMID 16375755.
- Elewaut D, Ware CF (2007). "The unconventional role of LT alpha beta in T cell differentiation.". Trends Immunol. 28 (4): 169–75. doi:. PMID 17336158.

