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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Gene Review: 

SARM1  -  sterile alpha and TIR motif containing 1

Homo sapiens

Synonyms: KIAA0524, MyD88-5, SAM domain-containing protein 2, SAMD2, SARM, ...
 
 
      
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High impact information on SARM1

  • Injury-induced axon self-destruction (Wallerian degeneration) requires SARM1 [1]. This function is conserved from insects to mammals.
  • SARM1 promotes neuronal cell death in response to some stimuli  [2] [3] [4].
  • SARM1 functions within the axon after injury to induce locally-mediated destruction [5].
  • TLR-independent control of innate immunity in Caenorhabditis elegans by the TIR domain adaptor protein TIR-1, an ortholog of human SARM [6].
  • Unlike all known TIR-domain adapter proteins, overexpression of the human TIR-1 homologue, SARM, in mammalian cells was not sufficient to induce expression of NF-kappaB or IRF3-dependent reporter genes that are activated by Toll-like receptor signaling [7].
  • A 0.4-kb antisense transcript was coordinately expressed with the SARM gene in the kidney and liver, while in the brain and malignant cell lines, it appeared independent of SARM gene transcription [8].
 

Biological context of SARM1

 

Other interactions of SARM1

  • Two additional adaptors are present in humans, termed Trif-related adaptor molecule (TRAM) and sterile alpha and HEAT-Armadillo motifs (SARM) [9].
  • SARM1-SARM1 homotypic interactions are mediated by sterile alpha motif (SAM) domains  [10].

References

  1. dSarm/Sarm1 is required for activation of an injury-induced axon death pathway. Osterloh, J.M., Yang, J., Rooney, T.M., Fox, A.N., Adalbert, R., Powell, E.H., Sheehan, A.E., Avery, M.A., Hackett, R., Logan, M.A., MacDonald, J.M., Ziegenfuss, J.S., Milde, S., Hou, Y.J., Nathan, C., Ding, A., Brown RH, J.r., Conforti, L., Coleman, M., Tessier-Lavigne, M., Züchner, S., Freeman, M.R. Science. (2012) [Pubmed]
  2. MyD88-5 links mitochondria, microtubules, and JNK3 in neurons and regulates neuronal survival. Kim, Y., Zhou, P., Qian, L., Chuang, J.Z., Lee, J., Li, C., Iadecola, C., Nathan, C., Ding, A. J. Exp. Med. (2007) [Pubmed]
  3. Mitochondrial dysfunction induces Sarm1-dependent cell death in sensory neurons. Summers, D.W., DiAntonio, A., Milbrandt, J. J. Neurosci. (2014) [Pubmed]
  4. Activation of the innate signaling molecule MAVS by bunyavirus infection upregulates the adaptor protein SARM1, leading to neuronal death. Mukherjee, P., Woods, T.A., Moore, R.A., Peterson, K.E. Immunity. (2013) [Pubmed]
  5. Neurobiology. SARM1 activation triggers axon degeneration locally via NAD⁺ destruction. Gerdts, J., Brace, E.J., Sasaki, Y., DiAntonio, A., Milbrandt, J. Science. (2015) [Pubmed]
  6. TLR-independent control of innate immunity in Caenorhabditis elegans by the TIR domain adaptor protein TIR-1, an ortholog of human SARM. Couillault, C., Pujol, N., Reboul, J., Sabatier, L., Guichou, J.F., Kohara, Y., Ewbank, J.J. Nat. Immunol. (2004) [Pubmed]
  7. Requirement for a conserved Toll/interleukin-1 resistance domain protein in the Caenorhabditis elegans immune response. Liberati, N.T., Fitzgerald, K.A., Kim, D.H., Feinbaum, R., Golenbock, D.T., Ausubel, F.M. Proc. Natl. Acad. Sci. U.S.A. (2004) [Pubmed]
  8. A novel human gene (SARM) at chromosome 17q11 encodes a protein with a SAM motif and structural similarity to Armadillo/beta-catenin that is conserved in mouse, Drosophila, and Caenorhabditis elegans. Mink, M., Fogelgren, B., Olszewski, K., Maroy, P., Csiszar, K. Genomics (2001) [Pubmed]
  9. The Toll-IL-1 receptor adaptor family grows to five members. O'Neill, L.A., Fitzgerald, K.A., Bowie, A.G. Trends Immunol. (2003) [Pubmed]
  10. Sarm1-mediated axon degeneration requires both SAM and TIR interactions. Gerdts, J., Summers, D.W., Sasaki, Y., DiAntonio, A., Milbrandt, J. J. Neurosci. (2013) [Pubmed]
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